Skin diseases in pregnancy

The dermatoses of pregnancy

can be classified into the following 3 groups:

physiologic skin changes in pregnancy,

dermatoses and cutaneous tumors affected by

pregnancy,

and specific dermatoses of pregnancy

 Outline
Normal skin changes during pregnancy.
Skin diseases during pregnancy:
1. Pemphigoid Gestationis
2. PRURITIC URTICARIAL PAPULES AND PLAQUES OF PREGNANCY (PUPPP)
3. ATOPIC ERUPTION OF PREGNANCY: Eczema, Prurigo,Pruritic folliculitis
4. PUSTULAR PSORIASIS OF PREGNANCY
5. Intrahepatic cholestasis of pregnancy(ICP)

Skin disaeses affected by pregnancy (psoriasis , fungal infection, melanoma ,acne)

Pemphigoid Gestationis
 Pemphigoid Gestationis
Herpes gestationis

A pregnancy-associated autoimmune disease.

It is not related to or associated with any
active or prior herpes virus infection.
named herpes gestationis on the basis of the
morphological herpetiform feature of the
blisters.
 PEMPHIGOID GESTATIONIS

Refers to a blistering disease that is clearly associated

with pregnancy and increased fetal risk.
It only occurs during pregnancy or with trophoblastic
tumors,such as hydatiform mole or choriocarcinoma.
Incidence 1/50000
HLA-DR3 and HLA-DR4 are more common among women
with this disorder.
 Clinical Manifestations

Pruritus may precede onset of visible skin

lesions, which erupt during the second or third
trimester or postpartum.
The rash typically begins on the trunk as
urticarial plaques or papules surrounding the
umbilicus ; vesicles may also be present .
Lesions may be seen on the palms and soles,
but rarely on the face or mucous membranes.
Mucosal lesions are present in less than 20
percent of cases.
The eruption spreads rapidly and forms bullae .
Periumbilical erythematous papules, vesicles,
erosions, and crusts are present in this patient
with pemphigold gestations.
Multiple tense bullae on skin.
 Course

Course Pemphigoid gestationis may remit prior to

delivery.
However, 75 percent of patients flare postpartum and
at least 25 percent subsequently flare with use of oral
contraceptive pills or during menses.

Most cases spontaneously resolve in the weeks to

months following delivery.
The disease usually recurs with subsequent
pregnancies and is often worse , but may also skip
pregnancies
Tense bullae are present on the arms of this
otherwise healthy 32-year-old primigravida
woman.
A close-up view of a blister reveals the tense primary lesion filled
with clear fluid.
 Etiology
Etiology The pathologic IgG antibody in patients with pemphigoid
gestationis binds to antigen in the BMZ of skin, which is known as bullous
pemphigoid antigen 2 (BP-AG2). BP-AG2 is a transcellular glycoprotein in the
hemidesmosome (a structure that connects the basal cell of the epidermis to
the basement membrane, thus helping to keep the epidermis attached to the
dermis), with both cytoplasmic and extracellular domain.

IgG triggers the classic complement pathway, eosinophils are recruited,

and proteolytic enzymes separate the epidermis from the dermis . It is not
known why some patients form these antibodies. It has been theorized
that paternal MHC class II antigens found in the placenta
induce maternal antibodies to the amniotic basement
membrane. These antibodies can then cross-react with skin and cause
maternal (and sometimes newborn) disease
 The initial clinical manifestations are erythematous urticarial patches and plaques,
which are typically periumbilical. These lesions progress to tense vesicles and blisters.
Some patients may present with urticarial plaques and may never develop blisters
(see the images below). These hivelike plaques differ from true urticaria because of
their relatively fixed nature. The rash spreads peripherally, often sparing the face,
palms, and soles. Mucosal lesions occur in less than 20% of cases. Patients may have
secondary infections at blister sites.
 Diagnosis
Two skin biopsies should be obtained to make
the diagnosis of pemphigoid gestationis.
Routine histology is performed on one
specimen and direct immunofluorescence is
performed on the other
 Skin biopsy (using routine histologic processing)
reveals a subepidermal vesicle with a perivascular
lymphocytic and eosinophilic infiltrate. Basal cell
necrosis and edema of the dermal papillae are
usually noted.
Immunofluorescent examination shows a
homogeneous, linear deposit of complement 3
(C3) at the basement membrane zone (BMZ) .The
presence of this C3 band is pathognomonic for
pemphigoid gestationis in a pregnant patient.
IgG is also present in 30 to 40 percent of patients.
Direct immunofluorescence microscopy shows linear
deposition of C3 along the dermal-epidermal
junction.
 Laboratory tests not necessary for
diagnosis.
Antithyroid antibodies are often present .
The degree of peripheral eosinophilia may
correlate with disease severity
 DDx
Pruritic Urticarial Papules and Plaques of
Pregnancy
Acute Urticaria
Allergic Contact Dermatitis
Cicatricial Pemphigoid
Dermatitis Herpetiformis
Drug-Induced Bullous Disorders
Erythema Multiforme
Linear IgA Dermatosis
 Treatment

