A CLINICAL STUDY ON THE EFFECT OF MANJISTADI LEPAM AND

MANJISTA KWATHAM IN VYANGA ROGA

Dissertation submitted in partial fulfillment for the degree of
Doctor of Medicine (Ayurveda)
In
Kayachikitsa
By

Dr. N. Sandhya Sundeepa

Co-Guide
Dr.S.Ramalingeswara Rao
M .D (AY)
T.A / Lecturer
P.G. Department of Kayachikitsa

Guide
Dr.Prakash chander
M .D (A .Y )
Professor & H.O.D
P.G. Department of Kayachikitsa

Dr.B.R.K.R.Govt.Ayurvedic College / Hospital

Hyderabad

Dr.N.T.R University of Health Sciences

Vijayawada.AP, India
2005-2008
1

r. N.T.R UNIVERSITY OF HEALTH SCIENCES

Vijayawada, A.P

Post graduate Department of Kayachikitsa

Dr.B.R.K.R.Govt. Ayurvedic College / Hospital
Erragadda, Hyderabad

CERTIFICATE
This is to certify that Dr.N.Sandhya Sundeepa of M.D. (Ayu) Kayachikitsa has
worked for the thesis on the topic A clinical study on the effect of manjistadi lepam
and manjista kwatham in vyanga rogaas per the requirements of the order laid down
by the Dr.N.T.R.University of Health Sciences, for the purpose. The hypothesis
submitted by her in the first year MD (Ayu) is one and the same to that of the dissertation
submitted.
I am fully satisfied with her work and hereby forward the dissertation for the
evaluation of the adjudicators.

Date
Place

: / / 2008
: Hyderabad

DR.PRAKASH CHANDER
MD(AY )
Professor & H.O.D
Post graduate Dept. of Kayachikitsa
Dr.B.R.K.R.Govt.Ayurvedic College,
Hyderabad, A.P.

Dr.N.T.R UNIVERSITY OF HEALTH SCIENCES

Vijayawada, A.P

Post graduate Department of Kayachikitsa

Dr.B.R.K.R.Govt. Ayurvedic College / Hospital
Erragada, Hyderabad

CERTIFICATE
This is to certify that Dr.N. Sandhya Sundeepa is a final year Post-graduate
scholar of M.D.(Ay) in the speciality of Kaya Chikitsa of this institute. She has written the
dissertation entitled A clinical study on the effect of manjistadi lepam and manjista
kwatham in vyanga roga in partial fulfillment for the degree of Doctor of medicine
under our direct supervision and guidance. The candidate has put in all his efforts in the
successful completion of this thesis.
Hence this dissertation is recommended for the evaluation of the adjudicators.

Dr.S.RAMALINGESWARA RAO
M.D (A y)
T.A / Lecturer
Post graduate Dept. of Kayachikitsa
Dr.B.R.K.R.Govt.Ayurvedic College,
Hyderabad, A.P.

Dr.PRAKASH CHANDER
MD(AY )
Professor & H.O.D
Post graduate Dept. of Kaya Chikitsa
Dr.B.R.K.R.Govt.Ayurvedic College,
Hyderabad, A.P.

Date : / / 2008
Place : Hyderabad

ACKNOWLEDGEMENTS
At this unforgettable moment, I prostrate my head on the feet of our Lord for
deputing me to serve the mankind.
I am deeply indebted to my honorable guide Dr.Prakash Chander, professor,
and H.O.D.P.G Dept. of Kayachikitsa and my sincere thanks to him for his unending
inspiration, valuable teachings, thought provoking ideas, constructive criticism and
encouragement at all levels in the progress of the work.
I express my heartful gratitude to Dr.V.Vijaya Babu, M.D.(Ayu), Reader, P.G
Dept. of Kayachikitsa, for his thought provoking lecturers, his constant support,
guidance, encouragement and kind co-operation in all aspects.
The practical outlook, clinical experience, proficient scrutiny of my co-guide
Dr.S.Ramalingeswara Rao has helped me to complete my work. I fall short of words as
well as eloquence to express my gratitude but Thanksholds formal.
I express my sincere thanks to Dr.B.Venkataiah, M.D, prof(retd) for his basic
guidelines, encouragement and suggestions in the selection of the topic.
I extend my thanks to the principal Dr.M.Sada Siva Rao, for providing facilities
for the research work.
It gives me immense pleasure to offer gratitude to my esteemed teachers,
Dr.v.vijaya laxmi, Dr.C.H.Rama Devi, Dr.P.Rama Rao for their valuable teachings,
suggestions, and guidance.
With deep sense of gratitude, I express my thanks to my co-scholars Dr.M.K.Jha,
Dr.Namratha, Dr.V.Jaya Laxmi and all my colleagues for their kind co-operation
during my course of study.
My special thanks to Smt.C.Ratna Kumari, librarian Research library GAH,
Sri.M.Ramgopal photographer Research Dept and Smt.G.C.R.Varakumari librarian
and P.Sudhaker library assistant GAC, Hyderabad.
My love and gratitude to my father Sri.N.J.Divaker, Lec(retd) for the confidence
he instilled in me.
I bestow my respects to my mother Smt. N.Madhurakshi Ass.prof(retd), who
has been a source of inspiration for all my academic achievements.
I am extremely thankful to my brother N.Ronald, Sister N.Saritha Saleena for
their co-operation by providing timely suggestions in completing the thesis work.
I am highly grateful to my unty Smt. O. Sowndarya Tilaka, sisters M.Sowjanya
Priyadarshini, M.Sowmya, and M.Sowdhamini for helping me in tacking care of my son,
during my course period.
It is my great pleasure to thank my husband M.Gnana Raju for his constructive
criticism, which has made me firm and dedicated to my work.
4

Special thanks to my son M.Sam Dheeraj for his understanding and co-operation,
with out creating any disturbance during my work.
I wish to express my special thanks to Smt.Katheeja for helping me in typing
work.
Last but not least, I thank all my patients, especially K.Sudhamani for introducing
many patients, who have co-operated with me by coming for the reviews and informing
the response periodically.
My special thanks to all my well-wishers and I lack words to express my all
associated acquitants and son on who has directly or indirectly helped me to shape this
thesis.

(Dr.N.Sandhya Sundeepa)

ABBREVIATIONS

Ada.Veda -

Adarvana vedam

Ag.Pu

Agnipuranam

A.H.

U.S
Su.S
Sa.S

Astanga Hrudhayam
Utarra stanam
Sutra stanam
Shareera sthanam

A.SA -

B.P

Be.S

Bhela samhita

Ch.Up

Chandogya Upanishad

C.S

Charaka Samhita
Chikitsa Stanam
Indriya Stanam
Vimana Stanam
Sutra Stanam
Shareera Stanam
Chakra Datta

Astanga Sangraham

Bava Prakasha
Po.K Poorva Kandam
Ma.K Madyama Kandam

Ch.Da

M.N

Madava Nidanam

S.K.D

Shabdha Kalpa Drumam

S.S

Ch.S
In.S
Vi.S
Su.S
Sa.S

Su.S Sa.S Ni.S Ch.S S.D.S

P.K U.K Sa.E.D
Va.Se
V.P
Yo.Ra
-

Susrutha Samhita
Sutra Stanam
Shareera Stanam
Nidana Stanam
Chikitsa Stanam
Sharangadhara Samhita
Poova Kandam
Uttara Kandam
Sanskrit English Dictionary
Vanga Sena
Vachaspatyam
Yoga Ratnakara

LIST OF TABLES
1. Showing the skin layers according to Charaka
2. Showing the skin layers according to Susrutha
3. Showing skin types as per prakruthi
4. Showing skin types as per sara
5. Showing the types of ahita ahara
6. Showing classification of hyperpigmentation according to its spread
7. Showing classification according to the color of pigmentation in genetic and
naevoid factors
8. Showing classification according to the color of pigmentation in acquired
hypermelanosis
9. Showing properties of rasa
10. Showing varities of madhu
11. Showing age-wise distribution of patients
12. Showing gender-wise distribution of patients
13. Showing marital-status wise distribution of patients
14. Showing religion-wise distribution of patients
15. Showing occupation wise distribution of patients
16. Showing education wise distribution of patients
17. Showing social-status wise distribution of patients
18. Showing locality-wise distribution of patients
19. Showing diet wise distribution of patients
20. Showing prakruthi-wise distribution of patients
21. Showing Cronicity-wise distribution of patients
22. Showing the level of discoloration in patients
23. Showing hormone therapy-wise distribution of patients
24. Showing prognosis of lesion-wise distribution of patients
25. Showing type of distribution-wise incidence in patients
26. Showing nidana-wise distribution of patients
27. Showing etiological factors-wise distribution in patients
28. Showing number of patches-wise distribution of patients
29. Showing location-wise distribution of patches in patients
30. Showing the T and P Values
7

31. Showing the total effect of the therapy

LIST OF FIGURES
1. Components of the integumentary system
2. Types of cells in the epidermis
3. Layers of epidermis
4. Synthesis of tyrosine from phenylalanine
5. Metabolism of tyrosine-biosynthesis of melanin
6. Diagram of a melanocyte showing dendrites and different stages of melanosomes.
7. Biochemical pathway for synthesis of melanin
8. Biochemical pathway for synthesis of phaeomelanin
9. Diffuse brown pigmentation of the cheek in chloasma
10. Root and plant of manjista
11. Dry roots of manjista
12. Madhu
13. Manjista kwatha churna
14. Fine powder of manjista and madhu
15. Handi-lens

LIST OF PLATES
1. Observation chart - 1
2. Observation chart - 2
3. Observation chart - 3
4. Photogarphs of the patients
5. Result chart

INDEX
PART I
SECTION I
SECTION II

INTRODUCTION
REVIEW OF LITERATURE

CHAPTER I

HISTORICAL REVIEW

CHAPTER II

SARIRA RACHANA
ANATOMY OF THE SKIN

CHAPTER III

SARIRA KRIYA
PHYSIOLOGY OF THE SKIN

CHAPTER IV

EXAMINATION OF THE SKIN

CHAPTER V

DISEASE ASPECT
NIDANA
POORVARUPA
ROOPA
SAMPRAPTHI
RUGVINISCHAYAM
SADYA-ASADYATA
UPADRAVA
CHIKITSA
PATHYA-APATHYA

CHAPTER VI

VYANGAM (PSYCHO PHYSIOLOGICAL

APPROACH)

CHAPTER VII

DRUG REVIEW
PART - II

SECTION III
SECTION IV
SECTION V
SECTION VI
SECTION VII
SECTION VIII

MATERIALS AND METHODS

OBSERVATIONS AND RESULTS
DISCUSSION
SUMMARY
CONCLUSION
APPENDIX
SPECIAL CASE SHEET FOR VYANGAM
BIBILOGRAPHY

Introduction

10

CHAPTER: I
INTRODUCTION
The word beauty is derived from the French word beauwhich is used to
mean fine and of late beloved too. On contrary, the word sundara which is the
adjective of the noun soundarya is derived from the Sanskrit root ardrikaroti chittam
iti meaning that which melts (is pleasing to) the mind. The difference in the concept
as well as the depth in the choice of the root denoting the suitable meaning are evident.
Sayings such as beauty lies in the eyes of the beholder and a thing of beauty is a joy
forver denote the subjective and objective aspects of beauty respectively. The Sanskrit
root ardrikarana suits both these aspects ably.
In modern science papillary dilatation is taken to be the subjective reaction to
sighting a pleasant or loved object. The mind automatically is more open and responsive
to the object in question, there by citing the psycho-social implications of beauty in
everyday life. This fact more than amply illustrates the effect of ardikarana on the
chitta. This chitta or a subtle psyche cannot be pleased but in close conjunction with the
atma or the eternal soul.
Swasthya and soundarya (Beauty is the essence of good health)
samadosha samagnischa samadhathumalakriya !
Prasannatmandreyamanah swasthya etyabhedeyathe [s.s.su 15/41 ]
We may note that the first half of this definition points out the physical state of
health with accent on the balanced functioning of the doshas, dhatus, malas, and agni.
The second half brings the aspect of the psyche and the eternal soul into focus which is
the inherent uniqueness of this science of life and excluding which any system of Indian
philosophy is incomplete.
Certainly, this feeling of well being, prasanna atma, indriya, and manas is
impossible without a basic sense of social acceptability and self assurance that is a result
of an appealing outward appearance. With modern concepts of health changing for every
decade, the WHO has finally settled for a definition for health as a feeling of complete
well being and not merely the absence of disease which has a close resemblance with
the swastha concept of ancient Ayurveda no dought, re-establishing its eternity and
supremacy.
Oriental sciences such as Ayurveda prefer calling any knowledge Anadi that is
not having a certain origin and inherent in any life form and Ananantam continouously
being improved upon. This is why the theories of Ayurveda are based on certain
fundamental and eternal concepts.
This simplistic approach in the concepts of Ayurveda has not been understood by
the changing generations. Ayurvedic and allied literature like the Vedas, Artha shastra,
and Kama sutra are resplendent with references on cosmetically rewarding internal and
11

external remedies. The present era lacking insight into its inherent versatility, and fed on
complicated western concepts, is looking forward for the natural herbal remedies.
Modern medicine has conquered life-threatening diseases and infections with the
advent of antibiotics. Modern cosmetology was born-albeit less than half a century ago as
compared to Ayurveda, which had a varnya concept centuries ago. Markets were flooded
with clinically approved topical applications, many of which gave satisfactory results and
people lapped them up to rid themselves of scars, patches, spots, rashes, pimples and
other skin ailments which were alarmingly on the rise especially in this century.
Then, suddenly all the euphoria died down with disturbing reports of the longterm damage caused by laboratory-created chemical formulations and the average
cosmetic-user became suddenly wary about these safe scientifically approved medicines.
As a direct result of this increased awareness, the modern cosmetic approach in
recent years has radically changed its hitherto attitude towards traditional medicine
which is still largely reliant on plants. This has developed a resurgent in herbalism. At
this juncture, with herbs ruling almost 60-70% of world market, a lot more people are
willing to use herbal products for health problems and especially for skin ailments.
Varnya and complexion
The colour and appearance of the face skin is known as complexion. Varnya
aushadas enhance the complexion, but according to some texts
vreeyatha ethi varna (vachaspatyam)
That which attracts or that which is selected is called varna.
varnya varnaya hitam(chakrapanidatta)
That which is conducive to the colour or that quality of attraction is a varnya dravya.
Here, a varnya dravya is not thought of as a lightener of the complexion but as an
instrument that restores and retains the natural hue and tone of the skin.
Varnya aushadhas have roughly been translated as cosmetics. Some say that the
modern day cosmetics has been confined to an external application on the skin, not
concerning itself with internal metabolism, while most of Ayurvedic varnya aushadahas,
including manjista used in present study, aim at correcting the factors distorting skin
colour from within and are to be taken orally.
Vyangam
Vyangam is one of the skin disorders described in Ayurveda under the kshudra
roga prakaranam. Vyangam is the disorder which is primarily seen on the face
(mukhamagatyam) according to brihat-trayi and laghu-trayi.
In this suppressed and crowded atmosphere, the most significant development is
the identity crisis and later, the exaggerated hunger for recognition otherwise known as
attention seeking. This is the urge that spurs man on to gain notice by excelling in all
aspects, personal appearance being the closest and immediately rewarding.
12

Indian philosophers have always held that the face is a reflection of the mind.
Now a days people have become more beauty conscious and are ready to spend handful
of money for cosmetic purposes. Commercializing change in the view of the people and
craze for the ayurvedic herbal products, many companies like Fair and lovely and
Emami has come up with ayurvedic fairness creams.
Vyangam is not a major disease but it may be a symptom of an underlying
disease. People get depressed by there looks i.e.with black patches on the face, and may
end up in many psychological problems.
This is an exceedingly common problem faced by many patients after
adolescence, particularly women. The skin becomes more darkly pigmented and the
pigmentation in some sites is particularly marked. Acurious pattern of uniform
pigmentation may occur on certain areas of the face, the cheeks, central zone of the forehead, the perri-ocular area, chin and temple. Skin may become pigmented to give a masklike appearance. The darker the normal skin colour, the more marked this alteration is.
There are many factors such as the sun-light i.e., cosmic rays (photo-sensitive
dermatitis), pollution, emotional upheavals, hormones, drugs and stress that may cause
the above problem. Skin is subjected to various external and internal onslaughts,
therefore vyangam needs special attention in view of the above factors.
Despite of rapid advancement in modern medicine there is no adequate and
complete treatment for this disorder even today. Although the pigmented areas are not
easy to lighten there are some preparations containing monobenzone or benoquin, with
side effects of dermatitis and excessive hypopigmentaton. Above medicine is reportedly
helpful but the desired effects are not seen.
Such a situation forces the research of other system of medicine to evolve a
comprehensive clinical trial of innumerable preparations prescribed for this disorder.
Hence the present work titled as A clinical study on the effect of manjistadi lepam
and manjista kwatham in vyanga rogamis undertaken.
Vyangam is caused by vitiation of pitta, the drugs selected are for pacifying pitta
i.e. manjista choornam with madhu for lepam and manjista kwatham internally. Manjista
is the drug of choice because it is mentioned as varnyam (charaka), pittasamshamanam,
raktashodhaka, (susrutha), and varnya krith (bhavamishra).
The properties of manjista are madhura, tikta, kashaya rasa, and guru,ushna
gunas, it is available freely, very economical with out any controversy, hence manjista is
selected along with madhu, which is in turn mentioned as yogavahi and varnyam.
The present study is aimed at establishing the efficiency of drugs/therapies
mentioned in classical literature in the management of vyangam. Manjista along with
madhu the promising formulation are selected for lepanam and kwatha panam
respectively. Results are recorded systematically and statistically after proper follow-up.

