Escolar Documentos
Profissional Documentos
Cultura Documentos
80-120 m2
pH
250-500 m2 20 m2
Constipação
Fezes normais,
principalmente tipo 4
Diarréia
ou
urgência fecal
m2
Célula Epitelial:
Somente Absorção?
A célula epitelial intestinal atua como
apresentadora de antígenos não
especializada, reconhece e responde a
antígenos bacterianos e virais em virtude de
sua expressão dos NODs e Toll Like
receptores e pode produzir uma variedade
de citoquinas e quimiocinas que influenciam
a resposta imune. Influencia na expansão
das células (linfócitos) T reguladoras no
intestino.
Wershil B.K; Furuta G, MD. Gastrointestinal mucosal immunity.
Journal of Allergy and Clinical Immunology - Volume 121,
Issue 2 Suppl (February 2008)
Os antígenos da luz
intestinal penetram
através das células M,
são englobados por
macrófagos e células
dendríticas, levados à
placa de Peyer onde
interagem com
linfócitos
CD4+
e
Linfócitos B.
Fígado
MALT
Mucosa
Associated
Lymphoid
Tissue
MALT
Mucosa
Associated Da orofaringe ao intestino
encontram-se estruturas
linfáticas (gânglios
Lymphoid linfáticos solitários,
placas de Peyer)
Tissue afins às de outros âmbitos
mucosos (vias respiratórias,
urogenitais, etc.)
Flora intestinal
“Tapete”, “filtro” sobre as vilosidades intestinais
MALT
Nariz (NALT)
Sistema MALT
(UALT)
Pele (SALT)
500 m!
2
Será coincidência?!...
SISTEMA IMUNE - MALT COLONIZAÇÃO BACTERIANA
Respiratory
tract
D 004-0047 06.10.2004
• http://nihroadmap.nih.gov/hmp
“Superorganismo
humano-microbiota”
Bactérias
Células
+
D 005-0114 11 06.08.2004
Aprox.
100.000.000.000.000
1012 células
humanas
Sinais de perigo!!!!
Regulação Disbiose
Inflamação Inflamação
fisiológica patológica
Hipotireoidismo Asma
Eczema
Patologia coronariana
Dematite atópica
Psoríase
Inflamação crônica
mínima persistente Fibromialgia
Urticária
Artralgias
Artrite reumatóide
Hipercolesterolemia Doenças por imunocomplexos
Esteatose hepática Osteoporose
Cirrose hepática
Hipersensibilidade química Cólicas
Diabetes Gases
Obesidade Distensão abdominal
Diarréias
Infecção urinária Disbiose intestinal Intolerâncias alimentares
Candididíase vaginal de repetição Alergias alimentares
Deficiências nutricionais
Síndrome da Fadiga crônica Sínd. Intestino Irritável
(desânimo, estresse, cansaço, Colite ulcerativa
Doença de Crohn
enxaquecas, mau-humor – “enfezada”,
Diverticulose
edema nas pernas, desinteresse no Polipose
trabalho, perda do apetite sexual, Câncer
mãos e pés frios)
Autismo Insuficiência venosa crônica
Úlceras de MMII
Leucemia
Tromboembolismo
3-5%
Flora 11 Flora
“Prejudicial” Bacteroides
Benéfica
(comensais +
Produção de toxinas, Bifidobacterium probióticas)
carcinógenos
Eubacterium
potenciais, putrefação Inibição das bactérias
intestinal metanógenos prejudiciais
Biodiversidade
Microecologia intestinal
Sinergia Microbiana
Defesa contra infecção é devida à interação de muitas
espécies bacterianas (e leveduras, helmintos,
protozoários e vírus).