mid to high potency topical corticosteroids for

initial therapy of localized disease.
Ointments tend to cause less stinging and may
be more effective than other topical
preparations, but are more cumbersome.
Nonsedating oral antihistamines are an
acceptable alternative. Topical antihistamines
are not recommended because they are not
effective and may induce an allergic response.
 If these drugs do not control symptoms, which
is common, then systemic corticosteroids
(eg, prednisone 0.5 mg/kg per day) are usually
effective. The dose may be tapered, and even
discontinued, in some pregnancies. However,
reinstatement of treatment postpartum will
likely be needed .
 Prognosis
Mild placental insufficiency
Fetuses are at risk for growth restriction and
prematurity.
Neonatal pemphigoid gestationis ;have a mild
course that resolves within weeks
There is minimal risk of adrenal fetal suppression
The mother is at high risk of recurrent
pemphigoid gestationis with subsequent
pregnancies .
Increased lifetime risk of Grave's disease.
 PRURITIC URTICARIAL PAPULES
AND PLAQUES OF PREGNANCY
(PUPPP)
 Is also called polymorphic eruption of
pregnancy (PEP),
Toxic erythema of pregnancy
linear IgM dermatosis of pregnancy
 Incidence
PUPPP is the most common specific dermatosis
of pregnancy.
The incidence is 1/160 .
Three-quarters of patients with the classic type
of PUPPP are nulliparous .
PUPPP is 8- to 12-fold more common in women
with multiple gestations
Possibly due to increased abdominal distension
or higher hormone levels
 Diagnosis

The diagnosis of PUPPP is clinical, based on

characteristic findings on history and physical
examination.
 Clinical Manifestations
PUPPP typically presents as erythematous papules within
striae .
Abdominal striae are the most common initial site (with
periumbilical sparing) and may be the only initial site .
The lesions then spread to the extremities and coalesce to
form urticarial plaques.
The face, palms, and soles are usually spared.
White halos often surround the erythematous papules in
patients with fair skin.
Lesions may also be target-like.
All patients have extreme pruritus .
PUPPP usually begins late in the third trimester (mean
onset 35 weeks), but may develop postpartum.
Erythematous plaques in the distribution of striae are present.
Erythematous plaques are present in areas of striae in this woman with
PUPPP.
In fair-skinned patients with PUPPP, a white halo may be present around the
erythematous papules and plaques.
 Etiology
The etiology of PUPPP is unknown and may be
heterogeneous .The degree of stretching of the
abdominal skin may play a role; PUPPP is more
common with excessive stretching .It has been
hypothesized that stretching may cause damage
to connective tissue, which results in exposure of
antigens that trigger an inflammatory response.
Another possibility is that it represents an
immunologic response to circulating fetal
antigens. As an example, one study demonstrated
fetal DNA in maternal skin lesions .
 Course Pruritus may worsen immediately
after delivery, but generally resolves by 15
days postpartum.
Laboratory There are no laboratory
abnormalities related to PUPPP
 Pathology Biopsy is not necessary for diagnosis, but
may be performed in cases of diagnostic uncertainty.
Histopathologic examination of skin biopsies reveals
nonspecific findings, such as spongiosis and parakeratosis in
the epidermis. The dermis contains a perivascular
lymphocytic infiltrate primarily composed of T-helper cells;
eosinophils or neutrophils are occasionally present. There
may also be dermal edema.
Immunofluorescent studies demonstrate C3 and IgM or IgA
deposits at the dermoepidermal junction (DEJ) .These
deposits are granular, not linear. (Linear deposits of C3
at the DEJ are considered pathognomonic for
pemphigoid gestationis).
 DDx
Acute Urticaria
Allergic Contact Dermatitis
Chronic Urticaria
Drug Eruptions
Erythema Multiforme;target lesion
Pemphigoid gestationis
 Treatment
low to mid potency topical corticosteroids as
initial therapy for relief of symptoms.
Nonsedating oral antihistamines are an
acceptable alternative.
Systemic corticosteroids
(eg, prednisone 0.5 mg/kg per day) are
occasionally required because of extreme
pruritus.
 Prognosis
PUPPP poses no increased risk of fetal or
maternal morbidity (other than maternal
pruritus.
The rate of recurrence has not been defined.