13

Historical review

14

CHAPTER: II
HISTORICAL REVIEW
Charaka samhita has grouped drugs under their curative and cosmetic activity as
jeevaniya, vayah stapana etc.1 apart from having an entire group of ten drugs (varnya
2
dashaymani) with varnya property. Many day to day activities or dina charyas have been
attributed with life-giving properties. Some of them are danta dhavana, gandusha,
shirastaila tarpana, abyanga, dhumapana and nasya. These not only have an impact on the
hygiene of the individual but also purify the blood, improve its supply to all the organs,
and clear the skin by flushing out toxins.
Achrya charaka has also indicated the importance of diet in maintenance of
3
beauty. The sense of normality and abnormality in appearance is reflected in the
classification of the ashtaninditiya purushas.4
The significance of beauty seems to have only grown greater by the period of
Susruta where disfiguring skin disorders has been allotted an entire chapter, kshudra
rogas.5 An entire range of drugs to prevent scar formation has been formulated under the
gana vaikritapaha, the upakrama for vrana.6
In the medieval period, where Rasa shastra began to dominate the proceedings,
cosmetic science caught the fancy of the rulers especially during the Moghul rule, and we
see inclusion of depilatory lepas, varnya lepas, snana and udvartana aiming at
7
improvement of the varna and prabha of the individual in Sarangadhara samhita. Still,
the original concept of beauty being only a part of health was retained throughout.

The description of the skin diseases are basically found from vedic period.
Vedas
In Rigveda, some names of skin diseases are mentioned, but they are not described in
detail.
In Adharvanaveda twak rogas have been dealt elaborately. Description of diseases
along with the treatment aspect has been discussed.
naktajathasyoushade ramekrushne asiknicha !
edda rajani rajai kilasa palitha cha ya the
The medicinal plants like rama, Krishna, asikini are the plants which bloom at
night times and has properties to give natural colour to the skin. By application of lepa of
above plants white colour of kilasa and palitham can be changed. 8
shama sarupakaraneprutivya adubdbutha !
edam shu pra sadaya puna rupane kalpaya
The herb called shama has the properties to restore the natural colour of th skin.
Like wise aasuri herb is also being described for the treatement of kilasa. 9
After vedic period, description of twak rogas canbe seen in upanishades,
puranas, samhitas and other latest Ayurvedic texts.
15

Upanishads:
In chandogya Upanishad, we find a reference regarding pama roga which is a type of
twak roga. In this, a story about Raikwa is told in which Jaanakshuti goes to Raikwa in
quest of knowledge and finds him lying underneath a cart and suffering with pama roga.10
Mahabharat:
na rajyamarshami twak doshopahathendriya
We find a reference about twak roga in Mahabharatam. Shantanus elder brother Devaapi
was declared unqualified to rule the kingdom because he was suffering with twak roga.11
Puranas:
kushtinacha tadha shastham panarda khadirodakam
1.In Agnipuranam, food regmens for khusta rogi, and use of drinks prepared from Kadira
12
along with herbal compound preparations like potions and pastes are described.
2.In Garudapuranam, the first chapter is called sarva roga nidana in which, we find the
description of kusta, visarpa, pandu and shodha roga nidanas.
Samhitas: (Bruhatraye)
1.Charaka samhita: A brief description of charma rogas, as shonitaja rogas has been delt
in vidhishonitheeya adyaya along with treatement.
kandhukotapidakakustacharmadaladayha
Kandu,kota,pidaka,kusta, and charmadala.13 Charaka mentioned some other skin
diseases viz. visarpa,pidaka in trisothiya adyaya.14
yasya prakupitta shonita prapya shushathi !
Tilaka piplava vyanga neelika tasya jayathe
When the aggravated pitta gets dried up in combination with rakta, causes skin
diseases like tilaka, piplava, vyanga and neelika.15 Vyanga has been mentioned as
bahirmargaja roga. 16
2.Susrutha samhita: The khudra roga was first and foremost coined by susrutha in
nidana stana. In this chapter 44 kshudra rogas are described, majority of these are skin
diseases. one among them is vyangam.
3.Vagbhata samhitas: Astanga sangraha has described 37 khudra rogas and Astanga
hrudayam has described 36 khudra rogas, vyangam is one amongst them.

Laghutraye

16

1. khudra rogas were given prominence by lagutraye. Madhavakara mentioned about 43

khudrarogas in 55th chapter and about vyangam in 55/38-39.
2. Sharangadhara has mentioned about 60 khudra rogas in purvakandha,about vyangam
in 7/95.
3. Bavaprakasha said about vyangam in khudrarogadikara chapter 14/36 in madyama
kandha chaturdha bhaga.
Finally the other Ayurvedic classical texts such as Yogaratnakara, Bhaisajya
ratnavali, Vaidya chintamani, Basavarajeeyam, Chakradatta etc. have kept up the trend of
ancient dermatology which is existing up to this date.
History of dermatology of other systems of medicine are as follows:1.The Chinese system of medicine falls in the period of 3000 to 2000 BC. In this system
they have given more or less accurate description of leprosy, scabies, icthyosis, vitiligo,
eczema, acne, carbuncles, warts, corn etc.
2.Hippocrates (460 to 375 BC) made the first attempt separating medicine from religious
cult. He described many skin diseases and divided them into two groups according to
their exogenous and endogenous causes.
3.The Roman authour Celsus mentioned about skin diseases in 8
medicine libro acts.

th

volume of De

4.Dermorbus cutaneous is the first book of the skin diseases on this earth written by
mercurialis in 1571.
References:
1. C.S.Su.S 4/8
2. C.S.Su.S 4/10
3. C.S.Su.S 5/8
4. C.S.Su.S 21/3
5. S.S.Ni.S 13
6. S.S.Ch.S 20
7. Sa.S.U.K 11/9-13
8. Ada.Veda 1/23-1
9. Adar.veda 1/23-4
10. Ch.Up 4-1-8
11. Briha.Devatta 8-156
12. Ag.Pu 279/11-16
13. C.S.Su.S 26/16
14. C.S.Su.S 18/23-24
15. C.S.Su.S 18/25
16. C.S.Su.S 11/55

Previous work done on the subject:

17

There is no work done on internal use of manjista in the Ayurvedic side. Though some
work has been done on the Ayurvedic approach to cosmetology.
1.There has been a theoretical compilation on the cosmetics of Ayurveda in the manual of
external diseases-Bahya Roga Nidarshaka, published by the Baidyanath Ayurveda
Bhavan, Nagpur in 1976.
2.A theoretical work on the correlative aspect of the Agnibala and varna has been done
by V.Shukla 1965.
3.The Ayurvedic magazine Dhanvantari had come out with an exclusive edition 1983 on
saundarya in the Ayurvedic view. Some of the papers presented are given belowa)Tomar G. had given a note on the Ayurvedic concept of maintenance of beauty.
b)Sharma H.S had published a paper on dealing with youvanapidakas, nyacha and
vyanga.
c)The role of panchakarma in the maintenance of beauty had been discussed by Kasture
H.S.
4.Goyal R,K had established a relation between prabha, chhaya and pratichhaya, shareera
Dept Jamnagar, 1969.
5.A study on varnyakara dravyas with an appraisal of the varnya principles had been
carried out by Nair R.V, DG.Dept. Jamnagar 1971.
6.Shah L.D had conducted a study on the pathological aspects and treatments of kshudra
kustas,K.C Dept, Jamnagar 1975.
7.The cosmetic approach of Ayurveda with special reference to varnya was established
by Mitendra P.Gohil Dept of Basic Principles, Jamnagar 1987.
8.The clinical management of vyanga with manjista madhu alepana with and without
kumkumadi taila nasyam was worked upon by Anita Lomite,S.S.P Dept,Hyderabad 1999.
9.An evaluative study on the botanical sources of tunga with special reference to its
varnya property by Madhavi M.Chandramohan DG.Dept, Hyderabad 2002.
10.Standardisation of purification process of guggulu and evaluative study on its varnya
property by R.Sirisha Devi DG.Dept, Hyderabad 2007.

18

Shareera rachana

Shareera rachana
Anatomy of the skin

CHAPTER: II
19

RACHANA OF THE TWAK

NIRUKTHI:
twacha samvarane, tanothi visthara yathiti(S.K.D)
twacha sparshavad dravya gocharam
twachati mamsam veshtayathi(V.C.P )
Twak covers muscles, bones, and all other organs, it envelopes entire body. Twak
gives protection, acts as excretory and sensory organ.
PARYAYPAD:
Twak, twacham, charma, asrugdhara, indriyaveshasha
Sparshagrahaka, valkala, dehavyapini 2

UTPATHI OF TWAK:
3

Twak forms as an upadhatu of mamsa from prasada paka during dhatu parinama.

In the sixth month of gestation, twak becomes manifested.

The layers of twak are formed during the development of foetus i.e, garbhavastha

from shukra and shonita by tridosha, during pachamanavasta as cream forms on the
boiled milk. 5

In the panchamahabhutatmaka shareera, datwagnis are the causative factor for

formation of saptatwacha during the process of digestion (pachamanavasta) of rakta
dhatu, just as the cream gets accumulated at the top of the surface of milk after
boiling.

During the pachamanavasta of asruja (blood), layers of skin forms as cream forms
on the milk, purity (twak prasada) of the skin is purity (rakta prasada) of the blood. 7

Twak and rakta are matruja bhavas i.e, entities which are particularly maternal and
are produced from mother. 8
9

Twak is considered as parthiva i.e, predominant in prithvi mahabhuta.

In panchbhutatmaka shareera the formation of twak and its sensory function is due
to rajoguna bahula vayubhuta.

10

SKIN LAYERS:
Skin layers according to Charaka:

11

20

There are six layers of skin, which cover the shadanga shareera
Table 1.Skin layers according to Charaka
No
Skin layer
Description
1. Udakadhara
Sustains the udaka
2. Asrugdhara
Sustains the rakta
3. Triteya
Adhistana for sidma and kilasa
4. Chaturdha
Dadru and kusta sambhava adhistana
5. Panchama
Alaji and vidradhi sambhava adhistana
6. Shasti
If this layer is cut, causes loss off
consciousness. Aromsika of Krishna rakta
varna, appears on stoolamula, which are
difficult to cure.
12

Skin layers according to Susrutha:

There are seven layers of twak formed in garbhavasta from shukra and shonita
Table 2. Showing skin layers according to susrutha
No Name of the layer Thickness in
Manifesting disease
vreehipramana
1. Avabhasini
1/18th
Sidma, padmakantaka, etc
2. Lohita
1/16th
Tilakalaka, nyachha, vyanga
th
3. Shweta
1/12
Charmadala, ajagalika, mashaka
4. Tamra
1/8th
Different kinds of kilasa, kushta
th
5. Vedhini
1/5
Kushta, visarpa
6. Rohini
1
Granthi, apachi, arbudh, galagand
7. Mamsadhara
2
Bhagandhara, vidradhi, arsha
Skin layers according to Vagbhata:
In the Astanga Hridaya, Vagbhata just said that the twak consists of seven layers
and did not go into further details. 13
In Astanga Sangraha, six layers of skin are mentioned and their description is done
14
according to Charaka. The sixth layer is called pranadhara (supporter of life).

ANATOMY OF THE SKIN:

21

fig.1 Components of the integumentary system

Introduction:
An appreciation of the skin, of the natural variations from region to region in the
same individual of the difference that are a reflection not of pathologic changes but of race,
age, occupation and above all physiologic and more specifically, endocrinologic states - an
appreciation of all these variations is necessary for a proper evaluation of the abnormal.
Measurements:
The skin is the largest organ of the human body and accounts for about 16% of total
body weight. In the average man it weighs about 4.8 kgs and in average women it weighs
about 3.2kgs. The surface area of the skin is about 0.25 square meter in the newborn, 1.85
square meters in the average-sized man, and 1.6 square meters in the average-sized women.
The thickness of the entire skin varies from about 0.5 mm in the eyelid to 3-6mm on the
palm or sole. Its specific gravity is about 1.25.
Embryology:
The skin is derived from both ectoderm and mesoderm. The epidermis and its
derivatives along with nerves originate from ectoderm. The remainder of the skin along
with subcutaneous fat is mesodermal in origin. At the beginning of the eigth week after
fertilization the ectoderm consists of simple cuboidal epithelium further which is called
periderm. By the fourth month all layers of the epidermis are formed and each layer
assumes its characteristic structure.
The dermis is derived from mesodermal cells in a zone beneath the ectoderm.
There they undergo a process that changes them into the connective tissues that begin to
form the dermis at about 11 weeks.
22

At about the third foetal month layer of cells forms into multilayered stratum
spinosum. In fourth month basophilic keratohyalin granules are seen in stratum granulosam
of face. In 5th month the desquamated cells of the stratum corneum along with sebaceous
secretion constitute the vernix caseosa. Stratum lucidum is seen at the eight month.15
Microsocpic anatomy of the skin:
Structurally the skin is formed of two main parts which are cemented to each other.
1. The outer thinner portion composed of epithelial tissue is called as Epidermis.
2. The inner thicker part composed of connective tissue is called as Dermis.
Beneath the dermis is a subcutaneous layer also called as, superficial fascia or the
hypodermis is seen.
EPIDERMIS:

fig.2 Types of cells in the epidermis

The epidermis is keratinized stratified epithelium. It contains four principal types of
cells.
a) Keratinocytes
b) Melanocytes
c) Lngerhans cells
d) Merkel cells
A. Keratinocytes:

23

Keratinocytes form the 90% of epidermal cells, which are arranged in four or five
layers and produce the protein keratin. Being the predominant cell type in the epidermis,
keratinocytes are intuitively considered to be the most important cell type for maintaining
epidermal structure integrity. The keratinocyte stem cells are known to locate at the basal
layer of the epidermis, from which they continuously divide in order to provide a sufficient
number of cells for the purpose of differentiating into the upper layers of suprabasal
keratinocytes, granular keratinocytes, and then simply keratins (at the stratum corneum).
These cells form a coherent structural frame by way of desmosome, an intercellular
adhesion network.
Keratin is a tough, fibrous protein that helps protect the skin and underlying tissues
from heat, microbes, and chemicals. Keratinocytes also produce lamellar granules, which
release a water-repellent sealant

B. Melanocytes:
About 8% of the epidermal cells are melanocytes which produce the pigment
melanin. Melanocytes are not original epidermal cells, but migrate into the epidermis
during embryonic development. Originating in the neural crest, melanocytes are important
pigment-producing cells in the skin. Primarily located in the basal layer, melanocytes
synthesize pigments in the form of the melanosomes, which are then transferred by way of
their dendrites to the neighboring suprabasal epidermal layer-located keratinocytes. Once
inside keratinocytes, the melanin granules cluster to form a protective veil over the nucleus,
on the side towards the skin surface. In this way, they shield the nuclear DNA from being
damaged by UV light.
C. Langerhans cells:
Langerhans cells are not original epidermal cells, but are bone marrow derived cells
that migrate into the epidermis during embryonic development. Localized in suprabasal
layers of the epithelia of skin and mucous membrane. Langerhans cells are dendritic cells,
with important immune functions. Accounting for about 5% of epidermal cells, they are
professional antigen-presenting cells that come into contact with foreign antigens passing
through the epidermis. Upon internalizing the antigen, the Langerhans cells migrate out
from the skin to regional lymph nodes with the help of integrin molecules, where they
present the processed antigen to T-cells by way of their surface MHC class II molecule,
and co-stimulatory molecules.
D. Merkel cells:
Merkel cells are the least numerous of the epidermal cells. They are located in the
deepest layer of the epidermis, where they contact the flattened process of a sensory
neuron, a structure called a tactile (merker) disc. Merkel cells and tactile discs detect
16
different aspects of touch sensations.

HISTOLOGY:

24

fig3. Layers of the epidermis

The mature epidermis is composed of the following strata
1. The basal cell layer or stratum germinativum / basale
2. The prickle cell layer or stratum spinosum
3. The granular layer or stratum granulosum
4. Stratum lucidum [seen in only thick skin]
5. Stratum corneum
The term Malpighian layer or rete malpighii, as generally used, refers to the
epidermis exclusive of the stratum corneum and stratum lucidum.
1. Stratum Basale:
The deepest layer of the epidermis is the stratum basale, composed of a single row
of cuboidal or columnar kerotinocytes. Some cells in this layer are stem cells that undergo
cell division to continually produce new keratinocytes. The cytoskeleton within
keratinocytes of the stratum basale includes scattered intermediate filaments; called
tonofilaments. keratin protects deeper layers from injury. Melanocytes, Langerhans cells,
and Merkel cells with their associated tactile discs are scattered among the keratinocytes of
the basal layer. The nuclei of keratinocytes in the stratum basale are large, and their
25

cytoplasm contains many ribosomes, a small Golgi complex, a few Mitochondria, and
some rough Endoplasmic reticulum.
2. Stratum spinosum:
Superficial to the stratum basale is the stratum spinosum, where 8 to 10 layers of
many-sided keratinocytes fit closely together. Cells in the more superficial portions of this
layer become somewhat flattened. These keratinocytes have the same organelles as cells of
the stratum basale, and some cells in this layer may retain their ability to undergo cell
division. Bundles of tonofilaments are inserting into a desmosome, tightly joining the cells
to one another. This arrangement provides both strength and flexibility to the skin.
Projections of both Langerhans cells and melanocytes also appear in this stratum.
3. Stratum Granulosum:
At the middle of epidermis, the stratum granulosum consists of three to five layers
of flattened keratinocytes that are undergoing apoptosis. The nuclei and other organelles of
these cells begin to degenerate, and tonofilaments become more apparent. Darkly staining
granules of a protein called keratohyalin are present in this layer, along with membraneenclosed lamellar granules, which release a lipid-rich secretion. The lipid-rich secretion
acts as a water-repellent sealant, retarding loss of body fluids and entry of foreign
materials.
4. Stratum Lucidum:
The stratum lucidum is present only in the thick skin of the fingertips, palms, and
soles. It consists of three to five layers of flattened clear, dead keratinocytes that contain
large amounts of keratin and thickened plasma membranes.
5. Stratum Corneum:
The stratum corneum consists of 25 to 30 layers of flattened dead keratinocytes.
These cells are continuously shed and replaced by cells from the deeper strata. The interior
of the cells contains mostly keratin. Between the cells are lipids from lamellar granules that
help, to make this layer an effective water-repellent barrier. Its multiple layers of dead cells
also help to protect deeper layers from injury and microbial invasion.17
DERMIS:
The second deeper part of the skin, the dermis, is composed mainly of connective
tissue containing collagen and elastic fibers. The few cells present in the dermis include
fibroblasts, macrophages, and some adipocytes. Blood vessels, nerves, glands, and hair
follicles are embedded in dermal tissue. Based on its tissue structure, the dermis can be
divided into two regions.