+ =
SP 007-0002 01 08.10.2007
Mucosal Integrity
D 0-00
Destruição de tight-junctions
Nusrat et al Infection and Immunity 2001
Conceito de Disbiose
Pai da Imunologia
Teoria Fagocítica
Alimentação inadequada
Stress
Consumo de álcool e
medicamentos (ATB,
inibidores de bomba de
prótons, AINH,
anticoncepcionais,
imunossupressores)
Viagens
Gravidez
Constipação
Idade
Amálgamas dentários
Sonda nasoenteral
Alteração no equilíbrio da
microbiota normal
Disbiose
Pesticidas
Citocinas
Resposta
predominante
IL-12 Patógenos
IL-2 IgG2a intracelulares
IL-12
IFN-g IgG3 (Micobactérias e
Th1 DTH
TNF-a Virus), Protozoários,
TGF-b Mac Células tumorais,
Th0 Hipersensibilidade
IL-4 tardia
IL-5 IgE
Th2 Patógenos
IL-4 IL-10 IgG1
IL-13 Eos extracelulares,
Parasitas, Alergia IgE,
Auto-imunidade por
Ac/Imunocomplexos
ReVieWS
F O C U S O N h O m E O S tat I C I m m U N E R E SRpEO
VNI ESW
ES
Innate
immuneimmune
pathologyregulation
114
. During a fatal T. gondii infection, to produce pro-inflammatory cytokines117. The exces- Adaptive immune regulation sIgA
excessive IFNγ production shuts down IL-2 production, sive expansion Commensal
of TReg cells in this latter stage of disease
TLA SEMA7A
triggering a homeostatic TReg cell contraction and allow- is likely to bebacterium an important mechanism that induces this
ing the development of immune pathology 79. A similar lymphocytic suppression118,119. Indeed, removal of surplus
effect can be initiated by IL-27 production in inflam- TReg cells in both mice and human patients seems to miti-
matory cells, which reduces IL-2 and hence the TReg cell gate immunosuppression119,120. This ‘over-filling’ of the
population, leading to autoinflammatory disease115. It is TReg cell niche is reminiscent of the excessive expansion
also notable that the correlation between effector func- that is observed in a partial depletion model in mice57. It
IL-25, breaks down with TH17 cell is therefore worth speculating that septic shock TSLP
tion and IL-2 production TSLP,syndrome
responses, as Aiolos IL-33, IL-25
(also known as IKZF3) expression consists of dual modalities of TReg cell homeostatic
TGFβ, failure: IEL APRIL,
IFNγ, IL-7, BAFF
by TH17 cells silencesTSLP
IL-2 production116. This mechanism a reduction of TReg cells during the acute phase,
TNF RA leading to
is thought to make TH17 cell responses more self-limiting hyperinflammation, followed by homeostatic expansion IL-15
IL-13,
compared with other TH cell responses, but it may also over-filling of TReg cells, leading to an anergic phase.
IL-1β,
amphiregulin
prevent efficient TReg cell homeostatic
IL-17,responses toIL-23strong IL-12
TH17 cell responses, which explains the dominant asso- Perspectives
IL-22
ciation of TH17 cells with autoimmunity. An additional The past year has provided striking new insights into IL-33 IL-10
mechanism by which the relationship between inflamma- the molecular machinery that controls TReg cell homeo-
tion and IL-2 availability can break down is through the stasis and differentiation into diverse functional subsets.
consumption of IL-2 by non-regulatory T cells. Indeed, The basal FOXP3-dependent transcriptional network ALARMIN IgA+ plasma cell
IL-25
activated effector ILC2
CD4+ T cells during infection with ILC3engaged by central
ILC1TReg cells induces a programme of
T. gondii, Listeria monocytogenes and vaccinia virus con- high turnover primed to react to minor changes in
sume sufficient IL-2 to reduce the amount available to conventional T cell activation status, which is primar-
TSLP
TReg cells to below homeostatic requirements78, a process ily sensed via IL-2. These properties DC allow for the rapid TReg cell
Lamina propria
that may contribute to immune pathology during these responses that are required from the TReg cell population
severe infections. Likewise, evidence suggests that, fol- at the earliest signs of reactivity owing to the dynamic TCR RA,
lowing excessive activation, CD8+ T cells can be induced nature of immunity and inflammation. The importance MHC TGFβ
to express CD25 to levels such that IL-2 consumption by of these properties is emphasized by the devastating
CD8 T cells may reduce IL-2 availability to levels too immune conditions that are caused by genetic or envi-
+
low to maintain TReg cell numbers, resulting in immune Macrophage ronmental disruption of TReg cell homeostatic networks.