Recurrence is also uncommon with menses or

oral contraceptives.
Several studies have reported a preponderance of
male fetuses in women with PUPPP.
ATOPIC ERUPTION OF PREGNANCY
Eczema in pregnancy, Prurigo of pregnancy, and
Pruritic folliculitis of pregnancy have been grouped
under the unifying term atopic eruption of pregnancy .
This classification scheme is based upon the presence
of shared clinical features, including a possible
association with atopy.
All three disorders may present with inflammatory
papules as a primary feature.
None of the disorders classified within this group are
associated with adverse effects on the fetus.
Eczema in pregnancy is strongly associated with a personal
history of atopy (seasonal rhinitis, asthma, and/or atopic
dermatitis) . Only 20 percent of affected women have a
preceding history of atopic dermatitis.
 Eczema Eczema is the most common
pruritic skin disorder occurring in pregnancy.

Eczema in pregnancy is strongly associated

with a personal history of atopy (seasonal
rhinitis, asthma, and/or atopic dermatitis)
 Clinical manifestations and diagnosis This
disorder often begins during the first or second
trimester. Symptoms frequently present in a
flexural distribution, similar to classic atopic
dermatitis.
Any area of the skin may be affected. Lesions
may be eczematous patches or intact or
excoriated papules.
The diagnosis is based upon the recognition of
clinical features.
A slightly lichenified, erythematous patch and excoriations are present in the
antecubital fold.
Numerous erythematous papules are present on the hands of this patient
with atopic dermatitis.
 Pathology Skin biopsy is not necessary in
most cases, and findings are non-specific.
Laboratory tests Although laboratory
testing is not indicated, up to 70 percent of
patients may have elevated serum IgE levels .
Etiology It is postulated that the
enhancement of Th2 cytokine production
known to occur during pregnancy may
contribute to the development of eczema .
 Differential diagnosis The earlier onset, predilection
for involvement of skin flexures, and the absence of
urticarial plaques in abdominal striae help to
distinguish this disorder from PUPPP.
Treatment Similar to non-pregnant patients with
eczema, these patients should be encouraged to
maintain adequate skin hydration through the use of
topical emollients. Low- to mid-potency topical
corticosteroids are useful for controlling symptoms.
Prognosis Eczema in pregnancy has not been
associated with adverse effects on the fetus.
 Prurigo of pregnancy :
Other terms that have been used to describe
prurigo of pregnancy include prurigo
gestationis of Besnier
Incidence 1 in 300 to 1 in 450
pregnancies
 Clinical manifestations and diagnosis The diagnosis of
prurigo of pregnancy is clinical, based on characteristic
findings on history and physical examination.
Prurigo of pregnancy usually begins in the second or third
trimester ,but has been reported in all trimesters.
Clinical diagnostic criteria consist of erythematous,
excoriated nodules, or papules on the extensor surfaces of
the limbs and trunk.
Lesions are grouped and may be crusted or appear
eczematous.
Course The eruption usually resolves in the immediate
postpartum period ,although it can persist for up to three
months .
 Laboratory Laboratory evaluation is unnecessary.
Two studies noted an elevated IgE concentration in
some patients.
Pathology Biopsy is not necessary for diagnosis
Skin biopsies of lesions are nonspecific. There is a
dermal perivascular mononuclear cell infiltrate without
eosinophils. The epidermis may show acanthosis,
hyperkeratosis, and parakeratosis.
Etiology The etiology is unknown. A relationship
with a history of atopy has been proposed, but remains
controversial .
 Differential diagnosis
PUPPP
pruritic folliculitis of pregnancy
Cholestasis
scabies, drug reactions
intrahepatic cholestasis of pregnancy
should be excluded by history and laboratory
testing (eg, bile acids)
 Treatment We suggest low to mid potency topical
corticosteroids as initial therapy for relief of
symptoms. Topical corticosteroids are usually
effective so systemic glucocorticoid therapy is
unnecessary.
Nonsedating oral antihistamines are an
acceptable alternative.
Prognosis There are no fetal effects, nor is
there long-term maternal risk .Prurigo of
pregnancy may recur with subsequent
pregnancies .
 Pruritic folliculitis of pregnancy Pruritic
folliculitis refers to sterile eruption of pruritic,
follicular lesions .
Incidence The incidence is unknown. In one
prospective series, one case was identified
among 3192 pregnant women.
 Clinical manifestations and diagnosis The diagnosis
of pruritic folliculitis is clinical. A pustule should be
cultured to rule out bacterial or candidal folliculitis.
Pruritic folliculitis of pregnancy usually presents in the
second or third trimester.
The eruption consists of follicularly-based papules and
pustules, primarily on the trunk, but sometimes
spreading to the extremities.
The appearance is similar to that of steroid induced
acne.
Course The eruption typically clears within two