1. Papillary region
2. Reticular region
1. Papillary region:
26

The papillary region is the superficial portion of the dermis is about 1/5th of the
thickness of the total layer. It consists of areolar connective tissue containing fine elastic
fibers. This contains dermal papillae that house capillaries, corpuscles of touch, and free
nerve endings. Different free nerve endings initiate signals that give rise to sensations of
warmth, coolness, pain, tickling and itching.
2. Reticular region:
The deeper portion of the dermis is called the reticular region. It consists of dense
irregular connective tissue containing bundles of collagen and some coarse elastic fibers. A
few adipose cells, hair follicles, nerves, sebaceous glands, and sudoriferous (sweat) glands
occupy the spaces between fibers. The combination of collagen and elastic fibers in the
reticular region provides the skin with strength, extensibility, and elasticity.
HYPODERMIS:
The tissue below the dermis is called hypodermis, which is abruptly distinct from
the upper layer dermis histologically. The hypodermis is areolar and adipose tissuepredominant region, but is functionally integrated with the upper layer dermis through
nerve, micro vascular, and lymphatic networks and the continuity of hair follicles into the
hypodermis. Mesenchymally derived, the adipocyte is the predominant cell type in this
layer. The tissues in the hypodermis serve as, insulator, cushion, an energy supplier,
protector of the skin and provide mobility over the underlying structures and also contain
nerve endings called lamellated corpuscles that are sensitive to pressure.
APPENDAGES OF THE SKIN:
The appendages of the skin are the nails, the hairs, the sebaceous and sweat glands.
Nails:
The nails are flattened, elastic structures of a horny texture, placed upon the distal
parts of the dorsal surfaces of the fingers and toes. The nail itself is a greatly thickened
stratum lucidum of the skin, and beneath it lies the germinative zone which, together with
the subjacent corium, forms the nail-bed.
The nail increases in thickness from its root to the distal edge of the lunule and the
remainder is of uniform thickness. On an average nails grow about 0.5mm a week. Nails
act as a rigid background for support of the digital pads of the terminal phalanges, and thus
may function in the tactile mechanism.
Hairs:
Hairs vary much in length, thickness, and color in different parts of the body and in
different races of mankind. A hair consists of a root, the part implanted in the skin, and a
shaft (scapus), the portion projecting from the surface. From the capillaries in the papilla
hair derives its nutrition. The hair-follicle consists of two coats an outer or dermic, and an
inner or epidermic.
The shaft of the hair consists, from within outwards, of the medulla, the cortex, and
the cuticle. Hairs are of three types Lanugo hairs (primary hairs), Vellus (secondary hairs),
and Terminal hairs. Growth of a hair occurs at the hair bulb, where the cells capping the
papilla proliferate and form the germinal matrix of the hair.
27

Sebaceous glands:
The sebaceous glands are small, sacculated, glandular organs, lodged in the
substance of the corium. They are found in most parts of the skin, but are especially
abundant in the scalp and face, they are also very numerous around the apertures of the
anus, nose, mouth and external ear, but are wanting in the palms of the hands and soles of
the feet.
The sebaceous gland is situated in the angle which the Arrector muscle forms with
the superficial portion of the hair-follicle and contraction of the muscle thus tends to
squeeze the sebaceous secretion out from the duct of the gland.
Sweat glands:
The sweat glands are found in almost every part of the skin, and are situated in
small pits on the under surface of the corium, or more frequently, in the subcutaneous
tissue, surrounded by a quantity of adipose tissue. They are especially large in those
regions where the amount of perspiration is great, as in the axillae and groin. They are
plenty in palms and soles.
The ceruminous glands of the external auditory meatus are modified sweat glands.
Most of the sweat glands are merocrine in nature i.e., they produce thin watery secretion
without demonstrable changes in the gland epithelium. Apocrine glands produce thicker
secretion by degeneration and shedding of the portion of the epithelial cell nearest the
18
lumen.
References:
1. S.K.D
2. V.P (Vol-IV)
3. C.S.Ch.S 15/17
4. A.H.Sa.S 1/57
5. S.S.Sa.S 4/4a
6. A.H.Sa.S 3/8a
7. A.SA.Sa.S 5/17
8. C.S.Sa.S 3/6
9. C.S.Sa.S 7/16
10. A.H.Sa.S 3/3
11. C.S.Sa.S 7/4
12. S.S.Sa.S 4/4b
13. A.H.Sa.S 3/8b
14. A.SA.Sa.S 5/17
15. Grays Anatomy
16. The skin
17. Animal models of Human Inflammatory Skin Diseases
18. Principles of Anatomy and Physiology

28

Shareera kriya
Shareera kriya
Physiology of the skin

CHAPTER: III
SHAREER KRIYA OF THE SKIN
Twak performs a number of vital functions related to the body. Some of them are
as follows
1. Twak is sparshanendriya.1 Factors known by touch and tactile faculty are
29

governed by vayu mahabhuta.

2. Twak is moola of mamsavaha srotas.3
4
3. It is brajaka pitta stana.
4. Twak acts as site for the absorption of nutrients by the foetus in garbhavastha.5
5. Paste applied in alepa, abyanga, avagaha etc enters in to hair follicles and virya
(potent fraction) permeates through sweat-carrying vessels. 6
6. When the body becomes hot, udaka comes out from hair follicles in the form of
7
sweat. Thus twak regulates the heat.
This being a work on varna vikriti, the factors influencing the varna of the twak
are analysed.
Factors influencing varna:
1.

2.
3.
4.
5.
6.
7.
8.

tasya raso balavarna kara

The foetus draws nourishment from mother in the form of rasa. The rasa (nutritive
8
fluid) promotes strength and complexion.
During garbhavastha varna is formed from rasaja and satmyaja bhava. 9
As per mythology, kanti or the glow of complexion is ruled by the Aswini
kumaras. 10
Among the mahabhutas, tejomahabhuta is the major factor influencing pitta, ushma,
11
kanthi and rupa of the body.
Varna and teja are due to agni mahabhuta.12
The pitta located in the skin is bhrajaka pitta, it helps in exhibition of color and
complexion.13
Prakruthi and vikruthi of brajaka pitta shows effect on varna, bhaya, krodha and
harsha. 14
udanavatasya balavarnasmruthikriya
Among five types of vata, udanavata affects the varna15

Normal and abnormal skin colour

Normal skin color:
1. With the predominance of tejomahabhuta, color formation is said to take place in
the following manner
Udaka---goura varna
Prithvi---krishna varna
Prithvi + akasa---krishnashama varna
16
Udaka + akasa---gourashama varna
2. Charaka has described normal colour to be of four types Krishna, krishnashama,
17
shamavadata, avadata.

Abnormal skin color:

1. The atikrishna, atigaura varna are mentioned under ashtanindita purushas.

18

2. Charaka has described abnormal color to be of five types neela, shama, tamra,
hareetha, shukla.

19

Chhaya and prabha:

30

Chhaya and prabha are the factors having a very close relation with skin colour.
Chhaya is said to mask the varna and is perceived only in close proximity whereas prabha
enhances the complexion and catches the eye from a distance itself. 20
Types of chhaya:
According to panchamahabhutas chaaya are classified in to five types
1. Nabhasi chhaya nirmala, neelavarna, snehayukta, saprabha
2. Vayavi chhaya ruksha, shavaruna, hataprabha
3. Agneya chhaya vishudha rakta, deeptabha, darshanapriya
4. Ambasi chhaya shudha vaidurya, vimala, susnigdha
5. Parthiva chhaya sthira, snigdha, Ghana, shlakshna, shama, shweta
Among the above, vayaviya alone is considered nindita (abnormal). While the
others fall under the purview of normal.21
Types of prabha:
Prabha based on color is of seven types rakta, peeta, sita, syava, harita, pandu,
and asita.
Varna is normal from birth to death except in case of arishta lakshana where
abnormal chhayas may indicate death. 22
Prakriti:
Prakriti is a result of, status of the parents of the individual during the
shukraartava samyoga, Kala, garbhashaya prakriti and pancha mahabhuta vikara
swabhava.23 This, coupled with the behaviour of the mother during pregnancy including
her food habits along with the atmaja bhava of the individual which he carries over from
his previous birth, determines the complexion of the individual.24
Skin type as per prakriti:

25

Table.3 Showing skin types as per prakriti

Prakriti
Skin type
Vata
Ruksha, parushavadana, prominent siras and kandaras
Pitta
Susceptible to piplu, vyanga, tila, pidaka, valipalitha and kalithya
Kapha
Avadata gatra, prasanna, snigdha
Sara: 26
Skin types as per sara:
Table.4 Showing skin types as per sara
Sara
Skin type
Twak sara
Snigdha, shlakshna, mrudhu, prasanna, sukumara loma, saprabha
Rakta sara
Snigdha, raktam, brajishnu
Mamsa sara
Guru, stira, mamsopachitha
Medha sara
Visheshata sneha yukta varna
31

Asthi sara
Majja sara
Shukra sara

Stira
Snigdha varna
Prasanna snigdha varna

Functions of Bhrajaka pitta:

The bhrajaka pitta is stated to be located in the skin and to impart its characteristic
color and luster.
Charaka has not described this pitta as a separate entity but he has included the
functions attributed to it among those of pitta in general. Marichi has stated that the
prakruthi and vikruthi of brajaka pitta effects varna, bhaya, krodha and harsha.27
Chakrapanidatta, in his commentary on the above, has stated that the regulation of
the body-heat and variations in the colour of the body are the functions of bhrajaka pitta
which is located in the skin.
Susrutha, Bhela, and Vagbhata have, made separate mention of this pitta, including
the functions ascribed to it.
According to Susrutha, the pitta located in the skin is known as bhrajakagni, it
enables the digestion and utilization of substances used for abhyanga, parisheka, avagaha,
28
alepa etc. It irradiates the glow of ones natural complexion.
Dalhana commenting on the above states that, bhrajaka pitta is located in the
bahyatwak, named as avabhasini and causes the radiation of luster.
According to Bhela, bhrajaka pitta is that which is responsible for the manifestation
of the specific characteristics of the body; it emphasizes its importance, creates different
prabha (hues) of the head, hands, feet, sides, back, abdomen, thighs, face, nails, eyes, and
29
hair. It also brightens them.
Vagbhata states that, bhrajaka pitta is located in the skin. It is so called because it
imparts luster to the skin and makes it radiate.30
Commenting on the above, Arunadatta states that, it is known as bhrajaka pitta
because, it performes dipana and pachana of substances used for abhyanga, lepa, parisheka
etc.

PHYSIOLOGY OF THE SKIN

The skin, apart from giving appearance and shape to the body, serves other important
31
functions
1.

Thermoregulation: The skin contributes to thermoregulation, the haemostatic

regulation of body temperature, in two ways: by liberating sweat at its surface and
by adjusting the flow of blood in the dermis.

2.

Protection:
Keratin in the skin protects from microbes, abrasion, heat, and chemicals
32

Lipids protect evaporation of water from the skin surface

The oily sebum contains bactericidal chemicals that kill surface bacteria

The acidic pH of perspiration retards the growth of some microbes

Melanin provides protection from UV light

Epidermal langerhans cells alert the immune system

Macrophages in the dermis phagocytize bacteria and viruses

3.

Cutaneous sensations: Sensations like pain arise in the skin. These include tactile
sensations touch, pressure, vibration, and tickling; as well as thermal sensations
such as warmth and coolness.

4.

Excretion: By evaporation of sweat, water and heat are removed from the body.
Sweat is also the vehicle for excretion of small amounts of salts, carbon dioxide,
and two organic molecules ammonia and urea.

5.

Absorption: Certain lipid-soluble materials penetrate the skin. These include fatsoluble vitamins A, D, E and K, certain drugs, the gases oxygen and carbon
dioxide.

6.

Synthesis of vitamin D: UV rays in the sunlight, activates precursor molecule in

the skin, to produce hormone calcitriol, which aids in the absorption of calcium
from foods.

PIGMENTATION OF THE SKIN:

32

Normal pigment cells:

The principal pigment determining skin color is melanin. The chemistry, quantity,
character, aggregation, and distribution of melanin are the major factors that determine
color and hue of cutaneous pigmentation. Three other pigments that contribute to normal
skin color are oxygenated hemoglobin, reduced hemoglobin, and carotenoids.
Embryogenesis:
All pigment cells arise from the neural crest except those of retinal pigment
epithelium, which are derivatives of the primitive forebrain. By the eighth week of
embryogenesis, pigment cells can be identified in the dermis.
Distribution of pigment cells:
Most melanocytes are located in the basal layer of epidermis. They also reside
within the papilla and matrix of the hair bulb. Melanocytes are a normal cellular component
of mucous membranes in oral cavity, nasal septum, respiratory tract, larynx, and
esophagus, eyes, ears, and leptomeninges.
Functions of the pigment system:
Pigment in the skin and hair protects against the harmful effects of sunlight.
Primary function of melanocytes is to remove free radicals formed in the skin during a
variety of inflammatory conditions. Melanocytes protect other cells of the epidermis from
damage caused by release of radical oxygens. Large quantities of melanin are an indicator
33

of an efficient and effective protective mechanism for elimination of detrimental effects of

many chemical and physical toxins.
Cytology of cutaneous melanocytes:

fig.4 Synthesis of tyrosin from

phenylaline

fig.5 Metabolism of tyrosinebiosynthesis of melanin

fig.6 Diagram of melanocyte

Melanocytes are oval and have a smooth cytoplasmic membrane and a round
nucleus. Dendrites extend outwards from the cell body. The cytoplasm is filled with many
organelles and a characteristic granule, the melanosome. The Golgi apparatus is prominent.
Intermediate filaments and microtubules are involved in the transfer of melanosomes from
the pigment cell into adjacent keratinocytes.
Melanosomes are formed by the fusion of several cytoplasmic suborganelles.
Vesicles with lamellae called premelanosomes are formed by the rough endoplasmic
reticulum. Other vesicles containing tyrosinase pinch off from the Golgi apparatus and fuse
with the premelanosome to initiate the synthesis of melanin.
The formation of the melanosome has been arbitrarily divided into four stages

Stage I: melanosomes are oval or spherical and contain a few filaments with
a characteristic periodic banding and the enzyme tyrosinase in an inactive
form.

Stage II: melanosomes are oval organelles with numerous filaments

organized into a lamellar substructure in which melanin is not present.

Stage III: melanosomes are partially filled with melanin

Stage IV: melanosomes are completely filled with melanin

The skin color is determined to a large degree by the number and size of
melanosomes, i.e, the quantity of melanin produced by the melanocyte and transferred in to
the surrounding keratinocytes.
34

Melanin synthesis:33
Human melanocytes are now known to produce 2 types of melanin: eumelanin and
phaeomelanin. Eumelanin is black or brown, and phaeomelanin is red. The ratio of the 2
types of pigment largely determines the hue of human hair and skin.
Eumelanin:

fig.7 Biochemical path way for synthesis of melanin

Eumelanin chemically is a polymer of indoles and quinines formed by the amino

acid tyrosine. These quinines and indoles, highly reactive chemically, are toxic to most
cells. Melanin synthesis probably is restricted to prevent these compounds from injuring
the cell.
A single enzyme, tyrosinase, performs 3 different catalytic functions in the melanin
pathway. This enzyme catalyzes the oxidation of tyrosine to dopa, the dehydrogenation of
dopa to dopaquinone, and the conversion of dihydroxyindole to melanochrome. Tyrosinase
is the best-characterized enzyme involved in melanin synthesis. Two other factors
dopachrome conversion factor and indole blocking factor seem to be involved in
regulating the rate of melanin formation. Dopachrome conversion factor is now well
characterized as the enzyme dopachrome oxidoreductase.
Phaeomelanin:

35

fig.8 Biochemical pathway for synthesis of phaeomelanin

Phaeomelanin is formed from 2 amino acids: tyrosine and cysteine. In the formation
of phaeomelanin, dopaquinone condenses with the amino acid cysteine to form cysteinyl
dopa. Cysteinyl dopa is oxidized into cysteinyl indoles, which condense to form a red
polymer, phaeomelanin. The melanosome in which phaeomelanin is formed is structurally
different from that of the eumelanosome. The phaeomelanosome is round, not oval, and
lacks the organized lamellar substructures characteristic of eumelanosomes.
Factors that stimulate melanin formation: 34

Many physical and chemical agents like metabolic, endocrine, nutritional, and
miscellaneous systemic causes stimulate pigment formation.
Short wave ultraviolet light (UVB; 290-320 nm), which is abundant in sunlight,
causes epidermal pigment cells to increase melanin formation. This process takes
several days to a week to be noticeable chemically.
Long wave ultraviolet light (UVA; 320-400 nm) rapidly alters the melanin
polymer, causing it to become darker.
Prostaglandin E2, estrogens, and other hormones also increase the amount of
pigment produced by pigment cells.
Some chemotherapeutic drugs, eg, bleomycin, darken the skin by inducing
melanin formation.
Ingested metals such as arsenic and silver also darken the skin by depositing in
the dermis.
Psoralens are tricyclic organic compounds fond in many plants such as limes,
celery, and parsnips.in combination with UVA, psoralens stimulate formation of
melanin.
Melanocyte-stimulating hormones (MSH) are the best-characterized stimulants of
melanin formation. Four different MSH peptides have been identified, each
formed in the pars intermedia of the pituitary gland. These different MSH
peptides probably have a variety of functions other than causing an increase in
skin color.

