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The Blood Type Diet Archives Volume 15


Posted By: ^heidi^ O iNFj
Date: Tuesday, 3 October 2000, at 6:23 p.m.

In Response To: I got it near my elbows, armpits (Sean (Be Negative))

I found this post on another message board that seems strangely full of vitiligo Q&A this past year. There are some valuable references attached, so I believe it will be of value.

Here is the text:

I have been diagnosed with Vitiligo (this is the correct spelling). The condition is considered to be autoimmune in nature and is characterized by the skin becomming depigmented (absence of melanocytes). They say there is no cure. In most cases, the areas of depigmentation are symetrically distributed on the body (left and right side of the body). The areas are usually on the top of hands, elbows, knees, chin, back of neck, corners of mouth and close to other body openings (around eyes, ears, genetals). People who are more susceptable include diabetics, and those with thyroid problems. In addition, persons with AIDS frequently develop vitiligo. The lesions to not hurt and there are no real symptoms other than the white spots themselves. It is noted that Vitiligo often occurs after stressful events or severe injury. They say it can happen at any age (including infants).

Clinical analysis has proved that there is an accumulation of hydrogen peroxide in the skin. This finding has led doctors to recently develop a treatment called psuedocatalase (catalase breaks down H202 into water) combined with UVB treatment. It appears to be successful at inducing repigmentation. Other methods include topical steroids and PUVA. Of course, none of these treatments address the underlying cause.

Here is where I need advice: I believe that Vitiligo is caused by CRS (even though there are no other symptoms) which in turn is caused by "leaky gut." To back this up, I am attaching several research studies I have found that seem to support my hypothesis. What I can not account for however, is the accumulation of hydrogen peroxide in the skin. Does anyone have a theory? Also, does my hypothesis hold water?

=name withheld=

Here are the articles:

Identification of autoantibody to melanocytes and characterization of vitiligo
antigen in vitiligo patients Park YK, Kim NS, Hann SK, Im S

Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea.

Patients with vitiligo have circulating antibodies to melanocytes. To identify vitiligo antibodies and characterize the antigens by vitiligo antibodies, sera of 18 patients with vitiligo, 18 with Behcet's disease, 22 with syphilis and 14 normal control subjects were analyzed by indirect immunofluorescence, live cell ELISA, and immunoblotting. In indirect immunofluorescent microscopy and live cell ELISA, most vitiligo sera showed positive immunofluorescence and high optical density on the surface of melanocytes cultured from normal and vitiligo patients, indicating that autoantibodies in the vitiligo sera may react with vitiligo antigens on the surface of melanocytes. When the same experiments were performed with malignant melanoma cell lines and fibroblasts, no significant differences in the immunofluorescence and optical density were observed between normal and vitiligo sera. And the sera of patients with Behcet's disease or syphilis showed no significant difference in the reaction of live cell ELISA to fibroblasts, IGR-3 and melanocytes. The antibody titers of vitiligo patients in live cell ELISA decreased following systemic steroid treatments. Immunoblot analysis demonstrated that 44% of vitiligo sera was directed to melanocyte antigen with a molecular weight of 65 kDa. Inhibition assay using rabbit anti-melanocyte antibody showed inhibition of reaction between vitiligo sera and melanocytes in ELISA and immunoblotting. These findings support the hypothesis that the sera of vitiligo patients have autoantibodies mostly directed to the 65-kDa antigen and this antigen may originate mostly from the melanocyte surface.

Purification and biochemical characterization of a 65-kilodalton mannoprotein
(MP65), a main target of anti-Candida cell-mediated immune responses in humans.
Gomez MJ, Torosantucci A, Arancia S, Maras B, Parisi L, Cassone A

Department of Bacteriology, Istituto Superiore di Sanita, Rome, Italy.

A 65 kDa-constituent (MP65) of a whole-cell mannoprotein (MP) fraction of Candida albicans was purified by immunoaffinity chromatography with monoclonal antibodies directed against periodate-insensitive, protease-sensitive MP epitopes, putatively polypeptide in nature. These antibodies were obtained by immunization of mice with concanavalin A bead-coupled, low-glycosylated MP from
hyphal cells of C. albicans grown in the presence of a subinhibitory dose of tunicamycin. The immunoaffinity-purified MP65 molecule had a pI of 4.1 and a protein/polysaccharide ratio of 1.8:1. It was resistant to hydrolysis by endoglycosidase H, endoglycosidase F, or N-glycoffanases but still reactive with
concanavalin A. The polysaccharide moiety of MP65 was composed exclusively of mannose and glucose at a ratio of 12.7 to 1. The protein moiety showed numerous potential O-glycosidic linkage sites as suggested by the high proportion of serine and threonine (together accounting for more than 20% of the total amino acid composition) and susceptibility to diluted alkali. This treatment and digestion with alpha-mannosidase caused a reduction in the MP65 molecular mass to around 54 kDa. The N-terminal sequence of MP65 protein moiety was rich in alanine and valine (7 of 13 amino acids) and did not show any significant homology with deposited sequences in data banks. Purified MP65, at doses of a few nanograms, induced extensive T-cell proliferation of human peripheral blood mononuclear cells. This proliferation was specifically inhibited, in a dose-response fashion, by the antigen-binding fragment of the monoclonal antibody used for immunoaffinity purification. Overall, these results highlight chemical and molecular details of MP65, a main target of human T-cell response to C.albicans.