weeks of delivery
Steroid induced acne
 Laboratory Laboratory tests are unnecessary other than
to exclude infection. Laboratory values are normal .
Pathology Biopsy is not necessary for confirmation of
the clinical diagnosis. Histopathology shows a perivascular
or interstitial lymphohistiocytic infiltrate and excoriation of
the epidermis, similar to polymorphic eruption of
pregnancy. An acute suppurative sterile folliculitis is
diagnostic.
Etiology The pathogenesis is unknown.
Differential diagnosis It may be difficult to distinguish
pruritic folliculitis of pregnancy from prurigo of pregnancy
or PUPPP. Infectious folliculitis must also be considered.
 Treatment We suggest low to mid potency
topical corticosteroids as initial therapy for relief
of symptoms .
Oral corticosteroids are rarely needed.
Nonsedating oral antihistamines are an
acceptable alternative.
Prognosis Maternal and fetal outcome appear
to be normal .
There are no data on recurrence with subsequent
pregnancies.
PUSTULAR PSORIASIS OF PREGNANCY
Is a newer name for impetigo herpetiformis. The
former is more descriptive and avoids the
implication of bacterial or viral infection, neither
of which plays a role in this disease.
It is debated whether pustular psoriasis of
pregnancy is truly specific to pregnancy .We favor
a true association as these women rarely have a
history of psoriasis and the eruption resolves
postpartum.
Incidence Pustular psoriasis of pregnancy is
exceedingly rare.
 Clinical manifestations and diagnosis clinically; however, we
suggest confirmation by histologic evaluation of a biopsy specimen,
given the potential consequences of the disease.
The disease can occur anytime during pregnancy. Lesions begin as
erythematous plaques with rings of pustules. The plaques then
enlarge from the periphery as the center becomes eroded and
crusted. There may be concentric rings of pustules.
The nails may become onycholytic.
The trunk and extremities are affected, while the hands, feet, and
face are usually spared.
Usually not pruritic. However, the patient feels ill with
symptoms such as malaise, anorexia, nausea, vomiting, diarrhea,
fever, and chills .
Post-inflammatory pigmentation occurs when plaques and pustules
resolve; however, scarring does not result.
 Course Pustular psoriasis of pregnancy
usually remits quickly postpartum, but may
also flare after delivery.
It recurs with subsequent pregnancies and
may also recur with menses or use of oral
contraceptive pills.
The disease tends to be more severe and have
an earlier onset with subsequent pregnancies
 Laboratory We suggest a complete blood count,
calcium level, electrolytes, and urinalysis. Leukocytosis
and an elevated erythrocyte sedimentation rate are
common. Hypocalcemia may be present, possibly
related to hypoparathyroidism and can lead to tetany,
delirium, and seizures. Albuminuria, pyuria, and
hematuria occasionally occur. Pustules are sterile.
Pathology We suggest biopsy for confirmation of
the diagnosis. The pathology is the same as in pustular
psoriasis in the nonpregnant patient. Spongiform
pustules with neutrophils are observed in the
epidermis. Psoriasiform hyperplasia and, possibly,
parakeratosis also occur .
 Etiology The etiology is poorly understood.
It may relate to hormonal changes of
pregnancy, particularly progesterone.
Hypocalcemia and hypoparathyroidism may
also be inciting factors
 Differential diagnosis
Infectious etiologies of pustules, such as
candidiasis and impetigo, should be excluded by
appropriate cultures.
dermatitis herpetiformis,
pustular drug eruptions
Pruritic folliculitis of pregnancy is pruritic and
exclusively perifollicular, neither of which is true
of pustular psoriasis of pregnancy.
Pemphigoid gestationis
 Treatment :systemic corticosteroids as initial therapy. High dose systemic
corticosteroids, such as prednisolone up to 60 to 80 mg per day, are given
for a few days and then slowly tapered as symptoms improve, with
monitoring in case a flare occurs.
Low-dose cyclosporine (2 to 3 mg/kg per day) may be a treatment option
for patients who fail to respond to systemic corticosteroids .Although
cyclosporine is a category C drug, data from studies in pregnant patients
with organ transplantation indicate that the risk of teratogenicity is low,
but premature labor and infants who are small for gestational age have
been reported.
For persistent cases, post-delivery in non-breastfeeding mothers, other
therapies include systemic retinoids and methotrexate .
Hypocalcemia must be corrected, when present, and fluid and electrolyte
balance should be maintained. These patients sometimes require early
delivery for relief of symptoms and for fetal safety
 Prognosis
Placental insufficiency
Miscarriage
Fetal growth restriction
Stillbirth
Antepartum fetal monitoring with nonstress
tests or biophysical profiles and ultrasound
assessment of fetal growth are indicated.
We report two successive pregnancies of a
patient with two different outcomes: stillbirth
in the first pregnancy; and a healthy newborn
in the second.
Intrahepatic cholestasis of pregnancy