Specific receptors for MSH are present on the surface of the pigment cell. When
attached to a receptor, MSH activates the enzyme adenylate cyclase to form cAMP, which
is one intracellular messenger involved in activating a protein kinase and initiating
formation of tyrosinase in the Golgi apparatus. The active enzyme is transported from the
Golgi to the premelanosome and synthesizes melanin. MSH also accelerates the movement
of melanosomes through the dendrites and their transfer into keratinocytes.
36

REFERANCES:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.

C.S.Sa.S 5/5
C.S.Sa.S 7/16
C.S.Vi.S 5/7-8
A.H.Su.S 12/14
C.S.Sa.S 6/23
S.S.Su.S 18/4
C.S.Sa.S 7/15
C.S.Sa.S 6/23
S.S.Sa.S 3/22-24
C.S.Sa.S 5/5
C.S.Sa.S 7/16
A.S.Sa.S 5/6
A.H.Su.S 12/14
C.S.Su.S 12/11
A.H.Su.S 12/5
S.S.Sa.S 2/36
C.S.In.S 1/8
C.S.Su.S 21/3
C.S.In.S 1/8
C.S.In.S 7/16-17
C.S.In.S 7/10-13
C.S.In.S 7/14-15
C.S.Vi.S 8/97
C.S.Sa.S 2/29
C.S.Vi.S 8/96-98
C.S.Vi.S 8/103-109
C.S.Su.S 12/11
S.S.Su.S 21/13
Bhela samhita
A.H.Su.S 12/14
Principles of Anatomy and Physiology
Dermatology a Lange medical book
Biochemistry of skin in health and disease
Essentials of Biochemistry

37

Examination of the skin

38

CHAPTER: IV
EXAMINATION OF THE SKIN
INTRODUCTION:
The skin is the outer layer of the human body, which forms a major interface
between man and his environment. The structure of human skin is complex, consisting of
a number of layers and tissue components with many important functions. Reactions may
occur in any of the components of human skin and their clinical manifestations reflect,
among other factors, the level in the skin in which they occur.
Accurate diagnosis of most skin lesions requires an adequate history, careful
examination of the patient and occasionally laboratory investigations.
HISTORY:
Detailed information should be sought concerning the present skin condition. This
should include the site of onset, mode of spread and duration of the disorder. Any
personal history or family history of skin disease, including atopy, is important. Previous
medical conditions should be noted, and a full drug history obtained, including any use of
over-the-counter preparations. The social and occupational history should be noted and in
some circumstances, details of recent travel may be important.
EXAMINATION:
The whole skin, including hair, nails and assessable mucosae, should be fully
exposed, preferably in natural light. Some times a magnifying lens is useful.
Four basic features of any cutaneous lesion must be noted and considered in the
examination of the skin like, the distribution of the eruption, the types of primary lesion,
the shape of individual lesions, and the arrangement of the lesions. The most important
abnormalities in the skin relevant to general examination are pallor, yellowness,
pigmentation, cyanosis and cutaneous eruptions. In dehydration the skin is dry and
inelastic, so that it can be pinched up into a ridge. The skin is atrophied by age and
sometimes after treatment with glucocorticoids. It is thickened, greasy and loose in
acromegaly.
Pallor depends on the thickness and quality of the skin and the amount and quality of the
blood in the capillaries.
Yellowness a pale lemon-yellow tint is characteristic feature of haemolytic jaundice, in
obstructive jaundice; there will be dark yellow or orange tint.
Pigmentation is most commonly racial or actinic. Mostly increased pigment is due to
increased melanin content or due to some other pigment. Generalized melanin hyper
pigmentation is seen in Addisons disease, nelsons syndrome, pregnancy, acanthosis
nigrican etc. Localized pigmentation are seen in melanocytic naevi, Mongolian spots,
naevus of ito etc.
Cyanosis is a bluish colour of the skin and mucous membranes due to the presence of
reduced haemoglobin in the blood. Two physiological types are central and peripheral.
39

Central cyanosis results from imperfect oxygenation of blood, as in heart failure and
some lung diseases and admixture of blood from venous-arterial shunts in the heart.
Peripheral cyanosis is due to excessive reduction of oxyhaemoglobin in the capillaries
when the flow of blood is slowed. This may happen on exposure to cold, when there is
venous obstruction, or in heart failure.
Cutaneous eruptions and lesions should be examined with special reference to their
morphology, distribution and arrangement, color, size, consistency, configuration,
margination and surface characteristics should be noted.
MOPHOLOGY OF SKIN LESIONS:
A.INSPECTION AND PALPATION:
Assessment of morphology requires visual and tactile examination.
b) Lesions should be felt
c) Smooth or rough, thin or thick
d) Dry or moist
e) Any visible sweating, either general or local
f) The elasticity of the skin

B.DISTRIBUTION OF SKIN LESIONS:

a) Symmetrical often implies an internal causation
Asymmetrical may imply external factors
b) Centrifugal erythema multiforme, eryhema nodosum
Centripetal chicken pox, pityriasis rosea
c) Flexor bias Atopic eczema in childhood
Extensor bias psoriasis in adults
d) Localised distribution may be due to contact

CASE HISTORY:
A complete history should be obtained to emphasize the following features
1. Evolution of lesions
a) Site of onset
b) Manner in which eruption progressed or spread
c) Duration
d) Periods of resolution or improvement in chronic eruptions

2. Symptoms associated with eruptions

40

a) Itching, burning, pain, numbness

b) If anything, has relieved symptoms
c) Time of day when symptoms are most severe
3. Current or recent medications
4. Associated systemic sysmptoms (eg-malaise, fever etc)
5. Ongoing or previous illnesses
6. History of allergies
7. Presence of photosensitivity
8. Review of systems

DIAGNOSTIC TECHNIQUES:
A) Tzanck preparation
This technique is useful for rapid diagnosis of vesicular infections or blistering
eruptions such as pemphigus.
B) Microscopical examination
This is useful in the diagnosis of scabies, pediculosis and fungal infection
(tinea and candidiasis)
C) Woods light
Woods light lamp emits long-wave ultraviolet light at a peak of 360nm.
Woods light examination is performed in a darkened room, it is useful in identifying
fluorescence of fungi and corynebacterial infection (erythrasma), in the localization of
pigmentary abnormalities.
D) Patch testing
This is an important and valuable tool for diagnosis of suspected allergic
dermatitis due to contact.
E) Skin biopsy
Biopsy is used to identify the nature of expanding or inflammatory lesions, in
diagnosis and in assessing the progress of skin diseases.

REFERANCES:
1.Hutchisons clinical methods

41

Disease aspect

nidana
poorvarupa
roopa
samprapthi
rugvinischayam
sadya-asadyata
upadrava
chikitsa
pathya-apathya

42

CHAPTER: V
DISEASE ASPECT
Description:
The disease vyangam is described under kshudra roga prakarana.
Kshudra roga = swalpa vyadhi (S.K.D)
Kshudra roga prakarana includes all those diseases whose dosha, dushya, etc,
have not been described in detail. Hence all the diseases in the kshudraroga prakarana are
in concise form.
Kshudra rogas have a simple hetu, lakshana and chikitsa. So, they are called as
kshudra rogas.
Some of the skin diseases are mentioned under kshudrarogas. Vyangam is one
amongst them.
There is difference of opinion regarding the total number of kshudrarogas.
According to Susrutha 44, Vagbhata 36, Madhavakara 43, Sharangadara 60,
Yogaratnakara - 44
The hyperpigmented patches effecting the face is called as vyangam. This can be
correlated with melasma or chloasma.
Nirukthi:
Vikruthani vyangani yasya (S.K.D)
vigata vikala vangha pradhikarma (V.P )
The meaning of vyangam is deformity, dark spots on the cheek.(San-Eng Dictionary)
Nidana:
1

yasya prakupitah pittah shonitah prapya shushati

krodhayasaprakupitho vayuh pittana samyuta 2
shokha krodhadhikupitadvathapittanmukkha 3
vata, pitta, rakta, krodha, shoka and ayasa are the main etiological factors which
cause the vyangam.
Vyangam is a skin disease, so any skin disorder would have the same nidana
karanas as for kusta, therefore the nidana kranas for kusta are being considered.
Ahara:
Importance of ahara:
4
Ahara is moola for bala, varna and oojas.
The food taken in proper quantity and quality, provides certainly strength,
complexion and happy life to the person

Ahita ahara:
43

Viruddha ahara have been mentioned to be the direct cause for the kusta rogas.
6
Charaka has mentioned some types of ahita ahara which are to be avoided.
Table.5 Showing types of ahitahara
Ahara dravya
Ahita aharra
Cereals
Yavaka
Pulses
Masha
Drinking water
River water during the monsoon
Salt
Ushara
Meat of animals
Young pigeon, frog
Fat of animals
Mahisha,kumbhira, chataka, hasti
Vegetable oil
Kusumbha
Ghee
Avika
Leafy vegetable
Sarshapa
Fruit
Nikucha
Rhizome
Aluka
Sugarcane preparation
phanita
The consumption of drava, snigdha, guru, nava anna pana, dhadhi,
mathsya and excessive intake of lavana, masha, mula, tila, kshira, guda are said to be
7
causes for skin diseases.
Vihara:
Vegadharana, especially chardivega dharana, vyayama after consuming heavy
food, not observing any regular regimen of diet, taking hot and cold foods in succession,
exposure to intense heat, not observing the regulations during fasting, consuming cold
water immediately after exertion, improer performance of panchakarma, sleeping during
the day etc.
Achara:
Apart from the above, certain antisocial activities or alakshmikara chesta like
disrespecting elders, holy men, places of worship are also responsible in accumulating
8
papa, which is a direct nidana for skin diseases.
Rakta as an etiological factor:
9
Pure blood imparts strength, complexion, and happy life to the persons.
When aggravated doshas attain stanasamsraya in the skin and blood, they produces
kustha and kshudra rogas.10
Vyangam is caused due to the vitiation of rakta dosha and is mentioned under the
raktajavyadhi.11
12
Charaka has mentioned vaivarna under the shonitaja roga.
Rakta prakopa karana:
Asruk undergoes aggravation by the same causes which aggravates pitta. Frequent
use of drava, snigdha, guru ahara, divaswapna, krodha, anala, atapa sevanam, shrama,
abhigatha, ajeerna virudha and adyashana causes rakta prakopa.13
Manovikaras:
44

14

Krodha, shoka are the psychological disorders. These psychological problems

arise when faced with non-fulfilment of desires and facing the undesired events.15
Aayasa:
shokaharshatayayasah sarva snehat pravathathe (V.P)
Exertion, Fatigue, Weariness (S.E.Dic)
Synonymas: shrama, klama, parisrama, prayasa, vyayama, klesha (S.K.D)
Defenition: Tiredness without doing any work, with improper perception of sense
organs and without rise of respiratory rate, this state is called as klama.16
Too much of shrama causes vitiation of rakta.17
Above all factors vitiate vata with pitta, & rakta causing shava varna mandalah on
face and manifests in to vyangam.
The etiological factors can be divided into bhahya hetu and abyantara hetu. In this
context shoka, krodha and aayasa are the bahya hetus where as vata, pitta and rakta
doshas are the abhyantara hetus.
Poorvarupa:
Poorvarupa of vyangam are not mentioned in any Ayurvedic classics. Infact the
word sahasa was used during the description of the disease, which means that lakshana
of vyangam appears suddenly or abruptly with out poorvarupa.
Roopa:
sahasa mukhamagatya mandalah visrujatyatha
neeruja tanukah shavah mukhe vyanga thamadishet(S.S)
The cardinal symptom of vyangam is the appearance of mandala, which is tanu,
18
neerujam and shava varna on the face.
19

As per Vagbhata, vyangam is classified in to 4 types

1. Vataja
2. Pittaja
3. Kaphaja
4. Raktaja
1. Vataja vyangam : Skin is rough with parusha sparsha and shava varna
2. Pittaja vyangam : The edges of the mandala are in tamra varna, with neela varna in the
central area.
3. Kaphaja vyangam: The edges are of shweta varna associated with kandu.
4. Raktaja vyangam: The edges has rakta varna with tamra varna in the central part
associated with tigling and burning sensation.
Samprapti:
On account of all causative factors, either independently or together, the pitta and
vata get vitiated and in turn vitiates rasa, and rakta dhatu along with manovaha srotas.
Chiefly the agni (brajaka pittam) gets vitiated here and the function of agni which is to
maintain varna is disturbed. When these dosha hetus are sustained, the dosha-dushya
45

sammurchana takes place and the morbid factors get lodged at the level of the stana i.e,
facial skin.
By the above measures, the samprapti ghattakas may be enumerated as below
1. Dosha
:
pitta, vata
2. Dushya
:
rasa, rakta, manas
3. Marga
:
bahya
4. Srotas
:
rasavaha, raktavaha, manovaha srotas
5. Adhistana
:
twak
6. Mala
:
sweda
7. Vyakti
:
vaivarna
Rugvinischayam:
1. Nyacha: Broad or small, shava or asita varna, painless patches on the skin of the body
20
is called Nyacha.
2. Nilika: Similar black patches as vyangam appearing in other parts of the body is
21
known as Nilika.
3. Jatumani: A congenital, slightly elevated, even, slakshna, slightly rakta Varna and
painless patch on the skin caused by kapha and rakta is known as
Jatumani.22
4. Masaka: Painless, immovable, black, round nodules on the skin resembling blackgram
23
caused by vata is called Masaka.
5. Tilakalaka: Black, painless spots resembling sesamum seeds, not raised above the
level of the skin, caused by vata, pitta and kapha together is known as
Tilakalaka. 24
Sadya Asadyata:
According to Bhavamisra, vikrits occurring in the twak and mamsa are
sukhasadya. According to all other Ayurvedic texts vyangam is a sadya vyadhi.
Upadrava:
Vyanga roga does not have any upadrava, but if this appears suddenly in the
25
diseased patient, it is considered as arista.
Chikitsa sutra:
shiravedhaih pralepascha tatha abyangarupachareth vyanga
The treatment indicated for vyangam is siravadham, lepam, and abyangam. 26
In addition to these Vagbhata has indicated navana nasyam with markava swarasa, kshira
and thoya. 27
Siravyadam:
The nearest vein, should be cut, then the paste of bark and sprouts of trees having
milky-sap made with milk should be applied.28
Siravyadam should be done near the lalata pradesha accordingly with the
practice and method. After the vyadana karma, the affected area should be rubbed with
samudraphena etc, and filled with the paste of the ksheerivruksha bark.29

Lepam:

46

Lepam is of three types pralepa, pradeha, and alepa. Alepam normalizes the
rakta and vata, cleans the skin and blood. 30 Alepa again is of three types doshagna,
31
vishagna and varnya. Varnya Kara alepa is used in vyanga roga.
Abyangam:
Abyangam is the process in which the persons body is oleated with medicated oil
with specific pressures and movement (gati). Uses of abhyangam are sharera
32
mardavakara, kapha, vata nirodhaka, dhatu phustikara, Varna and bala vrudhi kara.
Vadana abyangam with kumkumadhi tailam is said in Bavaprakasha. 33 Katutaila
34
abyangam in Chakradatta. Tribhuvanadhi churna udvartanam is mentioned in
35
Yogaratnakara.
Pathya Apathya:
Pathyam: phanita, madhu, navanita, raktashali, yava, rasona, matulunga etc,
Nutritional, and timely diet in proper quantity.
Apathyam: pitta and rakta aggravating ahara and vihara. Drava, snigdha guru and nava
anna pana. Dhadhi, mathsya and execessive intake of lavana, masha, mula, tila kshira,
and guda.
MELASMA; CHLOASMA

fig.9 Diffuse brown pigmentation of the cheek

in cholasma
36

Essentials of diagnosis:

Mottled macular pigmentation, usually on the face

Painless skin level hyperpigmentation

General considerations:
47

Melasma develops on the face of some women who are pregnant or taking birth
control pils. Estrogens may cause melasma by accelerating the formation of melanin and
also cause darkening of the nipples and areolas and the linea nigra on the abdomen, a
darkened line extending from the pubis to the umbilicus.
Melasma is not restricted to pregnant women. Many women who have neither
been pregnant nor received estrogen-contaning meducations have melasma, as do some
men.
Clinical findings:
A. Symptoms and signs: Melasma is a brown gray mottled discoloration most
prominent on the forehead, malar eminences, and cheeks anterior to the ears. Sometimes
it affects the upper lip and the chin.
B. Laboratory findings: the epidermis appears normal. The amount of melanin in
the darkened skin is increased compared to the normal skin. The number of pigment cells
is normal. Melanin may also be present in dermal macrophages (pigment incontinence)
and causes the gray-brown discoloration observed in some patients.
Complications:
Although there are no biologic complications from melasma, some patients are
markedly distressed emotionally by the cosmetic defects.
Differential diagnosis:
Other pigmented lesions that commonly occur on the face are nevus of ota,
freckles, solar lentigo, and post inflammatory hyperpigmentation.
Nevus of ota: This is a blue to gray-brown pigmented patch located on the face, usually
within the distribution of the ophthalmic and maxillary branches of the trigeminal
nerve.discoloration may be limited to the zygomatic arch or forehead or may cover half
the face.
Freckles: These are pigmented macules, usually with reddish tan, observed in sunexposed area on the skin. Seen mostly in children scattered across their cheeks and nose,
and macules darken following exposure to ultraviolet light.
Solar lentigo: Patients with history of chronic sun exposure develop solar lentigines,
usually after puberty and after age of 40 years. These are called liver spots or old-age
spots.lentigens are moderately dark brown and large. With irregular borders.they occur
on chronically sun exposed surfaces, on the face, and dorsum of hand.
Post inflammatory hyperpigmentation: This is caused due to a variety of inflammatory
conditions and infections of the skin. Eg, psoriasis, acne, lichen simplex, lichen planus,
trauma, herpes zoster, tinea versicolor and chicken pox.