Monocyte
pathology (S. Humblet-Baron, Naive T cell TReg cell
BasophilpersonalTypecommunication). Another important theme that has emerged is the
2correction specialization of T cells for tissue- and inflammation-
In all of these cases, the normal homeostatic
progenitor MPP Reg
mechanisms fail, such that there is insufficient IL-2 to specific responses. At the transcriptional level, many
support TReg cell expansion. In severe cases, this may lead familiar players seem to act in concert with the IL-10, Direct IEC e ect
to a positive inflammatory feedback loop that supports FOXP3-induced programme to drive TReg cell diversifica- B cell RA,
autoinflammation (FIG. 5c). Mast
tion. cell effector
Tailoring Basophil
TReg cell proliferative and apoptotic Indirect IEC e ect
TGFβ
Finally,
Peyer’s there is growing evidence that septic shock syn- controls to specific inflammatory milieu would promote
patch Immune response
ordrome involves defective TReg cell homeostasis. Sepsis and immune balance, allowing for appropriate antagonism
mesenteric Di erentiation
septic shock
lymph nodeare life-threatening
Basophilcomplications of infec- of inflammation during expansion, followed by relief of
tion. It has become clear that the initial response to septic immunosuppression during contraction. The contraction
Peterson LW, Artis D.
shock is a hyperinflammatory Intestinal
reaction, typically epithelial
mediated phase cells:
may regulators
prove to be important of barrier
for processes function
such as and
Figure 3 | IECs regulate innate and adaptive immunity. Intestinal epithelial cell (IEC)-derived cytokinesimmune homeostasis. Nat Revinterleukin-25
Immunol.
by endotoxin,
2014 releasing a plethora of pro-inflammatory the generation of immunological memory or healing in
Mar;14(3):141-53. Nature progenitors
Reviews | Immunology
cytokines and other mediators into (IL-25) and thymic
the circulation. stromal lymphopoietin
This non-lymphoid tissues. There is(TSLP)
a pressing elicit
needthe expansion and differentiation of basophil
to better and
acute stage is accompanied by a deficit multipotent progenitor
in TReg cells, which type
define the 2 (typemechanisms
homeostatic 2 MPP) cells, thatrespectively.
control central, IL-25, IL-33 and TSLP stimulate group 2 innate lymphoid
may contribute to the hyperinflammatory cells (ILC2s),
state . Most
117
whereas IL-25
effector andsuppresses
polarized TReginnate lymphoid
cell populations, cellthe
given subset 1 (ILC1) and ILC3 function by limiting macrophage
patients can survive this acute stage with best medical
production obvious potential for
of pro-inflammatory the targetedIL-1β,
cytokines modulation
IL-12ofand
TReg cells
IL-23. IECs condition dendritic cells (DCs) and macrophages
practice of pulmonary and cardiovascular support in an populations pertinent to pathology.
towards a tolerogenic
intensive care unit. However, patients surviving this acti- phenotype through the production of TSLP, transforming growth factor-β (TGFβ) and retinoic acid
(RA). These
vation phase often become immune suppressed, suchDCsthat promote
Note added theindifferentiation
proof of naive CD4+ T cells into regulatory T (TReg) cells and the maturation of B cells
the original infection is unresolved into IgA-secreting
and the patient is at Sinceplasma cells. Mucosal
this Review was accepted,cell-derived
a key paper DCs also imprint a gut-homing phenotype on primed B cells and
was pub-
risk of additional opportunistic infections.