Incidence :Geographic variations in the

rates of the disease may reflect differences in
susceptibility between ethnic groups.
PATHOGENESIS: The cause of ICP is unknown,
but genetic, hormonal, and environmental
factors are likely involved .
 Estrogens and progesterone
Estrogens are known to cause cholestasis in both
experimental and clinical conditions, and a role in
ICP is likely .ICP occurs mainly during the third
trimester when serum concentrations of estrogen
reach their peak. ICP is also more common in
twin pregnancies, which are associated with
higher levels of circulating estrogens than
singleton pregnancies
 ICP also may be associated with alterations in
progesterone metabolism, and the administration of
progesterone may be a risk factor for ICP. The
formation of large amounts of sulfated progesterone
metabolites, may result in saturation of the hepatic
transport system(s) utilized for biliary excretion of
these compounds in some genetically predisposed
women.
It is recommended that progesterone treatment be
avoided in pregnant women with a previous history of
ICP and immediately withdrawn when cholestasis
occurs during pregnancy.
 In patients with a history of cholestasis under
oral contraceptives or ICP, symptoms of
cholestasis may be observed after ovarian
stimulation for IVF;patients with a history of
cholestasis related to estrogen exposure
should be monitored carefully when
undergoing ovarian stimulation, and if
possible, mildly stimulated.
 CLINICAL MANIFESTATIONS
The onset of ICP is typically heralded by the development
of pruritus, which may be intolerable. It is often
generalized, but predominates on the palms and the soles
of the feet and is worse at night. Pruritus may precede
laboratory abnormalities .
Abdominal pain is uncommon. Encephalopathy or other
stigmata of liver failure are unusual, and their presence
should initiate a search for other causes of liver disease.
Physical examination is nonspecific, but may show
excoriations due to scratching. Jaundice occurs in less than
10 percent, typically after the onset of itching. The
presence of jaundice without pruritus is rare and should
prompt investigation of other causes.
 Laboratory findings
Serum total bile acid concentrations increase in
ICP and may be the first or only laboratory
abnormality
(Other laboratory findings ;elevations in the
serum concentrations of alkaline phosphatase,
and total and direct bilirubin concentrations.
Surprisingly, the serum concentrations of
gamma-glutamyl transpeptidase (GGT) are
normal or modestly elevated, which is unusual
in most other forms of cholestatic liver disease
in which GGT levels parallel other cholestatic
markers.
 Serum aminotransferases are elevated and
may reach values greater than 1000 unit/L.
The prothrombin time is usually normal.
ULTRASONOGRAPHY On ultrasonography,
the biliary ducts are not dilated, and hepatic
parenchyma appears normal
 DIAGNOSIS
Most women are diagnosed during the second or
third trimester.
The diagnosis of ICP is based upon the presence
of pruritus associated with elevated total
serum bile acids levels and/or aminotransferases,
and the absence of diseases that may produce
similar laboratory findings and symptoms. The
cardinal feature of ICP (ie, pruritus)
helps distinguish it from other types of liver
disease that can share similar laboratory features.
 TREATMENT Treatment for ICP focuses on
reducing symptoms and preventing maternal
and fetal complications. Several drugs have
been studied, and most focus on relieving
symptoms. Ursodeoxycholic acid(UDCA,
ursodiol) has emerged as the most promising
treatment.
 Ursodeoxycholic acid UDCA increases bile
flow and has been used to relieve pruritus and
improve liver biochemical tests in cholestatic