Examination:
48

Epidermal forms of hyperpigmentation usually respond to treatment. In contrast,

dermal hyperpigmentation (Mongolian spots or nevus of Ito and Ota) and dermal
melanosis do not respond to any medical treatments and usually is permanent.
It is important, therefore, to determine whether the pigmentation has mainly an
epidermal or dermal component. Examination of the patient with Woods lamp (black
light) in a totally dark room can facilitate this evaluation. Epidermal melanin turns
almost black when viewed with Woods lamp. In contrast, dermal pigmentation, when
observed with Woods lamp, will not be visible to the examiner, and the blemishes on the
patients skin will disappear.
Treatment:
Prevention of further hyperpigmentation is paramount. Patients with sun-induced
pigmentatory disorders must avoid habitual sun exposure. Sunscreens or sun blocks
should be applied prior to any outdoor activities.
The goal of therapy is to decrease the production of melanin without killing
melanocytes. Various bleaching medications must be applllied conscientiously 2 or 3
times every day, often for 6-12 months, to achieve optimal results.

Cream containing hydroquinone in 3-4% concentration, applied twice daily to the

dark areas may decrease the production of melanin by blocking the activity of
thyrosinase, the enzyme that is primarily involved in melanin synthesis. A side effect
from hydroquinone is mild skin irritation. At higher concentrations, colloid milia or
dermal pigmentation has been reported

The addition of a corticosteroid cream increases the effectiveness of the

hydroquinone and perhaps reduces the frequency of skin irritation. Caution must be
exercised when prescribing corticosteroids for prolonged periods. On the face,
steroids can cause telangiectases, atrophy, or acneiform lesions.
The more potent fluorinated corticosteroids should not be used on the face except
under special circumstances.

Tretinoin cream (Retin-A) can also be used in conjunction with hydroquinone or mild
corticosteroids, to decrease epidermal hyperpigmentation. Tretinoin can be very
irritating to the skin and cause erythema, desquamation, and soreness.
Gentle freezing with the liquid nitrogen can decrease the amount of color.
Melanocytes are particularly susceptible to destruction by this treatment and may
cause necrosis of the skin or blistering and permanent depigmentation in dark-skinned
patients.
Trichloroacetic acid, is effective in light-skinned patients. It must be used with great
caution, as it is extremely reactive chemically, and higher concentrations can cause
instantaneous necrosis of the epidermis that can leave severe scarring.

49

References:
1.C.S.Su.S 18/25
2. S.S.Ni.S 13/45
3. A.H.U.S 31/28
4. S.S.Su.S 1/28
5. C.S.Su.S 5/8
6. C.S.Su.S 25/39
7. C.S.Ch.S 7/4-8
8. C.S. Ni.S 5/6
9. C.S.Su.S 24/4
10. S.S.Su.S 21/33
11. S.S.Su.S 24/9, A.H.Su.S 11/8-9, A.SA.Su.S 19/4
12. C.S. Su.S 24/13
13. S.S.Su.S 21/25
14. C.S Su.S 7/42
15. C.S.Su.S 1/57
16.S.D.S.P.K 6/74
17. C.S Su.S 24/10
18. S.S.Ni.S 13/45-46
19. A.H.U.S 31/29-30
20. S.S Ni.S 13/43,
21. S.S.Ni.S 13/47,
22. S.S Ni.S 13/40
23. S.S.Ni.S 13/41
24. S.S.Ni.S 13/42
25. C.S.In.S 1/21
26. B.P.M.K 61/39, Va.Se Ks.Ro/43
27. A.H.U.S 32/33a
28. A.H.U.S 32/15
29. S.S.Ch.S 20/33-34
30. S.S.Su.S 18/8
31. S.D.S.U.K 11/1-2
32. S.S.Ch.S 24/30
33. B.P. M.K Ks.Ro/49
34. Ch.Da 55/50
35.Yo.Ra VOL-II Ks.Ro.N/123
36.Dermatology a Lange Medical

50

Vyangam
(psycho physiological
approach)

51

CHAPTER. VI
VYANGAM (PSYCHO PHYSIOLOGICAL APPROACH)
MANOVIGNANAM
A brief description of manas:
Nirukthi:
manyathe budyathe anenathi mana(S.K .D)
The functional unit which is responsible for percessiving knowledge and its
recollection is known as manas.
Conjunction of boby, sense organs, manas and atma is termed as Ayuvu. 1Manas is
ubayatmakam (karmendriya and gyanendriya) 2
Object of mind:
manasasthu chintyamartha
The object of mind is that which can be thought of (chintyam).3
Synonyms:
Athindriya, manah, satvasangyaka4
Seat of manas:
5
1. Hridayam
2. Shirastalvantara gatam 6
Manovishayas:
Chintyam, vicharyam, oohyam, dheyam, sankalpam are perceived by the manas
are known as manovishayas. 7
Manoguna:
8
Anutva, Ekatva are mano gunas.
Mano lakshana:
Gyana abhava and Gyana bhava are considered as mano lakshan.9
Mano kruthya:
Mano kruthyas are Indriyabhigraham, Swanigraham, Ooha, Vicharyam, and
10
beyond that is the jurisdiction of buddhi (intellect).
Mano doshas:
Rajas and tamas are the two manodhoshas.11
Mano vikara:
Psychological disorders like, Ersha, Shoka, Bhaya, Krodha, Maana, Dwesha etc
are caused due to pragnyaparadha.12

52

Causes for manovikara:

1. Perverted, negative and excessive use of kala, bhudhi, indriyardha are the threefold
13
cause of both psychic and somatic disorders.
2. Mano vikaras are caused due to, manodhoshas rajas and tamas.14
3.Psychological problems arise when faced with non-fulfilment of desires and by facing
the undesired situations.15
4.For both shareera and mano dhoshas, the three aggravating factors are astamendriyardha
16
samyogam, pragnyaparadam and parinamam.
5.Pragnyaparadam is the unwholesome activities performed by a person due to Dhi,
17
Druthi, and Smruthi bramsham, and this is an intellectual error.
Manovaha srotas:
Manas and bhuddhi are the moolas for manovaha srotas. Charaka has described
about this srotas in Unmada and Apasmara nidanam.
Description of krodha and shokha:
18
Krodha and shokha are considered as psychological disorders.
KRODHA:
Nirukthi:

prathikula sathi thaikshgamya prabhodha (V.P)

Anger, wrath (S.E. Dic)

Synonyms:

kopa, rosha, rudhra, krutha, krudha, rusha (S.K.D)

Lakshana: Injurious and destructive behaviour towards others, development of

inconsiderate violence and distress towards living creatures are the lakshnas of krodh.19
Causes:
20
Krodha is caused due to rajo guna.

When pitta dosha invades the sira, it produces the angry mind and irrelavent talk.

Abnormal state of sadaka pittam results in krodha.

Dhusta shonita causes klama and krodha.

Pitta prokopa causes krodha.24

21

22

23

Effects:
Krodha causes redness of face, increase in respiration and heart beat, and this leads to
hypertension and heart diseases.

Excessive anger and exertion causes the vitiation of rakta dhosha, which in turn
25

causes the skin diseases.

SHOKHA:
Nirukthi:

bandhadhi viyoghajanitha manah peeda(V.P)

Sorrow, grief, distress, deep anguish (S.E.Dic)
53

Synonyms:
Shuk, manyu, ityamara, shucha, neshama, khedh, shochanam (S.K.D)
Causes:
26
Shokha is caused due to tamo guna

Vata prakopa causes shoka

27

Effects:
28
Shokha causes emaciation of the body.

Shokha leads unto sever diseases 29 like shokhatisara.

Shokha causes the vitiation of vata

30

When krodha, ayasa, shokha inflict the manas, dhoshas are aggravated causing
other diseases like abhishanga jwara, unmade, apasmara etc31
Effect of krodha and shokha on dhoshas:

krodhashokhabhayaayasopittam prakopamapadyathe
32
Krodha, shokha and ayasa are the factors which causes the pitta prakopam.

kamashokhabhayadyauh, krodhatpittam..
33
Shokha causes vata prakopam and krodha causes pitta prakopam
34
Both body and mind effect each other in causing the diseases.
Psychic and somatic diseases sometimes continuing together are associated
mutually35
The sparshanendriya alone pervades all the sense organs and it is also associated
inherently with manas.36

PSYCHOPHYSIOLOGICAL STRESS:
Psychosocial stress may be an important factor in understanding skin problems.
No controlled study has been carried out which has examined relation between
psychophysiological stress and skin complaints. Potential role of psychophysiological
and organizational factors in the etiology and clinical course of skin diseases is to be
evaluated. 37
A comprehensive assessment of physiological, occupational and psychosocial
factors were performed, blood and urine samples were tested for the determination of the
levels of stress hormones (serum cortisol, prolactin, oestradiol, testosterone, thyroxin and
growth hormone and urinary concentration of adrenalin and noradrenalin). Rise in stress
hormone levels as well as subjective feelings of stress indicate the effect of stress on the
skin complaints. Physiological changes characterized by elevated metabolism and
38
increased dermal blood flow, may act as unconditioned stimulus.
There were no systematic differences noted refarding age, sex, distribution, job
functions, personality, socioeconomic factors, marital status, alchohol or coffee
consumption, or smoking habits and pigmentation ability. Further- more, for the persons
54

with skin complaints, a conditioning mechanism arising from a fear of health hazards is
probably of importance.
References:
1. S.S.Su.S 1/42
2.B.P.Po.K 1/106, S.S.Sa.S 1/6
3.C.S.Su.S 8/16
4.C.S.Su.S 8/4
5.C.S.In.S 5/41
6.Be.S.Ch.S 8/2
7.C.S.Sa.S 1/20
8.C.S.Sa.S 1/19
9.C.S.Sa.S 1/18
10.C.S.Sa.S 1/21
11.C.S.Su.S 1/57
12.C.S.Su.S 7/42
13.C.S.Su.S 1/54
14.C.S.Su.S 1/57
15.C.S.Su.S 11/45
16.C.S.V.S 6/6, C.S.Su.S 11/43
17.C.S.Sa.S 1/102, C.S.N.S 7/21
18.C.S.V.S 6/5, S.S.Su.S 1/24
19.S.D.S.P.K.5/117
20.A.SA.Sa.S 5/13
21.A.SA.Su.S 19/19
22.ON C.S.Su.S 12/11 Cakrapani commentary
23.C.S.Su.S 24/14
24.A.SA.Su.S 19/3a
25.C.S.Su.S 24/9-13
26.A.SA.Sa.S 5/14
27.A.SA.Su.S 19/3b
28.C.S.Su.S 25/40
29.S.S.Su.S 15/33
30.C.S Ch.S 3/115
31.C.S.Su.S 24/31
32.S.S.Su.S 21/21
33.C.S.Ch.S 3/115
34.C.S.Su.S 1/55
35.C.S.V.S 6/8
36.C.S.Su.S 11/38
37.Endocrine and dermatological concomitants of mental stress
38.Report published by National Institute for Psychosocial Factors and Health Sweden.

55

Disorders of
hyperpigmentation

56

CHAPTER: VII
DISORDERS OF HYPERPIGMENTATION:
Hyperpigmentation is a common problem, especially in patients with dark skin.
Most cutaneous irritants cause an increase in pigmentation. However, patients of any race
can suffer significant cosmetic disfigurement from ocalised or generalized
hyperpigmentation. Hyperpigmentation may be a cutaneous sign of a serious metabolic or
nutritional disorder. Fortunately, most types of hyperpigmented lesions are benign. Some
are malignant eg-melanomas. Usually one thinks of hyperpigmentation as affecting only
the skin. However, it can also affect the nails or mucous membranes.
Abnormality of pigmentation can be subdivided in to
a) Melanocyte population densities (increased or decreased)
b) Melanin production (enhanced or diminished)
c) Melanosomal packing and distribution
d) Miscellaneous abnormalities (usually nonmelanotic)
The depth of pigmention deposition in the skin, whether in the epidermis or abnormally
in the dermis, also affects the overall perceived color. These vroad groupsof
clinicopathologic disorders are further divided into
a) Congenital or genetic diseases
b) Acquired diseases
A. CONGENITAL OR GENETIC HYPERPIGMENTATION DUE TO AN EXCESS
NUMBER OF MELANOCYTES
1. Lentigo simplex

Onset during infancy or early childhood

Small brown macules
Not limited to sun-exposed areas
Low malignant potential

3.Multiple lentigines syndrome or leopard syndrome

Lentigines
Electrocardiographic abnormalities
Ocular hypertelorism
Pulmonary stenosis
Abnormalities of the genitalia
Deafness
There are increased number of melanocytes in the basal layer and
increased melanisation. The melanosomal contents is expanded, and gaint
melanosomal complexes are noted.

57

3.

Nevus spilus

4.

Mongolian spot

5.

Present at birth or occasionally early infancy

Light brown patch speckled with dark brown macules, usually is a
congenital
The usual location is the trunk or proximal extremity

Blue-black pigmentation of the sacrogluteal region

Present at birth
Spontaneous resolution
Bipolar melanocytes filled with melanin are scattered in the papillary and
reticular dermis

Nevi of ota

Blue to gray-brown pigmented patches

Facial location
Permanent
Pigmented patch located, usually within the distribution of the ophthalmic
and maxillary branches of the trigeminal nerve

6. Nevi of ito

Blue to gray-brown pigmented patches

Unilateral location on shoulders and neck
Permanent
It occurs along the distribution of the supraclavicular and brachial nerves

B. ACQUIRED HYPERPIGMENTATION DUE TO AN EXCESS NUMBER OF

MELANOCYTES
1. Solar lentigo (senile lentigo)
Onset after puberty and usually after age 40yrs
History of chronic exposure to solar radiation
Lesions confined to sun-exposed areas
Solar lentigines are moderately dark brown and large, often 1cm or more in
diameter with irregular borders
2. Ultraviolet-induced hyperpigmentation (suntan)
Light brown or golden brown coloration of exposed skin
Sharp demarcation lines between exposed and normal skin

B. CONGENITAL
DEFECTS

HYPERPIGMENTATION

DUE

TO

MELANOSOMAL

Neurofibromatosis ( Recklinghausens disease)

58

Neurofibromas: Usually soft, pedunculated, flesh colored papules and nodules,

buttonhole deformity
Caf-au-lait macules
Axillary freckles
Lisch nodules: Yellow or brown papules on the iris
Neurofibromatosis is one of a group of disorders of neural crest-derived cells, the
neurocristopathies. They include pheochromocytoma, neuroblastoma, and other
syndromes

D. CONGENITAL HYPERPIGMENTATION DUE TO ABNORMALITIES OF

TYROSINASE
1. Familial progressive hyperpigmentation
Dark-skinned individuals only
Reticulated, deeply pigmented patches on the skin, present at birth
3. Hereditary hyperpigmentation in blacks

Futchers line is a sharply demarcated line of pigmentation visible on the

anterolateral side of the deltoid and the upper part of the arm
In others hyperpigmented line extending across the nose from one nasolabial fold
to the other is seen

4. Periorbital hyperpigmentation
Darkened rings around the eyes, seems to vary with stress or lack of sleep.
This may be due to vascular changes. The trait is transmitted as an antosomal
dominant defect
5. Peutz-jeghers syndrome
Brown or black macules, especially on the lips and buccal mucosa
Polyps of the intestines
Autosomal dominant inheritance
6. Incontinentia pigmenti (Bloch-sulzberger syndrome)
Female predominance (X-linked dominant)
First stage :- streaks of vesicles
Second stage :- streaks of verrucous papules
Third stage :- streaks of whorled hyperpigmentation
Associated with multiple defects of the central nervous system
Streaks develop most commonly over the extremities and trunk
D. ACQUIRED HYPERPIGMENTATION DUE TO ABNORMALITIES OF
T YROSINASE
1. Freckles (ephelides)
Tan or red macules 1-5mm in diameter in sun exposed areas
Especially in fair-skinned people
Freckles scatter across cheeks and nose in children

2. Melasma (chloasma)
59

Mottled macular pigmentation, usually on the face

Most commonly during pregnancy (mask of pregnancy)

3. Beckers nevus
Light brown patch usually on the unilateral shoulder and back
Male predominance
Hypertrichosis within the pigmented patch
4. Postinflammatory hyperpigmentation
Patchy distribution following pattern of original dermatoses
Very common in dark-skinned patients
5. Systemic causes of hyperpigmentation
a) Metabolic
Porphyria cutanea tarda
Advanced liver cirrhosis
Hemochromatosis
Chronic renal failure
Gauchers disease
Niemann-pick disease
c) Endocrine
Addisons disease
ACTH and MSH producing tumors
Pregnancy
Oral estrogen therapy
Acromegaly
d) Nutritional
Pellagra (niacin deficiency)
Pernicious anemia (Vit B 12 deficiency)
Kwashiorkor
e) Miscellaneous
Scleroderma
Inflammatory bowel disease
Cronkhite-canada syndrome
Bleomycin therapy
Fluorouracil therapy
Busulfan therapy
Arsenical ingestion
Fixed drug reaction
5. Adrenal insufficiency (Addisons disease)
Generalized brown hyperpigmentation
Accentuation in creases, sun-exposed sites and genitalia
Excessive ACTH and MSH production
7. Drug-induced hyperpigmentation
60

a) Heavy metals
Silver :- blue-gray color called argyria
Bismuth and arsenic :- brown hyperpigmentation
c) Tetracycline
Minocycline
Methacycline (blue-grey hyperpigmentation is seen, melanin may also be present
in epidermis)
d) Cytotoxic agents
Bleomycin :- Skin becomes deeply tanned
Cyclophosphamide
Melphalan (hyperpigmentation in nails)
e) Miscellaneous drugs
Antimalarial drugs
Chlorpromazine
Clofazimine (reddish-brown hue)
Table.6 Showing classification according to the color of pigmentation in genetic and naevoid factors
GENETIC AND NAEVOID FACTORS
BROWN COLOR

GREY, SLATE OR BLUE COLOR

1. Ephelides (freckles)

1. Mongolian spot

2. Lentigines

2. Naevus of ota

3. Multiple lentigines syndrome

3. Naevus of ito

4. Peutz-jeghers syndrome

4. Blue naevus

5. Cafe-au-lait and freckle-like macules in 5. Diffuse melanocytosis

Albrights syndrome

6. Incontinentia pigmenti ( Bloch-

6. Acanthosis nigricans (juvenile type)

sulzberger)