T cellsThis immunethelished
through describingof
production a role
RA.for a new
After population to
trafficking of tissue-
the intestine, TReg cells are expanded in number by macrophages
paralysis has been found to be associated with a reduc- resident TReg cells in muscle repair, further extending our
that are conditioned to produce IL-10 by TSLP-mediated
tion of circulating effector T cells with curtailed potential understanding of TReg cell specialization . 121 stimulation and through contact-dependent interactions with
IEC-expressed semaphorin 7A (SEMA7A). The production of a proliferation-inducing ligand (APRIL) and B cell-activating
factor (BAFF) by IECs and by TSLP-stimulated macrophages and DCs promotes class-switch recombination and
1. Liston, A. & Piccirillo, C. A. Developmental plasticity
of murine and human Foxp3+ regulatory T cells.
4.
the production of IgA by B6.cells
Mabarrack, N. H., Turner, N. L. & Mayrhofer, G.
in theT cellsintestinal lamina
Samstein, R. M. et al. Extrathymic generation of
Recent thymic origin, differentiation, and turnover of
regulatory in placental mammals propria. IEL, intra-epithelial lymphocyte; IFNγ, interferon-γ;
mitigates
2.
Adv. Immunol. 119, 85–106 (2013).
Hsieh, C. S., Lee, H. M. & Lio, C. W. Selection of (2008).
sIgA, secretory IgA; TCR, T7.cellmaternal-fetal
receptor;
regulatory T cells. J. Leukocyte Biol. 84, 1287–1297
TLA, thymus leukaemia antigen; TNF, tumour necrosis factor.
conflict. Cell 150, 29–38 (2012).
Josefowicz, S. Z. et al. Extrathymically generated
regulatory T cells in the thymus. Nature Rev. Immunol. 5. Atarashi, K. et al. Treg induction by a rationally regulatory T cells control mucosal TH2 inflammation.
12, 157–167 (2012). selected mixture of Clostridia strains from the human Nature 482, 395–399 (2012).
3. Paiva, R. S. et al. Recent thymic emigrants are the microbiota. Nature 500, 232–236 (2013). 8. Thornton, A. M. et al. Expression of Helios, an Ikaros
preferential precursors of regulatory T cells This study demonstrated the direct capacity of transcription factor family member, differentiates
differentiated in the periphery. Proc. Natl Acad. Sci. microbiota and microbiota-derived metabolic thymic-derived from peripherally induced Foxp3+ T
USA 110, 6494–6499 (2013). expansion of previously primed regulatory T cells .
products to induce TReg cells in the colon.
126
regulatory cells. J. Immunol. 184, 3433–3441 (2010). and myeloid cell phenotypes that promote the develop-
CX3CR1hi macrophages promote tolerance in the intes- ment of type 2 cytokine responses at mucosal sites130–133.
NATURE REVIEWS | IMMUNOLOGY tinal lamina propria through the production of IL-10,
VOLUME 14 | MARCH 2014 | 163 These cells include a distinct population of basophil pro-
© 2014 Macmillanwhich leadsAllto
Publishers Limited. suppression
rights reserved of inflammatory cytokine genitors and a population of multipotent progenitor cells,
production by colitogenic T cells and promotion of which undergo extramedullary haematopoiesis and rep-
regulatory T cell function127,128. IECs maintain this resent an innate link between IEC-derived signals and the
Innate lymphoid cells tolerogenic function through their production of solu- polarization of TH2 cell immune responses to helminths
(ILCs). A group of innate ble factors, such as TSLP, TGFβ and retinoic acid103,104,110, and allergens132,133.
immune cells that are as well as through contact-dependent interactions
lymphoid in morphology and
involving IEC expression of the integrin ligand sema- Innate lymphocyte function. In addition to the myeloid
developmental origin, but lack
properties of adaptive B cells phorin 7A, which induces IL-10 expression by CX3CR1hi cell and granulocyte populations, a recently identified
and T cells such as recombined macrophages and promotes intestinal homeostasis129. innate immune cell population of innate lymphoid cells
antigen-specific receptors. IECs also play an important part in the induction of (ILCs) plays a crucial part in intestinal immune homeo-
They function in the T helper 2 (TH2) cell responses during helminth infec- stasis. ILCs lack properties of adaptive lymphocytes, such
regulation of immunity, tissue
homeostasis and inflammation
tion. In this setting, the IEC-derived cytokines TSLP as recombined antigen-specific receptors134. They are
in response to cytokine and IL-25 promote the expansion and differentiation of found at barrier surfaces, including mouse and human
stimulation. haematopoietic progenitor cells towards mononuclear lung 135, skin136 and intestine137, where they function
Subpopulações Th
IFN-gama
-
Th1 - IL-10 Th2
Resposta balanceada
Intestinal responses to gut flora during homeostasis (healthy intestine) and IBD.