liver diseases.
300 mg three times a day (or 15 mg/kg per
day) until delivery.
 Complications
fat-soluble vitamin deficiency
MATERNAL FOLLOW-UP AND OUTCOME
The maternal prognosis in ICP is good .
Pruritus usually disappears in the first few days
following delivery, accompanied by normalization of
serum bile acid concentrations and other liver tests.
We follow liver biochemical tests and bile acid
concentration six to eight weeks after delivery to
confirm that previously noted abnormalities have
resolved.
The patient should be referred to a liver specialist to
assess for underlying hepatobiliary diseases if
laboratory abnormalities do not return to normal.
Recurrence in subsequent pregnancies Cholestasis
recurs during subsequent pregnancies in 60 to 70
percent.
 Association with other disorders
Population-based studies suggest that ICP
may be associated with subsequent
development of hepatobiliary cancer,
immune-mediated disease, and cardiovascular
disease.
 Hormonal contraception
Estrogen-progestin The administration of estrogen-progestin
contraceptives to women with a history of ICP rarely results in
recurrent cholestasis
The Centers for Disease Control and Prevention and the World
Health Organization consider estrogen-progestin contraception an
acceptable choice for women with a past history of ICP since the
benefits generally outweigh the risks. However, in women with
cholestasis related to use of estrogen-progestin oral contraceptives,
non-estrogen methods of contraception are preferred due to the
increased risk for recurrent cholestasis .
Progestin-only A history of ICP or cholestasis related to use of
estrogen-progestin oral contraceptives is not a restriction to use of
progestin-only contraceptives .The risk of recurrent cholestasis is
low.
Breastfeeding ICP is not a contraindication to breastfeeding.
FETAL FOLLOW-UP AND OUTCOME
ICP carries significant risk for the fetus .
Prematurity
Meconium-stained amniotic fluid
Intrauterine demise
Neonatal respiratory distress syndrome (which
appears to be associated with bile acids entering
the lungs.)
The risk of spontaneous fetal death is the most
concerning issue.
 We deliver women with ICP at 36 weeks
(360/7ths to 366/7ths) of gestation or upon
diagnosis if ICP is diagnosed at 37 weeks of
gestation.
CONDITION RASH PRESENTATION PREGNANCY RISK TREATMENT
Pruritic urticarial Intensely pruritic urticarial plaques and papules with or No identified adverse Oral antihistamines and
papules and plaques of without erythematous patches of papules and vesicles; rash effects topical corticosteroids for
17
pregnancy first appears on abdomen, often along striae and occasionally pruritus; systemic
involves extremities; face usually is not affected corticosteroids for extreme
symptoms
1
Prurigo of pregnancy Erythematous papules and nodules on the extensor surfaces No identified adverse Midpotency topical
of the extremities effects corticosteroids and oral
antihistamines
Intrahepatic Excoriations from scratching; distribution is nonspecific Risk of premature delivery, Oral antihistamines for mild
cholestasis of meconium-stained pruritus; ursodeoxycholic
1,18,19
pregnancy amniotic fluid, intrauterine acid (ursodiol [Actigall]) for
fetal demise more severe cases
Pemphigoid Pruritic papules, plaques, and vesicles evolving into Newborns may have Oral antihistamines and
20,21
gestationis generalized vesicles or bullae; initial periumbilical lesions may urticarial, vesicular, or topical corticosteroids for
generalize, although the face, scalp, and mucous membranes bullous lesions; risk of mild cases; systemic oral
usually are not affected premature deliveries corticosteroids for severe
andnewborns who are cases
small for gestational age