7. xeroderma pigmentosum

7. Naegelli-franceschetti-jadassohn

8. Fanconis syndrome

syndrome

9. Dyskeratosis congenital
10. Familial progressive hyperpigmentation

Table.7 Showing classification according to the color of pigmentation in acquired hypermelanosis

61

ACQUIRED HYPERMELANOSIS
CAUSATIVE FACTOR
BROWN COLOR
A. Endocrine

B. Chemical

C. Physical

D. Nutritional

E. Post inflammatory

F. Tumours

1. ACTH and MSH

producing pituitary and
other tumours
2. Addisons disease
3. ACTH therapy
4. Pregnancy
5. Contraceptive pills and
oestrogens
6. Melasma (chloasma)
1. Arsenic
2. Busulphan
3. Bleomycin
4. Cyclophosphsmide
5. Adriamycin
6. Psoralens
7. Berloque dermatitis
8. Phytophotodermatitis
1. UV light
2. Ionising radiation
3. Trauma
1. Kwashiorkor
2. Pellagra
3. Sprue
4. Vit B12 deficiency
1.Eczema
2. Lichen planus
3. Lupus erythematosus
4. Lichen and macular
amyloidosis
5. Systemic sclerosis
6. Morphoea
1. Malignant melanoma
2. Acanthosis nigricans with
adenocarcinoma
3. Malignant tumours

GREY, SLATE OR BLUE

COLOR

1. Minocycline
2. Fixed drug eruptions
3. Barbiturates
4. Phenolphthalein
5. Phenothiazines
6. Chlorpromazine

Chronic nutritional
deficiency

1.Pinta
2. Erythema dischromium
3. Perstans

Metastatic melanoma with

melanogenuria

62

CLASSIFICATION OF HYPERPIGMENTATION ACCORDING TO ITS SPREAD

Table.8 showing classification of hyperpigmentation according to its sprea
GENERALIZED
LOCALISED HYPERPIGMENTION
HYPERPIGMENTATION
1. Addisons disease
6. Melanocytic naevi
2. Nelsons disease
7. Mongolian spots
3. Pregnancy
8. Naevus of ota
4. Acanthosis nigricans
9. Naevus of ito
5. Primary
10. Neurofibromatosis
haemochromatosis
11. Peutz-jeghers syndrome
6. Secondary
12. Albrights syndrome
haemosiderosis
13. Chloasma
7.Hepatic cirrhosis
14. Post-inflammatory hyperpigmentation
(particularly biliary 10. Lichen planus
cirrhosis)
11. Fixed drug eruption
8. Chronic renal failure
12. Atopic dermatitis
9. Glycogen storage
disease
10. Gauchers disease
11. Vagabonds disease
12. Heavy metal
intoxication
(Arsenic ingestion,
silver, bismuth and
gold preparations)
13. Modern drugs
(Minoxycycline,
Amiodarone,
phenothiazines,
chlorpromazine
etc)
14. Carotenaemia
15. Canthexanthin
16. Methaemoglobinaemia
17. Sulpha
emoglobinaemia

Referances:
1. Roxburghs common skin diseases
2. Histopathology of the skin
3. Dermatology

63

HYPERPIGMENTATION DISORDERS IN AYURVEDA

1

1. Vidhradhi
Vataja vidhradhi Krushna, aruna varna
Pittaja vidhradhi Shava varna
Raktaja vidhradhi Krushna, shava varna
2

2. Vataja vrana Shava varna

3

3. Kushta
Kapala kushta Krushna, aruna varna
Ruhyajihva kusta Raktaparyantam, Antashyavam
Kitiba kusta Shavavarna kina
Vispota kusta Shava, aruna basa
Shataru kusta Rakta, shava
Vicharchika Shava
4. Kshataja visarpa Shavashonitam4
5. Kshudra rogas5
Jatumani Krushna
Mashaka Krushna, mutsanna
Tilakalaka krushna
Vyanga Shava
Nyacha(lanchana) Shava
Nilika Krushna
6. Vataja pandu black red discoloration of skin6
7. Asadhya madatyaya Black or blue discoloration of lips, teeth, gums7
8. Haleemaka blackish yellow discoloration of skin 8
9
9. Vishaja unmade Shava
10. Krimija hridroga - Shava 10
11
11. Vatodara bluish or brownish discoloration of skin
12. Vataja sleepada Blackish swelling is seen12
Referances
1. M.N 40 /4,5,10
2. M.N 42 /2
3. M.N 49 /10,13,18,21,22
4. M.N 52 /23
5. M.N 55 /34
6. M.N 8/4
7. M.N 18/22
8. M.N 8/23
9. M.N 20/15
10. M.N 29/6
11. M.N 35/7
12. M.N 39/9

64

Drug review

65

CHAPTER: VIII
DRUG REVIEW
CRITERIA FOR SELECTION OF THE DRUG
The drug selected for the present clinical study is manjista kwatha internally and
manjista madhu lepam externally.
The administration of manjista kwatha for varnya vikaras is mentioned in charaka
samhita sutrastana 5/8
The use of manjista madhu lepam is described in Susrutha samhita, Vagbhata
samhita, Bavaprakasha and in many classical Ayurvedic texts.
The preparation is non controversial, easily available, easy to prepair and free
from toxic effects.
manjista madhura tikta kashaya swaravarna krut !
Raktatisara kustasavesarpa vrana mehanut1
Manjista has madhura, tikta, kashaya rasa and it has varnya, kustagna, and
raktashodaka properties.
sowkumaryam sukshmam param srotovishodanam
2
Kashanurasam lady prasadajanakam param Varnyam,Yogavahe
Madhu has madhura, tikta as anurasa. It bestows suppleness, enters into minute
pores and cleanses the srotas. It has varnya and yogavahi properties.
Properties of rasa
Table.9 Showing the properties of rasa
RASA
PROPERTIES
Twachya
Madhura
Varnya
Kustaprashamana
Kusta, pitta kapha jayate
Tikta
Kusta, raktagadapaha
Shleshma, rakta pitta prashamana
Kashaya
Pitta, kapha vishodhana, twak prasadana
Capa, rakta, pittagna twak prasadana

SAMHITA
C.S.Su 26/62
A.H.Su10/8,B.Pr.Po.k 5/155
C.S.Su 26/70
A.H.Su 10/14-15
B.Pr.Po.k 5/199
C.S.Su 26/72
A.H.Su 10/19-20
B.Pr.Po.k 5/203

Because of brajaka pitta avabasini twak layer has its normal complexin .pitta vikruthi
causes rakta dhusti resulting in varna vikaras of the skin. Along with these if vitiation of
vata and kapha occurs, theye will cause disturbances in brajaka pitta functions resulting
in shava, aruna and shukla varna of the skin. 3
Vyanga roga is caused due to psyco-somatic disturbances, and it being a skin
disease, rakta dhatu dhusti is also seen and more-over this is a varnya vikara.
Manjista has the varnya, kustagna and raktashodaka properties. When it is given
internally it has tranquilizing effect on the brain.
Madhu is also a varnya dravya and it pacifies vata and pitta dhoshas. 4 when honey
is mixed with various formulations it alleviates many diseases as it is an excellent
synergist, because of being composed of, number of factors. 5 madhu is yogavahi- that
which exerts action similar to that of the drugs in combination.
66

Keeping in view all the facts mentioned above manjista, madhu are selcted for the
present trial.
FORMULATIONS
A review of formulations employed in the study
1. Manjista, madhu lepam (B.P.M.K.4A.14/39)
2. Manjista kwatham (C.S.Su 4/8)
The above mentioned preparations are selected for present clinical study
Review of ingredients

1. Manjista

fig.10 Root and plant of manjista

Botanical name: Rubia Cordifolia

Family: Rubiaceae
Synonyms: manjistha, vikasa, samangi, Kalameshika, manduka parni, yojanavalli,
rasayana, raktangi, raktayastika, manjusha, vastra ranjani.6
Vernacular names: 7
Sanskrit
Hindi
English
Telugu

:
:
:
:

Manjista
Manjit
Indian madder
Tamravalli

Gana
Varnya, Jwarahara, Vishagna (Charaka)
Priyangvadhi, Pittasamshamana (Susrutha)
Varnya gana (A.H.S)
Parts used;
Roots
Botanical description:
67

A perennial climbing herb; roots long, cylindric, with a thin red bark; stem very long,
rough, grooved; Branches scandent, quadrangular, often prickly on angles. Leaves in
whorl of 4, ovate, 4-9 + 1.5-3.5cm, lower leaves longer than the upper, scabrous above,
margins with minute prickles, all 5-(rarely 7-) nerved from the base; Flowers small,
greenish, in terminal, panicled cymes; Fruits didymous or globose, 4-6mm in diameter,
purplish black when ripe.
Distribution:
It is found through out India, ascending to an altitude of 3750 from North-West
Himalayas eastward.
Actions:
The roots are astringent, alterative, anti-inflammatory, anodyne, antiseptic,
carminative, anthelmintic, depurative, vulnerary, emmenagogue, diuretic, ophthalmic,
febrifuge, rejuvenating, tonic and it has tranquilizing effect on the brain.
Uses:
The roots are useful in dropsy, paralysis, rheumatoid arthritis, neuralgia, cephalalgia,
dyspepsia, flatulence, leucoderma, pruritus, wounds, ulcers, upper respiratory infections,
menstrual disorders, discolouration of the skin, tubercular condition of the skin and
mucosal tissue, spleen and liver disorders, pectoral diseases and general debility.
Properties:

Rasa

Madhura, Tikta, Kashaya

Guna

Guru, Ruksha

Veerya

Ushna

Vipaka

Katu

Doshaghnata :

Kaphapitta shamaka

Karma

Swara varna krut, Shothahara, Vranaropana, Kushthaghna,

Deepana, Pachana, Stambhana, Raktashodhaka, Pramehaghna,
Balya, Rasayana and Vishaghna.

Amayika
prayoga

Shota, Vrana, Charmaroga, Agnimandha, Amadhosha, Rakta

Atisara, Yoni, Akshi, Karna ruk, Visarpa, Kusta, Prameha, Jwara,
Varnavikara, Daurbalya, Vishavikara.

Dose
:
Kwatha
Pharmacognosy of roots:

:-

50-100ml, Powder

:-

1-3 gms

68

fig.11 Roots of manjista

Root is long, cylindric, fexuose, smooth and reddish. In transverse section, the
root is circular in out line. Outer 5-7 layers of cells form the cork tissue, occasionally
containing tannin. Secondary cortical cells are thin walled and polygonal in shape. Many
of these cells contain tannin. Phloem cells are thin walled, some of them contain tannin.
Cambium is 2-3 layered. Secondary xylem consists of vessels and tracheids. Primary
xylem is triarch.
Chemical constituents:
Roots contain resinous and extractive matter, gum, coloring matter and salts of
lime. Free alizarin and its glucoside, purpurin, xanthopurpurin, munjistin, glucose,
sucrose, ruberythric, acid, pseudo purpurin, 1,4-dihydroxy-2-methyl anthraquinone,
physcion, nordamnacanthal, scopoletol, ten fatty acids with saturated long chains,
anthraquinones, naphthohydroquinones, mollugin, furomollugin and dehydro-alphalapchone.9
Pharmacological activities:
Antioxident, antibacterial, anticancer, anti-inflammatory, antitumour, antiviral,
haemostatic, anti-lipid peroxidative activity, and hypoglycaemic.
Therapeutic evaluation:
1. 45 patients suffering from scabies with secondary infection were treated with the
Aragwadha kwatham, for external application Pamari ointment( paranthimoola,
dinesavalli, manjista) was used. About 51% cases were completely relived within 20-50
days.
2. 32 cases prescribed with Alstonia scholaris bark extract (60ml twice a day) internally
and Pinda taila (manjista and shariva) applied externally showed relief from minor skin
diseases in 10-30 days.
3. A paste made with manjista roots and honey is a valuable application for the freckles
and other skin discolorations, in external inflammation, ulcers and skin diseases such as
pityriasis, versicolor etc, roots are said to act against staphylococcus. (Wealth of India
CSIR)
References:
1. B.P.Po.K.Ashta varga 5/178
69

2. B.P.Po.K.Madhu varga 5/1-5

3. Chakrapani comentary on C.S.Su 4/8
4. S.S.Su 45/132
5. S.S.Su 45/142
6. B.P.Po 5/176-177
7. Dravyaguna vignanam Vol II
8. Danvantari negantu
9. Data base on medicinal plants in Ayurveda(Vol - V)
MADHU

fig.12 Madhu

Biological source
Honey is the sugary substance produced from the nectar of flowers by the worker
bees and deposited by them in the cells of the honey comb. Honey dew, a secretion of the
leaves of various trees and plants, is also gathered by bees.
Scientific name
Family
Order

:
:
:

Apis mellifica and A.dorsata and other species of apis

Apidae
Hymenoptera

Vernacular names:
Sanskrit
Hindi
Telugu

:
:
:

Madhu
Shahadh
Thene

Synonyms
Madhu, maksika, madhvika, ksaudra, saragha, maksika vanta, varati vanta,
bhrngavanta, pusparasodbhava.1
Characters:
Honey is thick, syrupy, translucent liquid. The colour varies from almost
colourless to nearly black according to its botanical source and to conditions of
processing and storage it has undergone. The difference in the aromatic constituents
altering the taste and aroma of the honey varies, according to the plants from which the
nectar is obtained.
70

At normal temperature honey is frequently supersaturated with respect to glucose

and exists as clear syrup mainly preferred by consumers. However on storage, coarse
granulation or crystallization can occur, which may lead to fermentation, in some cases.
The tendency to granulate depends on, number of factors, some of which remain
unknown. The ratio of sugar components and moisture have a major effect in granulation,
e.g- glucose and water ratio of 2:1 or more granulate rapidly.2
Charecters of madhu according to Ayurvedic texts:
Madhu has sheeta veerya, it is easily digestable, sweet, causes dryness, grahi,
sacrificant, good for eyes, kindles digestive fire, good for voice, cleanses and heals
ulcers. Bestows suppleness, enters into minute pores, cleanses the srotas, has astringent
as secondary taste, bestows contentment, improves complexion and intelligence, is
aphrodisiac, removes tastlessness, cures leprosy and other skin diseases, good in piles,
cough, bleeding diseases, diabetes of kapha origin, exhaustion, worms, obesity, thirst,
vomiting, dyspnoea, hiccup, diarrhea, constipation, feeling of burning sensation, wounds
in the lungs, is yogavahi (enhances the effect of the drug with which it combines) and
aggravates vata slightly.4
Composition:
The main constituents of honey are moisture, glucose (dextrose), fructose,
maltose, sucrose, dextrine, formic acid, volatile oil and mineral matter. In addition to
these, traces of enzymes, vitamins (Vit B), proteins, aminoacids are also present in honey.
Pollen is invariably present in comb honey, but may be absent in some honeys which
have been very finely strained. Enzymes present cause changes in the proportions of the
original sugars present and the sucrose may disappear completely on storage.
Chemical constituents: 4
Water (%)
:
Nitrogen (%db)
:
Ash (%db)
:
Reducing sugars(%db) :
Dextrin (%db)
:
Proteins
:
Free acid (ml 0.1m
:
NaOH/100g)
PH
:

15 22
0.05 0.38
0.04 0.93
85 94.9
1.70 5.22
> 1%
12.9 58
3.6 5.6

Carbohydrates in honey:
The principle sugars present in honey are fructose and glucose together with
maltose, a little sucrose and dextrin. Dextrin fraction includes a mixture of at least 22
di-tri and higher oligosaccharides. Ratio of fructose to glucose in pure honey is 106119:100.