M. Nedim Ince, MD & David E. Elliott, MD. Immunologic and Molecular Mechanisms in Inflammatory Bowel Disease.
Surgical Clinics of North America - Volume 87, Issue 3, June 2007
MALT
Colite Ulcerativa
Manifestações
Extra-intestinais
SARTOR, R. B. Role of the enteric microflora in the pathogenesis of intestinal inflammation and
arthritis. Alimentary Pharmacology and Therapeutics. Volume 11 Supplement 3 December 1997 pp
17-23
http://www.ncbi.nlm.nih.gov/pubmed/21475195
Oferta de glicose
Inflamação crônica
Déficit imunológico
Célula normal (Focos dentários)
Déficit mineral e vitaminas (Se, Mg, Zn, Célula tumoral
Vitamina D)
Metais pesados
Hiperproteinização / hiperacidez
Disbiose
Alergia alimentar
Campos de interferência/Focos (dentes)
Geopatia, radiação
http://pt.slideshare.net/ctorgan/microbiome-sport
http://pt.slideshare.net/ctorgan/microbiome-sport
http://pt.slideshare.net/ctorgan/microbiome-sport
http://pt.slideshare.net/ctorgan/microbiome-sport
http://pt.slideshare.net/ctorgan/microbiome-sport
• Overlap among
inflammatory conditions
of the upper and lower
airways.
• Diseases of an integrated
mucosal system.
8
7
6
5 Atópico
4 No atópico
3
2
1
0
Clostr Bifido Lacto
Eckard Hamelmann 2004
Kalliomaki M et al. J Allergy Clin Immunol 2001 Jan;107(1):129-34
SP 015-0037 26.04.2005
INSUFLAÇÃO RETAL
§ Linfócitos T da submucosa
(GALT): resposta anti-
inflamatória e
imunossupressora
§ Permeabilidade intestinal
§ Indução da resposta
antioxidante
RETOCOLITE ULCERATIVA
(Knoch et al. „Aktuelle Koloproktologie“)
Fem, 45a
Insuflação retal
20-30 µg/ml
300-500 ml
4 semanas
Estágio florido de retocolite Biópsia de controle após 4
• destruição do epitélio semanas:
RETOCOLITE ULCERATIVA
Masc, 62 a (Knoch et al. „Aktuelle Koloproktologie“)
Insuflação retal
8,5-27 µg/ml
300 ml /day,
3x/semana
4 semanas
Biópsia de controle após 4
Estágio florido de colite semanas:
Bocci
Concentração
20 30 35 40
(mcg/ml)
Volume
100 100 150 200
(ml)
Ozonioterapia
Insuflação Retal
PRÉ
4 dias depois
PÓS
Enema de Café
u Os enemas são realizados por meio da
introdução de uma sonda fina no reto e têm como
objetivo principal promover a desintoxicação do
fígado e dos rins.