Impetigo Round, arched, or polycyclic patches covered with small Reports of increased fetal Systemic corticosteroids;
22,23
herpetiformis painful pustules in a herpetiform pattern; most commonly morbidity antibiotics for secondarily
appears on thighs and groin, but rash may coalesce and infected lesions
spread to trunk and extremities; face, hands, and feet are not
affected; mucous membranes may be involved

Pruritic folliculitis of Erythematous follicular papules and sterile pustules on the No identified adverse Topical corticosteroids,
1
pregnancy abdomen, arms, chest, and back effects topical benzoyl peroxide
(Benzac), or ultraviolet B
light therapy
Psoriasis during pregnancy
Psoriasis improves during pregnancy in 40 to 60 percent of women, worsens in 10 to 20
percent, and remains stable in the remainder. In women who improve, the degree of
improvement can be dramatic. In the postpartum period, psoriasis severity remains the same or
worsens in most women

Ideally, women should plan pregnancy when they are in remission and off medication or taking
the minimum effective dose of medications that have the best fetal safety profiles. However,
postponing pregnancy until a period of remission often is unrealistic. The selection of
treatments with good fetal safety profiles is particularly important for these patients.
.
For women with limited psoriasis (ie, non-debilitating psoriasis that involves less than 5 to 10
percent of the body surface area), we suggest topical rather than systemic therapy . Emollients
and moisturizers are useful for reducing bothersome scale. Our first-line medical treatment is a
low- to medium-potency topical corticosteroid

For women with psoriasis that cannot be managed adequately with topical therapy (ie,
resistant or extensive disease), we suggest narrowband ultraviolet B (UVB) phototherapy rather
than systemic therapies because of the safety and efficacy of phototherapy in pregnancy .
Because psoriasis often improves during pregnancy, women who required systemic treatment
prior to pregnancy may be able to transition to phototherapy.

Topical tazarotene, methotrexate, and acitretin are contraindicated during pregnancy.