Varieties of Madhu:
Table.10 Showing varities of madhu
CHARAKA5
SUSRUTHA6
1. Makshika
1. Pauttika

BHAVA PRAKASHA7
1. Maksika
71

2. Bhramara
3. Ksaudra
4. Pauttika

2. Bhramara
3. Ksaudra
4. Maksika
5. Chatra
6. Arghya
7.Auddalaka
8. Dala

2. Bhramara
3. Ksaudra
4. Pauttika
5. Chatra
6. Arghya
7. Auddalaka
8. Dala

Varga:
Madhu is mentioned among the Madhura varga, Kashaya varga (A.H.Su.S 10/24&31)
Pharmacological and therapeutic properties: 8
Rasa

Kashaya, Madhura(Caraka)
Madhura, Kashaya anurasa (Ba.Pr)
Guna
:
Guru, Sheeta, Ruksha (Caraka)
Laghu, Sheeta, Ruksha (Ba.Pr)
Veerya
:
Sheeta
Vipaka
:
Katu
Doshagnata :
Tridosha prashamana
Action and uses:
Slightly aggravates vata, alleviates rakta, pitta and kapha, grahi,
Lekhana, deepana, swarya, sowkumarya kara, srotovishodhana,
Varnya, kusta hara, yogavahi.
Specific properties of madhu:
1. Madhu pacifies vata and pitta due to madhura, kashaya and picchila bhavas. 9
2. Madhu is composed of many factors, when it is mixed with various formulations, it
10
alleviates many diseases as it is an excellent synergist.
3. Old (pakva) honey is tridhosha haram, where as new honey is tridhosha karam.11
12
Madhu after one year is considered as purana madhu.
References:
1. Ba.Pr.Po.K. 6(mv)/1
2. Pearsons chemical analysis of food
3. Ba.Pr.Po.K 6(mv)/1-5
4. AIDS to analysis of food and drugs
5. C.S.Su.S 27/243-244
6. S.S.Su.S 45/133
7. Ba.Pr.Po.K 6(mv)/6
8. Madhu ke upayog
9. S.S.Su.S 45/132
10. S.S.Su.S 45/142
11. S.S.Su.S 45/143
12. Ba.Pr.Po.K 6(mv)/126
METHOD OF PREPARATION OF THE MANJISTA KWATHA:
A brief description of kwatha:
Kwatha:
72

1. Definition: The preparation, prepaired by boiling a drug on fire is known as kwatha or

srutha. 1
2. Kwatha is one of the panchavidha kashaya kalpanas viz swarasa, kalka, kwatha, hima
and phant.2
Synonyms:
Srutha, kashaya, niryuha, kadha 3
Preparation:
One pala (4 tola) of coarsely powdered drug is boiled with 16 parts (64 tola) of
water in an earthen pot over a mild fire till the liquid is reduced to 1/8 th of the original
4
quantity. Thus obtained liquid is known as kwatha.
Administration:
1. In vata and kapha pradhana vyadhis ushna kwatha and in pitta pradhana vyadhis
sheeta kwatha should be administered.5
6
2. Ancient, physicians advise administration of kwatha after the digestion of food.
Dose:
4 tola in slightly warmed media
kwatha churna:

fig.13 manjista kwatha churna

1. Kwatha churna are compounded coarse powders which are intended for usage
whenever a particular type of decoction is required.
2. Churna should not be powdered finely. If the powder is very fine, the decoction is
not easily filtered into a clear liquid, this is due to the fine particles passing through the
filter.
3. The kwatha churna is potent for nearly one year, if protected from moisture and
insect
Preparation of manjista kwatha :
Manjista is cleaned, dried, powdered coarsely, and stored in glass jars. 30gms of
coarse powder of manjista is washed in water and taken in clean and dry vessel. Vessel is
then filled with 480ml of water and then kept on mild fire, with out covering it with the
lid, and stirring the contents till the liquid reduces to 60ml (1/8 th of the total content).
73

Then the decoction is filtered and used, when it is warm. Thus prepared kwatha should be
used with in 12hrs.8
Dose: 30ml Twice Daily
MANJISTA MADHU ALEPAM
Brief description of lepam:
Nirukti:
lipyathe anenathilepa
turushka nama gandha dravyam
Classification:
Lepas are of three types, Pralepa, Pradeha, Alepa
1. Pralepa: This is cold, thin layer, moist or dry (sheeta, tanu) and should not be
applied in the nights eg.chandana lepam
2. Pradeha: This may be ushna or sheeta, thick layer (bahala) and moist, pacifies vata
and kapha, cleanses, heals and alleviates inflammatory swelling and pain, it is used in
open and closed wounds, and can be applied in day and night times.
3. Alepa: This cleans skin and normalise blood and muscle. Its thickness is of medium
character, normalizes rakta and pitta.1
Alepa types:
Alepa is of three types doshagna, vishagna and varnya based on the action. This is also
termed as mukhalepa.
1. Doshagna: It is applied in vata, pitta dhosha and shotadi conditions. Applied in 1/4
angula pramana (app 0.175 inch)

th

2. Vishagna: It is applied for the vanaspati, prani and kanija visha effect in 1/3rd angula
pramana (app 0.205 inch)
3. Varnya: It is applied in vyanga, charmakeela, kshudraroga in angula pramana (app
0.325 inch)
As per susrutha, the thickness of alepa should be equal to moist skin of
buffalo (mahisha ardha charma) 3
Indications and contraindications:
1. The lepa on skin should be applied always in pratiloma direction i.e down to
upwards. By applying romabhimuka, the medicine is adequately absorbed
through siramukha and romakupa. Where it shows its effect.4
2. Lepa should be applied warm for vata and kapha, for pitta it should be applied
very cold. 5
3. The lepa applied over is removed when it is wet and never allowed to dry
because it becomes nirveerya and causes harmful effects. 6
4. Lepa should not be applied in the night, to avoid complications arise due to nonexit of heat suppressed by coldness.7
74

5. one should never apply stale paste nor additional applications over a paste
applied, due to thickness, it might cause, vedana, daha and ushma.8
6. After application of lepa, the person should avoid day sleep, speaking for long
hours, exposure to fire and sunlight, sorrow and anger. 9
7. Lepa should not be administered to persons suffering from peenasa, ajeerna,
dattanasya (who has received nasya), hanugraha, arochaka and has done
ratrijagarana. 10
Absorption of lepa:
In Dalhana commentary on susrutha samhita, during the description of abyanga,
Dalhana commented that the sneha takes 400 matrakala to reach the skin (S.S.Chi.S
24/30 Dalhana vyakya). Since the procedure of lepanakarma can be compared to some
extent with abyanga, the time factor can also be taken as the same, therefore the lepa
applied on the face should be kept for 5 minutes or more, and then washed away.
Action of lepa:
1. If lepa is done properly, it cures akala palitha, vyanga, vali, timira and neelika.11
2. For those who apply mukhalepa the vision becomes keen and the face smooth,
resembling a lotus flower. 12
Procedure adapted for application of manjista madhu alepam:

fig14.Fine powder of manjista and madhu

In this trial, patient is instructed to mix madhu with manjista choorna in a bowl
and to apply it with right hand middle finger upon the effected part from medial to
lateral side 2-3 times a day for 5 to 10 minutes. Then patient is asked to wash away the
lepa and instructed not to expose to sun-light and heat for a period of 1/2hr. In this way,
the medicine is applied regularly for a period of eight weeks.

References:

1. S.S.Su.S 18/8
2. Sha,S.U.K 11/1-2 & A.H.Su.S 22/14
3. S.S.Su.S 18/10
75

4. Sha.S.U.K 11/73
5. A.H.Su.S 22/14
6. Sha.S.U.K 11/74
7. S.S.Su.S 18/12
8. S.S.Su.S 18/13
9. A.H.Su.S 22/16
10. A.H.Su.S 22/17
11. A.H.Su.S 22/18
12. A.H.Su.S 22/22

76

Materials and methodas

77

PART II
SECTION III : MATERIALS AND METHODS
1. Selection of the patient: Thirty patients attending the OPD of Kaya chikitsa
department of GAH, Hyderabad presenting with features of vyangam are selected for the
clinical study irrespective of gender, age, occupation, chronicity etc.,. Patients with
notable systemic disorders are excluded. Special attention is made to notice the incidence
of gender, age, occupation, social status, diet, prakruthi, chronicity in relation to the
diseases.
2. Selection of the drugs: Manjista kwatham (ref C.S.Sutrastanam) is selected for
internal use and manjista madhu alepam (ref B.Pr.Madyama Kanda) is selected for
external use.

3. Method of preparation of the drug: Manjista roots are purchased by the reliable
person from the market, then cleaned, dried, and powdered coarsely for kwatha churnam,
and fine powder is obtained to use for alepam. Madhu from reliable manufacturing
company is taken.

4. Method of administration of drugs: Thirty patients are selected for clinical study,
and treated with manjista kwatham and manjista madhu alepam daily for a period of 60
days. Manjista madhu alepam is applied on the hyperpigmented patches on the face, 2-3
times a day, kept for 5 to 10 minutes. Manjista kwatham is taken in the dose of 30ml
twice a day.

5. Criteria for diagnosing the disease: The clinical features mentioned in the text are as
follows:
1. Tanu (thin/less in quantity)
2. Neeruja (painlessness)
3. Shyava (dark brown or dark dusky)
4. Mandala (circular patches)
These are the symptoms on the face, which are considered for the diagnosis of the
condition, but in practice, itching is an added symptom observed in some patients.

6. Critera for the assessment of results: The changes in the signs and symptoms such
as, color variation of hyperpigmented patch, size reduction of the patch, and
improvement of the associated symptoms such as itching are the chief parameters for
assessing the results.
a) Color: The color of the hyperpigmented patch, before and after the treatment is
recorded based on the fairness meter.
78

fig15. Fairness meter

Scoring / grading:
1. Mild discoloration
2. Moderate discoloration
3. Severe discoloration

:
:
:

1-8 shades
9-16 shades
17-24 shades

b) Size: The size of the discolored patchs is measured before and after the treatment by
using handi-lens, length and breadth of the patch is recorded in cms. Any reduction in the
size is considered as a positive sign.

fig16.Handi-lens

c) Number of patches: The numbers of hyperpigmented patches on the face were

counted before the treatment. Any reduction in the number was considered as an
improvement.
d) Associated symptoms: Before treatment any associated symptoms such as itching,
oozing, scaling, etc., are noted. Relief from these symptoms is considered as
improvement.
e) Assessment of the treatment: Effect of the therapy on the selected abnormality is
assessed on the basis of three categories responded, partially responded, not responded.
1. Good result: The color of the hyperpigmentd patch fading to 1-3 shades on the
fairness meter is considered as good result.
2. Moderate result: The color of the hyperpigmented patch fading to 4-6 shades on
the fairness meter is considered as moderate result.
3. Mild result: The color of the hyperpigmented patch fading above the 6 th shade on
the fairness meter is considered as mild result.
f) Follow up: Variations of color, size, and relief from associated symptoms are recorded
every week till the completion of treatment, later once in a month upto three months.
Type of study: The type of study opted here is single blind.
79

Observations and results

80

SECTION IV : OBSERVATIONS AND RESULTS

OBSERVATIONS
The clinical management of vyangam with manjista kwatham along with manjista
madhu alepam was conducted at GAH, Hyderabad. 30 cases were selected at random,
irrespective of gender, age, occupation, religion, diet, social-status, prakruthi, level of
discoloration, and cronicity.
The patients who have left the treatment and who did not turned up for the follow
up have been excluded from the study. The data of the regular patients who continued the
treatment is being presented here.
Table 11. Age-wise distribution:
S.No Age
No of patients
Percentage
1
15-24
4
13%
25-34
8
27%
2
3
35-44
9
30%
45-54
8
27%
4
55-64
1
3%
5
There is a peak evidence of discoloration in the age group 35-44 suggesting either
the use of oral contraceptives, or the pregnancy factor, stress and strain in females and
stress at the working place and over exposure to the pollution and sun might be the reson
for the disease occurring in males. And the pitta dhosha is predominant in the middle
aged persons.
Table 12. Gender-wise distribution:
S.No
1
2

Gender
male
female

No.of Patients
7
23

Percentage

23%
77%

Females outnumbered the males in the case of discoloration, suggesting excess mental
and physical stress and strain in daily life and role of hormonal imbalance.
Table 13. Marital status-wise distribution:
S.No
1
2

Marital status
Married
Unmarried

No of patience
26
4

Percentage
87%
13%

From observing the cases it is clear that married persons has the highest level of
discoloration, this may be due to responsibilities, stress and strain.
Table14. Religion-wise distribution:
S.No Religion No.of patients Percentage
1
Hindhu
21
70%
2
Muslim
5
17%
3
Christian
4
13%
Out of 30 cases visited the GAH 70% patients are Hindhus, 17% are Muslims and
13% are Christians.
Table 15. Occupation-wise distribution:
81

S.No Occupation No of patience

1
Students
3
2
Working
10
3
House wifes
17

Percentage
10%
33%
57%

More number of house wifes are affected with this disease, because of mental and
physical stress and strain due to house hold activities, next affected are working class due
to exposure to sunlight, pollution, and stress due to work load.

S.No
1
2
3
4
5

Table 16. Education-wise distribution:

Education
No of patients
percentage
7
23%
Uneducated
st
th
13
43%
1 -10 class
2
7%
Intermediate
5
17%
Graduation
3
10%
Post-graduation

More number of patients are in basic education group (1 st-10th ), with low
economic background prone to more stress and strain and low standerded of living. Next
is the uneducated group who does strenuous work and are exposed to pollution and sun.
Other groups are affected with the disease due to mental stress at work place and
improper dietry habits.

S.No
1
2
3

Table 17. Social-status wise distribution:

Social status
No of patients Percentage
Upper middle class
11
37%
Lowere middle class
16
53%
Lower class
3
10%

Lower middle class people are more prone to the disease due to there standered of
living with more mental stress and strain with high responsibilities and low income.
Lower class people are least affected, suggesting their sathmya with the surroundings and
thus having vyadhikshamatva. Average occurance in upper middle class indicates their
affordability to avoid some of the etiological factors.

S.No
1
2

Table 18. Locality-wise distribution:

Area
No of patience
Percentage
Urban
28
93%
rural
2
7%

More number of patients are from urban are due to pollution and exposure to sun
and demanding city life habits. Rural area people are less affected with the disease due to
there way of living with out tensions.

S.No

Table 19. Diet-wise distribution:

Diet
No of patients
Percentage
82

1
2

mixed
Vegetarians

22
8

73%
27%

People with mixed diet are more in number suggesting that derangement of pitta
is caused in them due to non vegetarian food stuffs are cooked with high chilly and spicy
content.
Table 20. Prakruthi-wise distribution:
S.No Prakruthi
No of patients
Percentage
1
V
8
27%
2
P
17
56%
3
K
5
17%
Pitta prakruthi persons are affected more in number as vyangam occurs in pitta
prakruthi persons due to predominance of pitta dhosha.

S.No
1
2
3
4
5

Table 21. Cronicity-wise distribution:

Cronicity range No of patients Percentage
Upto one year
Upto two years
Upto three years
Upto four years
Above four years

10
11
4
2
3

33%
37%
13%
7%
10%

More number of patients are in the chronicity range between 1-2 yrs shows that
people are more conserned about there looks.
Table 22. Level of discoloration:
S.No Discoloration No of patients
Percentage
1
Moderate
21
70%
2
severe
9
30%
More number of patients are having moderate discoloration which shows that disease is
less cronic.
Table 23. Hormone therapy-wise distribution:
S.No Hormone therapy
No of patients Percentage
1
Not used
21
70%
2
Used
7
23%
3
Using
2
7%
From the observation the harmone therapy is not an major etiological factor in
producing the the disease.
Table 24. Prognosis of lesion-wise distribution:
S.No Prognosis of lesion No of patients
Percentage
Progressive
21
70%
1
Non-Progressive
9
30%
2
Progressive hyperpigmented lessions are seen in more number of patients.
Table 25.Type of Distribution-wise incidence:
S.No Distribution No of patients Percentage
1
Diffuse
14
47%
83

2
Localised
16
53%
Localized hyperpigmented patches are seen in more number of patients.
Table 26. Nidana-wise distribution:
Nidana
No of patients percentage

S.No
Ayasa
14
47%
1
Krodha
7
23%
2
Shoka
6
20%
3
Ayasa & Krodha
1
3%
4
Ayasa & Shoka
2
7%
5
More number of patients are affected with the disease due to nidana karana, ayasa
followed by krodha and shoka.

S.No
1
2
3
4
5

Table 27. Etiological factors-wise distribution:

Etiological factors No of patiences Percentage
Melasma
Ultra-Voilet radiation
Drug induced
hyperpigmentation
Hormonal therapy
Post inflammatory
hyperpigmentation

20
4

67%
13%

10%

7%

3%

More number of patiences are effected by the etiological factor melasma, followed by
ultra-voilet radiation, drug induced hyperpigmentation, hormonal therapy, post
inflammatory hyperpigmentation.
Table.28 Number of patches-wise distribution
S.No
No of patches
No of patients Percentage
1
1-2
14
47%
2
3-4
12
40%
3
5-6
3
10%
4
7-8
0
0%
5
9-10
1
3%
Only one patient has nine patches, majority of patients has 1-2 patches on there
face followed by the patients with 3-4 patches on the face.

S.No
1

Table.29 Location of patch-wise distribution

Area
Location of patch No of patients
Area II
Around the rt.eye
2

Percentage
2%
84

2
3
4
5
6
7
8
9

Area - III
Area - IV
Area V
Area VI
Area VII
Area VIII
Area IX
Area - X

Around the lt.eye

Rt.Temporal region
Lt.temporal region
Rt.cheek
Lt.cheek
Nose
Around mouth
Fore head

2
4
4
27
27
11
5
12

2%
4%
4%
29%
29%
12%
5%
13%

Peak level of hyperpigmentation in Area VI and Area VII shows that, cheeks are the
more susceptible areas to develop vyangam, and we can see the similarity in both right
and left side of the face, followed by fore head, nose, temporal region and around eye.

parameter
Color variation

measurments

RESULTS
Table.30 Showing T and P values of the parameters
Mean
Percentage S.D S.E
T-value P-value
B.T | A.T Of relief
15.7
4
74.5%
2.76 0.50 23.22
0.001
18.75 16.06 14.35%
1.99 0.36 7.4
0.001

Chi-square test
B.T
| A.T
12.46
20
1.73
2.4

Table.31 Effect of treatment

S.no

Effect of therapy

No of patients

1
2
3

Good result
Moderate result
Mild result

19
8
3

Percentage
63%
27%
10%

85

MASTER CHART

S.No

Regd
No

Age/Sex

Occup

Diet

Prakriti

6728
6930
7170
7718
8122
11198
11442
29964
30131
31609
32911
33220
33231
33261
33412
33533
19521
21433
21441
21649
21997
22685
23249
23132
23154
23588
23812
24036
24880
25111

29y/F
40y/F
48y/F
35y/M
50y/F
23y/M
26y/F
40y/F
28y/F
40y/F
25y/M
24y/F
35y/F
45y/F
35y/F
32y/F
40y/F
30y/F
50y/F
32y/F
43y/F
45y/F
35y/F
28y/M
48y/F
51y/M
49y/F
23y/M
60y//F
18y/M

H-W
H-W
H-W
Wor
H-W
Stud
H.W
H.W
H.W
H.W
Stud
Wor
H.W
Wor
H.W
H.W
Wor
Wor
H.W
H.W
H.W
Wor
Wor
Wor
H.W
Wor
H.W
Stud
H.W
Wor

Mix
Mix
Veg
Mix
Mix
Mix
Mix
Mix
Veg
Veg
Mix
Mix
Mix
Veg
Mix
Mix
Mix
Mix
Veg
Veg
Mix
Mix
Mix
Mix
Veg
Mix
Mix
Veg
Mix
Mix

K
V
P
P
P
P
P
V
V
K
P
V
P
P
V
P
V
K
P
K
V
P
V
P
K
P
P
P
P
P

2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30

Color Variation
% of
BT
AT
relief

10
17
13.5
14
14
10
15
17
15
20
14
15
14
22
12
16
15
10
15
16
16
23
12
17
14
20
16
13
21
24