Enema de Café
ImuPro 300
Alergias alimentares tardias – IgG e Imunocomplexos
D 005-0044 19.08.2004
SP 017-0023 16.04.2005
SP 017-0026 25.04.2005
c c. Aplicação preventiva de
ozônio como insuflação
retal (15 sessões)
Tipos:
• A – autoimune – 6% (junto com tipo C)
• B – bacteriana por H. pylori – 94%
• C – etiologia química e refluxo gastroesofágico
Óleo ozonizado
400 IP (índice de
peróxido) – iniciar
com 5 ml até 20 ml
Conventional therapy of chronic purulent otitis media has been actual for a number of years. It is
mainly aimed a control of inflammatory process in otitis media in chronic mesotympanitis,
accompanied by marked mucositis. The existence of numerous methods of mucosites treatment
proves these techniques to be of insufficient efficiency. Ozone is known to produce a marked effect on
cellular metabolism when it is used in definite concentrations. It contributes to the elimination of
intracellular hypoxia, activation of carbonic, fat and protein exchange, bringing synthetically,
regeneratory and secretory functions of epithelial cell to normal level. Definite ozone concentrations
produce bactericidal effect which is of no less importance in the course of chronic inflammatory
process. We have developed an ozone therapy technique in controlling chronic mucositis of otitis
media, based on ozone/oxygen irrigation of tympanic membrane and auditory tube mucous.
40 patients underwent a course of treatment that consisted of 7-10 daily procedures. Control group of
10 patients was on a conventional therapy. The results demonstrated that ozone therapy have no
negative effect on internal ear or labyrinth function, even in prolonged applications of high ozone
concentrations effecting mucous membrane of medial wall. Clinical effect was observed in
inflammation control of mucous membrane, discharge reduction and restoration of auditory
tube function. The use of ozone therapy in combination with complex therapy of chronic purulent
mesotympanitis shortens the period of hospitalization. The developed method can be recommended
as a stage during the preoperation preparation for myringoplasty.
The persistent inflammation of the middle ear adopt several forms owing to anatomical, physiological
and bacterial factors. Patients with this disease suffer of continuos ears infections or relapses,
presenting most of them a hearing loss, in relation with an injury in the sound-transmitting mechanism
and a cochlear damage by toxicity or a direct propagation of the infectious process. The aim of this
study is to evaluate the effectiveness of ozone therapy in patients maintaining suppurative chronic
middle ear disease after conventional medical treatment and regional surgery. A clinical trial was
performed in 17 out-patients coming from external otorrhine office of Guevara Hospital and Mártires de
las Tunas Hospital, between March and December/96. Patients received a cycle of treatment
consistent in 15 sessions of rectal ozone applications, with an ozone concentration of 50 mg/L,
and also installation of 2 drops of ozonized oil (OLEOZON®) for 12 hours in each ear during 15
days. This cycle of treatment is repeated 3 months later. The results demonstrated that 16 patients
(94 %, p<0.05) had negative bacteriological study at the end of the second cycle of treatment. Only in
one patient remained septic conditions (pseudomones + proteus). The otoscopy showed 10 patients
(59 %) with tympanic membranes completely recovered and in 7 patients still remained a little point
without epithelization. According to audiometry, 14 patients (82 %, p<0.05) improved their hearing
loss. Mastoid X-ray studies demonstrated improvement in 13 patients (76 %). It is concluded that
ozone therapy is effective in the treatment of suppurative chronic middle ear, without any side effect.
Vestn Otorinolaringol.
1998;(6):11-2.
Use of gaseous ozone and ozonized solutions in the
treatment of chronic suppurative otitis media
[Article in Russian]
[Article in Russian]
[Article in Russian]
Muminov AI, Khushvakova NZh.
Inflammatory diseases of the front sinuses, rather
common now, run often an atypical complicated cpirse.
102 patients with chronic purulent frontal sinusitis
received treatment consisting in irrigation of the
paranasal sinuses with ozone-oxygen mixture. A total
of 5-7 procedures were given (one course). The control
group of 30 patients was treated conventionally. 89% of
the irrigated patients recovered faster than the
controls.
L. Silva, R. Wong.
Medical and Surgical Research Center, Cuba.