Immunological cross reactivity between Candida albicans and human tissue.
Vojdani A, Rahimian P, Kalhor H, Mordechai E
Immunsciences Lab Inc., Beverley Hills, CA 90211, USA.

An old concept to account for autoimmunity is the existence of immunologic cross reactions, or shared determinants between an exogenous agent and self antigen. To study molecular mimicry between the Candida antigen and an autoantigen, sera from clinical specimens were screened, based on seronegativity or positivity for thyroid, ovary and adrenal antibodies. Compared with tissue antibody negative sera and sera from healthy controls, samples from positive tissue antibody subjects exhibited significantly higher levels of Candida IgG (P < 0.001) IgM (P < 0.001) and IgA (P < 0.01) antibodies. While Candida antibodies were elevated in 60% of tissue antibody positive samples, these antibodies were present in only 7.5% of tissue antibody negative subjects and in 10% of healthy controls. Since PAGE electrophoresis showed similar bands mobility in Candida and different tissues, these positive antibodies and rabbit anti Candida antibodies were reacted in immunodiffusion and Western Blot Assay against Candida and tissue antigens, simultaneously. The results of immunodiffusion showed a clear precipitation line against tissue antigens when rabbit anti Candida or human positive Candida serum was used. Similarly, Western Blot Assays with rabbit or human anti Candida serum showed several positive bands with Candida and one or two positive bands with different tissues. The common antigens were located in the regions of 72 and 36 KD. The 72 KD was detected in capsule antigens, placenta, ovary, adrenal, thymus, liver, pancreas, spleen, brain and kidney, but not in sperm or epithelial cell antigen. The 36 KD antigen was positive in placenta, spleen adrenal, pancreas and capsule tissues. Absorbtion of sera containing high levels of Candida antibodies with tissue antigens caused 10-15% reduction in antibody titers. Moreover, treatment of thyroid antibody positive sera with C. Albicans caused a similar reduction in thyroid antibody levels. These reductions in antibody levels are an additional support for cross reactivity between C. Albicans and mammalian tissues. A demonstration of immunological cross reactivity between Candida and human tissues may be associated with the possible pathogenic role of Candida Albicans in the development of
autoimmune diseases which warrants further investigation.

Candida albicans suppresses transcription of melanogenesis enzymes in cultured melanocytes.

Kippenberger S, Bernd A, Menzel I, Loitsch S, Ramirez-Bosca A, Kaufmann R
Abteilung 1, Klinikum der Johann Wolfgang Goethe-Universitat, Frankfurt/Main, Germany.

Human skin can be colonized by different yeasts that may have an impact on skin pigmentation. In order to study this effect normal human melanocytes were cultured with different yeasts. Reverse transcription polymerase chain reaction (RT-PCR) analysis gives evidence that Candida albicans suppresses the transcription of melanogenesis enzymes.

The effect of UV-light on human skin microorganisms.

Faergemann J, Larko O

Pityrosporum orbiculare, Candida albicans, Staphylococcus epidermidis and S. aureus were irradiated with UVA and UVB light in vitro. UVB inhibited growth much more effectively than UVA. P. orbiculare was the most sensitive and S. aureus the least sensitive organism. With a dose of 900 mJ cm-2 of UVB a 50 times reduction in number of colony forming units was seen for S. aureus and for the other organisms a total inhibition of growth was seen. When P. orbiculare was irradiated with monochromatic light at 300, 330 and 360 nm the highest antimicrobial activity was seen at 300 nm. If these in vitro observations correlates with the effect of UV-light treatment of various skin disorders is still unclear.

Chronic mucocutaneous candidiasis.
Kirkpatrick CH
Department of Medicine, University of Colorado Health Sciences Center, Denver.

Chronic mucocutaneous candidiasis is a complex disorder in which patients have chronic and recurrent Candida albicans infections of the skin, nails, and mucous membranes. There are several subgroups of patients with chronic mucocutaneous candidiasis, and these can be identified by associated disorders such as autoimmune diseases, endocrinopathies, thymoma, and interstitial keratitis, as well as the distribution and severity of the Candida infections. Several other disorders may coexist in patients with chronic mucocutaneous candidiasis. These include other infectious diseases, endocrinopathies, dental enamel dysplasia, vitiligo, and alopecia totalis. Successful treatment programs should include antifungal drugs and manipulations that correct the immunologic abnormalities that predispose the patient to Candida infections.

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