2
5
3.5
6.5
2
2
2
2
5
3
2
6
5
13
1
3
5
2
1
2
6
12
1
3
1
3
4
2
3
13

80%
71%
74%
70%
85%
80%
87%
88%
67%
85%
86%
60%
64%
41%
92%
81%
67%
80%
93%
88%
63%
48%
92%
82%
93%
85%
75%
85%
86%
46%

Measurement
% of
BT
AT
relief

7.75
26.2
18.2
13.6
39
2
6.66
15.6
39
23.36
5.25
5.13
30.5
10
3.65
52.92
10.38
7.75
27.5
16
25.25
49.75
3.25
29
2.28
43.5
17
8.75
21.56
1.67

5.25
21.5
14.5
11.3
35.86
1.6
5.23
12.2
33.6
19
4.75
4.4
29
8.7
3
48.67
9
5.75
21.86
12.5
22.5
47
2
22.33
1.8
36.5
14.36
7.17
18.5
1.65

32%
18%
20%
17%
8%
20%
21%
22%
14%
19%
10%
14%
5%
13%
18%
8%
13%
26%
21%
22%
11%
6%
38%
23%
21%
16%
16%
18%
14%
2%

Result

Good.R
Mode-R
Good.R
Mode-R
Good.R
Good.R
Good.R
Good.R
Mode-R
Good.R
Good.R
Mode-R
Mode-R
Mild-R
Good.R
Good.R
Mode-R
Good.R
Good.R
Good.R
Mode-R
Mild-R
Good.R
Good.R
Good.R
Good.R
Mode-R
Good.R
Good.R
Mild-R

86

OBSERVATION CHARTS
Education-wise distribution

Age-w ise distribution

14
12
10
8
6
4
2
0

No of patients

10
8
6
4
2
0
15-24 25-34 35-44 45-54 55-64

un-e 1-10t inter grad p.gra

Age in years

education

Etiological factors-w ise distribution

20
18
16
14
12
10
8
6
4
2
0
D-I-H Hor
Mel P-I-H U-R

12
10
8
6
4
2
0

No o f patients

no of patients

cronicity-w ise distribution

upto upto upto upto abov

1
2
3
4
4
cronicity range in years

Etiological factors

Gender-w ise distribution

N o o f p at ien t s

Nidana-wise distribution
15
male
23%

10

male

female

0
Ay

Kr

Sh

female
77%

A-k A-s

Nidana

Plate no.1

87

Religion-w ise distribution

Occupation-w ise distribution

Chirstian
13%
Muslim
17%

Students
10%

Hindu
Muslim
Hindu
70%

Chirstian

Upper
middle
class
37%

Low er
middle
class
53%

Working
Students

Marital-status distribution

Social status-wise distribution

Low er
class
10%

House w ifes
House
w ifes
57%

Working
33%

Upper middle
class

Unmarrie
d
13%
Married

Low er middle
class

Unmarried
Married
87%

Low er class

Locality-w ise distribution

Diet-w ise distribution

Rural
7%

Vegitarian
27%

Urban

Mixed
Mixed
73%

Vegitarian

Rural
Urban
93%

Level of discoloration

Prakruthi-w ise distribution

Kapha
17%

Severe
30%

Moderate
Moderate
70%

Vata
27%

Vata
Pitta

Severe

Pitta
56%

Kapha

Plate no.2

88

Prognosis-w ise distribution

Horm one therapy-w ise distribution

Using
Used 7%
23%

Non
progressi
ve
30%

Not used
Used
Not used
70%

Non
progressive
Progressive

Progressi
ve
70%

Using

Distribution

Number-wise distribution

1-2

10% 0%3%

3-4

Diffuse

47%

Localised
40%

5-6
7-8
9-10

location-wise distribution
n o of patients

Localised
53%

Diffuse
47%

30
25
20
15
10
5
0
Area Area Area Area Area
II
IV
VI
VIII
X
location

Plate no.3

89

Effect of the drug

Plate no.4

90

Plate no.5

91

SECTION:V DISCUSSION
Vyangam is a disorder in which hyperpigmented patches are noticed on cetain
areas of the face. By considering the symptomology, it is comparable to Melasma /
Chloasma. Vyangam is one among the 44 kshudra rogas, Charaka has mentioned it in
bahirmargaja rogas and Susrutha has described in kshudra roga prakarana. In vyangam
increased pigmentation is seen, particularly affecting the skin of the face. The study
entitled A clinical study on the effect of manjistadi lepam and manjista kwatham in
vyanga rogamwas conducted at Govt. Ayurvedic Hospital, Hyderabad. Total 30 cases
were selected at random and were treated with manjista madhu alepana and manjista
kwatham 30ml twice daily for 60 days.
From observations female population (77%) is more effected than males (23%)
with this disorder. This may be due to mental and physical stress and atrain in daily life
and role of hormonal imbalance. More over, the disorder has cosmetic significance, so
the female gender is more concerned and approach for the treatment.
There is a peak incidence of this disease in the age group of 35-44 years. Out of
30 cases, 30% were in this age group, they belong to pre-menopausal phase, there is a
high alteration of hormonal balance in this age group. Equal number of cases was
moderately affected in 25-34 and 45-54 (27%) age groups. Least effected patients are in
the age groups of 15-24 and 55-64.
More number of patients was under the married group (77%), this may be due to
the responsibilities, stress and strain.
It is observed that out of 30 cases, 21patients (70%) were Hindus, 5 patients
(17%) were Muslims and 4 patients (13%) were Chirstians, this can be emulated to their
religious customs and beliefs pratcised.
Occupational status reveals that 57% are house-wifes, 10% are working, and 3%
are students. More number of house-wifes are effected with this disease, because of
mental and physical stress and strain due to house hold activities, next effected are
working class due to exposure to sunlight, pollution and stress due to work load.
Among 30 cases 43% are among basic education group (1st -10th class), 23% are
uneducated, 17% are graduates, 10% are post graduates, and 7% are of intermediate
education. More number of patients are in basic education group, with low economic
background prone to more stress and strain and low standered of living. Next is the
uneducated group who does strenuous work and are exposed to pollution and sun. other
groups are effected with the disease due to mental stress at work place and improper
dietry habits.
According to the social status out of 30 cases 53% are of lower middle class, 37%
are of upper middle class and 10% are of lower class. Lower middle class people are
more prone to the disease due to there standered of living with more mental stress and
strain with high responsibilities and low income. Lower class people are least effected,
suggesting their sathmya with the surroundings and thus having vyadhikshamatva.
Average occurance in upper middle class indicates their affordability to avoid some of
the etiological factors.
92

It is observed that 93% patients were from the urban area, due to pollution and
exposure to sun and demanding city life habits. Rural area patients were 7% due to their
way of living with out tensions.
Among 30 cases, 22 patients (73%) have mixed dietary habits, most of them
prefer non-vegetarian food. Generally these food items are hot and spicy, so vitiation of
pitta dosha is suspected.
When prakruthi of the patients was taken into consideration 56% belonged to pitta
prakruthi, 27% belonged to vata prakruthi, 17% belong to kapha prakruthi. From
observation it is clear that pitta prakruthi people are more susceptible to vyangam.
About range of chronicity of these pigmentary changes- out of 30 cases, 37%
cases fall under cronicity range of upto 2 years, 33% upto1 year, 13% upto 3years, 10%
above five years and 7% upto 4 years. From this it is clear that the disease is moderately
chronic, despite of rapid progress in modern medicine, there is lack of satisfactory
treatment for this disorder. Further, chronic use of various drugs may precipitate the
problem.
Level of discoloration among 30 cases, moderate level of discoloration is noted in
70% of patients and severe level of discoloration is noted in 30% of patients. This shows
that 70% of patients has less cronic disease.
Taking in to consideration, prognosis of the hyperpigmented patch among 30
cases, 70% patients has progressive lesion and 30% patients has non-progressive lesion.
Regarding the type of distribution of the hyperpigmented patch, among 30 cases,
47% has diffuse type of lesion and 53% has localized type of lesion.
Nidana wise distribution of 30 cases shows that, 47% patients has ayasa as nidana karana,
23% has krodha as nidana karana, 20% has shoka as nidana karana, 7% has ayasa &
shoka as nidana karana and 3% of patients has ayasa & krodha as nidana karana
Taking in to consideration of the etiological factor among 30 cases, 67% patients
has melsama as etiological factor, 13% has exposure to ultra-voilet radiation, 10% has
drug induced hyperpigmentation, 7% has hormonal therapy as etiological factor and 3%
has post inflammatory hyperpigmentation.
According to the number of patches in 30 cases, 47% of patients has 1-2 patches,
40% of patients has 3-4 patches, 10% has 5-6 patches and 3% of patients has 9-10
patches on the face.
It is observed that among the 30 cases around Rt. and Lt. eye 2+2 patches (4%),
on Rt. and Lt. temporal region 4+4 patches (8%),on Rt. and Lt. cheeks 27+27 (58%), on
nose 11 patches (12%), around mouth 5 patches 5%, and on fore head 12 patches (13%)
are present. Cheeks are the more effected areas on the face, followed by fore head, nose,
mouth, temporal region and eyes.
It has been observed that there was no spread of lesion in the patients who has
taken the treatment.
93

The results were divided into good result, moderate result and mild result groups.
They were assessed on the basis of color variation and measurement of the lesion before
and after treatment. Out of 30 cases 19 patients (63%) showed good result, 8 patients
(27%) showed moderate results and 3 patients (10%) showed mild results. This scoring
has been obtained by taking color fading level scoring on fairness meter. From any shade
if the color fades to 1-3 levels on the fairness meter, it is considered as good result. From
any shade if the color fades to 4-6 levels on the fairness meter, it is considered as
th
moderate result. From any shade if the color fades to, above 7 shade on the fairness
meter it is considered as mild result.
From the results obtained we can observe that there is marked variation in the
color but only one or two centimeters of lesion is reduced.
Manjista kwatham is given 30ml twice daily along with manjista madhu alepam
on the hyperpigmented patches for 60 days. Manjista mentioned as varnyam and pitta
shamanam by Charaka and Susruta respectively, having the properties such as madhura,
tikta, kashaya rasa pacifies the pitta which is one of the etiological factors of vyangam.
This pitta can be stated as bhrajaka pitta- asper the claim of Ayurveda, there exists in the
avabhasini layer of the skin, a pitta known as bhrajaka which is responsible for providing
the skin with that pigment which imparts to it its normal color. This pigment can be
called as melanin which is metabolically produced by specialised cells in the skin by the
enzyme tyrosinase. The roots of manjista contains coloring matter such as purpurin,
manjistin, xanthine etc., which may be effective in restoring the normal skin color and
complexion of the face by acting as a skin bleaching agent and inhibiting melanin
synthesis in the melanocytes of the skin.
Madhu or makshika, with its tridosha prashamana property may effect vata and
pitta which are vitiated in the disorder vyangam. Madhu is described as varnyam hence,
bestows color or complexion. The topical drug treatment (lepana karma) aims at
providing high concentrations of the drug at the site of application. Madhu with its
yogavahi guna is taken as base or vehicle and it enhances the properties of manjista.
Madhu may function as a reservoir for manjista, allow local release of suitable amounts
of the active drug, assist in the absorption and provide a reasonably safe in infra-structure
for practical application. In addition to these, it has lubricating effects. The paste of
manjista and madhu also protect the skin from external irritants and from sunlight.
Thus it can be concluded that the manjista kwatham and the manjista madhu
alepam had good effect on vyangam.

94

summary

95

SECTION: VI
SUMMARY

1. The present clinical study entitled A clinical study on the effect of manjistadi
lepam and manjista kwatham in vyanga rogam was conducted at GAH,
Hyderabad in 30 patients presenting with the features of vyangam.
2. The disorder vyangam has close resemblance with Melasma / Chloasma.
3. Vyangam has no systemic effects but it is of cosmetic significance and concerned
with the beauty of the face.
4. Vyangam occurs due to psycho-physiological changes caused due to krodha,
shoka and ayasa. Other etiological factors like, ahitahara sevana, pitta
prakopakara ahara sevana cause pitta prakopa along with vata, which manifests as
vyanga roga on the face.
5. Females (77%) are more effected than males (23%). This is due to improper diet
habits, stress and strain due to excess work and high responsibilities in
maintaining the family.
6. Localised hyperpigmentation is seen as a side effect of several of several systemic
medications and also due to the photosensitivity of the skin.
7. Results were assessed on the bases of signs and symptoms before and after the
treatment.
8. Drugs used in the clinical trial were varnyakara and has pittashamana properties.
9. Manjista, and madhu has coloring matter, hence they proved to be good skin
bleaching agents.
10. Lepana karma was effective, because the drug entered the skin in adequate
concentration from the site of application.
11. Manjista has pitta shamana properties so it also pacifices rakta dosha as well.
12. Results are found to be encouraging, they are compiled and analyzed statistically.

96

conclusion

97

SECTION: VII
CONCLUSION
1. Manjista madhu alepam and manjista kwatham is proved to be an effective drug
in the disorder vyangam.
2. Irrespective of the cause of the hyperpigmentation i.e., hormones; drug induced
hyperpigmentation; photosensitivity; and combination of the above the treatment
proved to be effective.
3. it is advisable to conduct the clinical trial on more number of patients and on all
types of discolored patches on the face.
4. It is also advisable to have more effective parameters or investigations like biopsy
(scrapings of patches) / melanin assessment / hormonal assays.
5. It is also advisable to assess the role of manjista as coloring agent locally on the
face as well as all over the body.
6. It is proved that the disorder vyangam is comparable to hyperpigmented patches
caused by either exposure to ultra-voilet radiations or drug reactions or allergy to
certain chemicals and cosmetics or hormonal imbalances or oral contraceptives.
7. From observation fading of patch takes place more than two months, so treatment
may be continued for four to five months.

98

RESEARCH CASE SHEET FOR VYANGA

P.G.DEPARTMENT OF KAYA CHIKITSA
DR.B.R.K.R.AYURVEDIC GOVERNMENT COLLEGE/HOSPITAL
S.R.NAGAR, HYDERABAD-38
PARTICULARS OF PATIENTS:
Name

Occupation

Age

Marital status

Sex

Date

Address

S.No

Religion

OP/IP No

Education

Ward/Bed No

Social Status :

Probable Diagnosis :

PRADANA VEDANA (CHIEF COMPLAINT):

ANUBANDA VEDANA (ASSOCIATED COMPLAINTS):

ADYATANA VEDANA VRITTANTA (HISTORY OF PRESENT ILLNESS):

POORVA VYADHI VRITTANTA (HISTORY OF PREVIOUS ILLNESS):

KULA VRITTANTA (FAMILY HISTORY):

99

VAIYAKTIKA VRITTANTA (PERSONAL HISTORY)

Ahara(Food):
Agni(Apetite):
Vihara(Activities):

Mala Pravritti( Bowel):

Nidra(Sleep):

Mootra Pravritti(Micturition):

Vyasana(Addictions):

ATURA PAREEKSHA (EXAMINATION OF THE PATIENT):

A. SAMANYA PAREEKSHA(GENERAL EXAMINATION):
Prakriti

Nadi:

Height:

Temp:

Weight:

B.P:

B. VESHASHA PAREEKSHA( LOCAL EXAMINATION OF SKIN):

a) LOCATION OF THE LESION:

100

b)TWAKGATA STANIKA PAREEKSHA:

1. Prograssive/Nonprograsive
:
2. Localised/Diffuse
:
3. Colour
:
4. Size
:
5. Shape
: Irregular/Flat Round/Oval/Rectangular
NIDANA (ETIOLOGICAL FACTORS):
1. a)Krodha
b)Ayasa
c)Shoka
2. Ultra-Violet radiation(Exposure to sunlight)
3. Melasma / Chloasma
4. Drug induced hyperpigmentation
5. Hormonal therapy
6. Allergy to chemicals
7. Post-Inflammatory hyperpigmentation
8. Allergy to certain cosmetics
9. Systemic causes of hyperpigmentation

LEVEL OF VAIVARNYATA-SCORING:
1. MILD DISCOLORATION
2. MODERATE DISCOLOURATION
3. SEVERE DISCOLOURATION

SAMPRAPTI GHATAKAS:
Dosha

Udbhbava stana

Dooshya

Sanchara stana

Srotas

vyakta stana

Prakara

Rogamarga

Agni

Swabhava

VYADHI VINISCHAYA (DIAGNOSIS):

CHIKITSA (TREATMENT):
Dravya (Drug):

Matra (Dose):

Kala(Duration):

Upayoga vidhi(Mode of Administration):

Dietary advice: Pathya

101

Apathya--PROGNOSIS:
Observation chart:
Lakshana

Before
Treatment

9th
Day

18 th
Day

27th
Day

36th
Day

45th
Day

52nd
Day

60th
Day

Remarks

Vaivarnyata
Measurement
Of lesion
Other signs &
symptoms

RESULTS:
1. Good result
2. Moderate result
3. Mild result

Signature of the scholar

Signature of the Supervisor

INFORMED CONSENT
I -----------------son/daughter/wife of -----------------am exercising my free
will to participate in the above study as a subject. I have been informed to my satisfaction
by the attending physician the purpose of clinical evaluation and the nature of the drugtreatment. I am also aware of my right to opt out of the treatment schedule at any time
during the course of the treatment.

Patient signature

102

My commitment increases my level of energy. My energy increases my level of action. My

action increases my level of success. My success increases my level of commitment.

Research in any field is the most important section of development. Ayurveda is in

service is for ages to the needy mankind to relieve their ailments and recording the facts
for the future generations. At present the Ayurveda research scholar, developing the
Ayurveda and understanding under the limelight of contemporary scientific backgrounds.
The plagiarism is more and more now a day in the scientific community. This is
happening as the researches of the various institutions are not available for the common
researcher. We wish to control this plagiarism by contributing the dissertations for
scientific community. If you find any thesis is a copy of the previous publication, we take
this issue to the university authorities for proper action. The solution to prevent copy cats
is http://ayurvedaresearch.wordpress.com/

Dr. Shiva Rama Prasad Kethamakka

technoayurveda@gmail.com,