3rd International Symposia on Ozone Applications - June 27th through 30th 2000,
Havana City, Cuba
Este trabajo tiene como objetivo mostrar la evolución de 1 000 pacientes tratados con
ozonoterapia intratonsilar con diagnóstico de amigdalitis crónicas, las pacientes han
sido seguido hasta un año posterior al tratamiento, realizándoles controles microbilógicos
(exudado faringeo y TASO), así como exámenes físicos de la región orofaringea. Otro
objetivo fue demostrar que no se ha producido estrés oxidativo en los pacientes tratados,
mediante estudios en sangre y lavados bronquiales. Para lograr este objetivo se
escogieron 10 pacientes a los que se les realizó diagnóstico de estrés oxidativo en
sangre, antes y después del tratamiento y otro grupo de 10 pacientes que se les realizó
lavado bronquial, para determinar si existía ó no estrés oxidativo. Los resultados
obtenidos en ambos grupos fueron satisfactorios, así como la evolución de los pacientes,
tanto desde el punto de vista del examen físico, como del aspecto microbiológico.
[Article in Russian]
Silva L. (Cuba)
The present study summarizes the evolution of 2 300 patients with diagnosis of
tonsillitis, treated by the method of ozone therapy intratonsillar, during the
last eight years. The ozone concentration used was 50 mg/L and a volume of
5 mL, in each tonsil. The main number of ozone applications was four. To
these patients, an exam of its pharynx, as well as microbiological pharyngeal
studies were performed, at the beginning and at the end of the treatment and
along a year after the treatment. A system for oxidative stress diagnosis,
measuring different antioxidants and pro-oxidants biomarkers, was performed
in 10 patients. The oxidative stress results demonstrated that these patients
were in no stress condition after the ozone treatment. Outstanding results were
obtained in 97 % of patients. No relapse was presented along the year of
evaluation. Also, the economic advantages in comparison with the traditional
surgical method (amigdalotomy) were pointed out.
Herpes labial
Resultado
Melhora significativa das
lesões e da sintomatologia
em 48 horas
Melhora completa em 72
horas (estágio final de
cicatrização das lesões e
remissão de todos os
sintomas)
RESUMEN
Se evaluó la efectividad del aceite ozonizado en el tratamiento de la
estomatitis subprótesis grados I y II. Se seleccionaron 64 pacientes del
Servicio de Prótesis Estomatológica de la Facultad de Estomatología, que
requerían nuevo tratamiento protésico y presentaban estomatitis subprótesis. A
32 pacientes se les aplicó el oleozón y otros 32 se tomaron como grupo
control, a los cuales se les aplicó la nistatina en crema. Ambos grupos (estudio
y control) se subdividieron en 2 subgrupos, según el grado de estomatitis I y II,
con 16 pacientes en cada uno. Se confeccionaron tablas que muestran los
resultados generales alcanzados según el número de aplicaciones diarias.
Según los resultados obtenidos podemos inferir que el tratamiento con ambos
medicamentos ha sido efectivo, pero con la aplicación del oleozón los
resultados alcanzados en la curva de la estomatitis subprótesis fueron
más rápidos y se necesitó un menor número de aplicaciones.
Pacientes asmáticos
Tratamento por 1 ano com 3 ciclos de ozonioterapia (5-6 meses cada)
3 grupos: GAHT 4 mg, GAHT 8 mg, Insuflação retal 10 mg
Técnica
3 grupos:
• GAHT 4 mg (15 sessões)
• GAHT 8 mg (15 sessões)
• Insuflação retal 10 mg (20 sessões)
Avaliação laboratorial: IgE sérica, HLA-DR, biomarcadores de estresse
oxidativo (glutationa reduzida,glutationa
peroxidase, glutation redutase, glutationa
S- transferase)
Função pulmonar
Sintomas
Resultados:
• GAHT 8 mg (15 sessões) melhor do que
Insuflação retal 10 mg (20 sessões), melhor do
que GAHT 4 mg (15 sessões)
•Diminuição da IgE sérica e do HLA-DR
•Aumento dos biomarcadores de estresse oxidativo (glutationa
reduzida, glutationa peroxidase, glutation redutase, glutationa S-
transferase)
• Melhora da função pulmonar (somente com GAHT 8 mg e Insuflação
retal 10 mg)
• Melhoras dos sintomas (dispnéia, sibilação, uso de medicação)
IgE values before first and after third cycle of ozone therapy in patients
with real atopic asthma.
* Statistically significant.