Fungal infections
Require longer duration of ttt
 Moles \ melanoma
What is the appearance of moles in pregnancy?
What to look for?
During pregnancy, moles can get darker and
larger, particularly on the belly and breasts. These
benign changes are usually symmetric. Therefore,
any asymmetric change in size, shape or colour
should be examined by your dermatologist.
A dermatoscopic evaluation (examination moles
with a hand-held microscope) of the mole during
pregnancy may reveal some modifications in the
structure which will often completely resolve
after delivery
What is the appearance of melanoma in
pregnancy?
What to look for?
The appearance of melanoma in pregnancy is
identical to that in non-pregnant women. Any
spot that changes in colour, size, or shape or
bleeds, becomes an open wound (ulceration),
painful, or itchy must be examined by a
dermatologist.
How is melanoma treated in pregnant patients?
Are these investigations safe for the baby?
When the doctor suspects a melanoma, a dermatosopic examination followed by an excision of the spot
will be performed and the tissue examined under a microscope (histopathologic examination); this will
take 1 to 2 weeks. This examination will establish whether it is a melanoma and, if so, the thickness of the
melanoma. The condition is staged in the same way in pregnant as in non-pregnant women.
In order to establish the stage of the melanoma, various features must be considered including:
- the thickness (how deep the melanoma has grown into the skin
thin melanoma (<1mm deep) usually has a very good outlook)
- the type of the melanoma
- involvement of lymph nodes
- the spread of the melanoma into other organs (metastases)
Usually no further tests are done for thin melanoma.
Some other medical tests may be used for staging the melanoma: sentinel lymph node biopsy,
ultrasounds, or MRI (magnetic resonance imaging). All these procedures are safe in
pregnancy. Sentinel node biopsy is used in some cases to know if the melanoma has spread beyond the
skin, and is done by biopsy of the first lymph node into which the melanoma drains. Sometimes it may be
worth waiting until after delivery, but if essential there is no evidence that the blue dye used harms the
baby, but occasionally the mother can have a serious allergic reaction to it, which could harm the baby.
Methods using X-rays or radioactive isotopes must be avoided.
How is melanoma treated in pregnancy?
What are the implications of the treatment for the baby?
The treatment depends on the stage of the melanoma. The first treatment of all
melanoma is surgical (removal of the melanoma under local anaesthesia); no further
treatment is needed for thin melanoma. This procedure is safe for the unborn baby.

For thick melanoma or ones that have spread chemotherapy may be considered. This
should only be given after the first three months of pregnancy, and careful
consideration given to use later in pregnancy because it can affect the baby. Another
form of treatment for melanoma is immunotherapy which is not advised in pregnancy
because it increases the risk of spontaneous abortions.

Can melanoma spread to the baby?

In most cases of melanoma the baby will not be affected by the melanoma or by the
treatment (surgical).
If the disease is at a late stage, when lymph nodes or internal organs are involved
(advanced disease), the disease may spread to the placenta and the baby. In this
situation the placenta should be examined and baby watched for any signs of
melanoma in the following months; however, this situation is very rare.
Does pregnancy worsen the prognosis of melanoma?
Pregnancy itself does not worsen the prognosis of melanoma.
However, in pregnancy diagnosis and treatment are often delayed which
may lead to a late stage melanoma with a worse prognosis. It is therefore
important to remove a mole that is suspicious for melanoma as early as
possible.
Also, the melanoma does not influence the outcome of the pregnancy for
mother and baby
 ACNE
acne is common during pregnancy. In fact, more than one out of every
two pregnant women can expect to develop acne. In some cases, the acne
may be severe.
The primary cause of acne when you're pregnant is the increased
hormone levels in the first trimester. The higher level increases the skin's
production of natural oils. It's hard to predict who will develop pregnancy
acne. You have a higher risk, though, if you have a history of acne or have
acne flares at the start of your menstrual cycle. If you do not develop acne
during the first trimester, it's unlikely you'll have breakouts that are out of
the ordinary during the second or third trimesters.
Managing acne when you're pregnant can be tricky. That's because many
prescription and over-the-counter treatments come with a high risk
of birth defects. In general, you should avoid any medication that has even
a remote chance of harming your baby.
It usually subsides when hormone levels return to normal. So the safest
thing to do is to avoid any prescription acne medications or over-the-
counter chemical spot treatments. Instead, you can rely on drug-free
home remedies.
Isotretinoin is an oral medication that has revolutionized the way severe
acne is treated. However, it's especially dangerous when you are
pregnant.
That's because the drug can affect a fetus and cause serious birth defects.
Drug category x ..never used in pregnancy
Because the risks are so high, women of childbearing age who take the
drug need to be on two forms of birth control starting at least one month
before they begin therapy. They also need to stay on two forms of birth
control for at least one month after therapy ends. Also, women must
have pregnancy testsbefore, during, and after treatment