MAHT a fte r
8 MG. b e fo re
400 MAHT
4 MG.
350
300
*
250
RI 10 MG.
*
IU / m L
200
150
100
50
Calunga
HLA-DR values before first and after third cycle of ozone therapy in
patients with real atopic asthma.
* Statistically significant.
MAHT a fte r
4 MG. MAHT 8MG. b e fo re
50
RI 10 MG.
40
*
P e rc e n ta g e
30
*
20
10
0
Calunga
AHT-8 80 20 0
AHT-4 46 20 33
Calunga
RESULTADOS
Variables funcionales al inicio y final del
estudio. * p<0.05
Calunga
RESULTADOS
Variables funcionales al inicio y final del
estudio. * p<0.05
10mg
Calunga
Técnica
Infiltração submucosa da borda das úlceras com solução salina ozonizada
(2-3 ml) a 5 µg/ml
Higienização da via aérea diária com a mesma solução (40-60 ml)
Ozonioterapia em Ginecologia
Constipação crônica
Miomas uterinos
Ovários policísticos
Endometriose
Tireoidite crônica
Ela desejava ficar grávida e muitos médicos
disseram que seria muito difícil...
Março 2007
KyberKompact
#1
Março 2007
KyberPlus # 1
Março 2007
A.G., fem, 32 a
Tratamento:
Prosymbioflor
Ômega 3
Hepeel + Traumeel
5-HTP
Fitoterapia chinesa (fígado e baço)
Terapia anti-homotóxica (Solidago compositum
+Thyreoidea compositum + Thuya Injeel + Hormeel)
Vitaminas e minerais VO e EV
Enemas de café e insuflação retal de ozônio
Sauna com ozônio
Terapia neural (cicatrizes)
Ajustes nutricionais (evitar alimentos com alto IG)
KyberKompact # 1 KyberKompact # 2
A.G., fem, 32
Set 2007
A.G., female, 32
OZONIOTERAPIA RETAL
• Usar sonda retal ou uretral
• Em adultos , iniciar com 20 mcg/ml e ir aumentando
gradativamente a concentração, até o máximo de
40mcg/ml.
• Observar esquemas terapêuticos
Indicações:
• Qualquer patologia que temos necessidade de estimular
as propriedades das indicações do ozônio e a GAHT
não seja possível, devido às condições venosas ou de
custos.
• Patologias intestinais, patologias prostáticas
• Fístulas Perianais
INSUFLAÇÃO RETAL
nOOOcAUT
Núcleo de Ozonioterapia de Combate ao Autismo
nOOOcAUT =
núcleo de
OOOzonioterapia de
combate ao
AUTismo
5x/semana
Semana 1 Semana 2 Semana 3 Semana 4
3x/semana
Semana 5 Semana 6 Semana 7 Semana 8
2x/semana
Semana 9 Semana 10 Semana 11 Semana 12
Ozonioterapia em Ginecologia
INSUFLAÇÃO VAGINAL
Infecções GAHT ou
(otites, sinusites, Insuflação retal,
rinites,amigdalites, Bolsa
abscessos)
Patologias
OTORRINOLARINGOLOGIA
vasculares
(surdez súbita, Modulação
Meniére, Imunológica &
presbiacusia,
Inflamatória
metabólicas, (alergias. doenças
úlceras) auto-imunes, dor
crônica, ATM,
neoplasias)
GAHT ou Insuflação
retal, Bolsa
GAHT ou Insuflação retal, PAHT, Injeção
subcutânea, Injeção intramuscular, Injeção
intra/periarticular
Ozonioterapia em
Otorrinolaringologia
30 mcg/ml, 120-180 ml
“Insuflação Nasal”
Inalação de Óleo Ozonizado
(Mollica)
INALAÇÃO DE ÓLEO
OZONIZADO (CUBA)
Infiltração amigdaliana
Infiltração amigdaliana
Abaixar a língua
Concentração: 10 µg/ml
2
3
2
3
Ozônio é apaixonante...
+55 11 9 9902-0560