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At the Problem Psoriasis Clinic at the University of Tennessee, Memphis, we use an antimicrobial approach for the treatment of psoriasis. This method is described for patient history, physical examination, and laboratory tests as well as treatment.

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The recent discovery that human epidermal cells themselves make and secrete the components necessary for activation of the alternative complement pathway appears to provide an explanation for how human skin is ordinarily able to avoid colonization by molds and other organisms. It also helps clarify the mechanisms underlying clinical and laboratory findings seen in chronic mucocutaneous candidiasis, dandruff, and psoriasis. Psoriasis seems best explainable as a visible, late stage of the inflammatory sequelae of activation of the alternative complement pathway in the epidermis.

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It has been suggested previously that psoriasis is best explained as a distinctive inflammatory response to a variety of microbial stimuli, all acting primarily through activation of the alternative complement pathway. For the past several years we have conducted a "Problem Psoriasis Clinic" based on that premise. Patients are questioned, examined, and subjected to microbiologic laboratory investigations in an attempt to identify possibly relevant microorganisms, and then are treated with antibiotics. This article lists the most commonly found microorganisms in psoriasis patients and describes the usual treatment for each. Results obtained with this approach compare favorably with those achieved with more usual anti-psoriasis treatments. We recommend that a microbiologic investigation and a trial of antimicrobial treatment should precede any plan to treat psoriasis patients with anything more than the simplest topical agents.

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Bimolane, an analog of razoxane has been used in China with comparable efficacy but less toxicity than razoxane in the treatment of psoriasis. In an attempt to characterize further its mode of action it was administered both systemically and topically in the Malassezia ovalis animal model of psoriasis. Intravenous methotrexate and topical 0.1% betamethasone valerate were also used as positive control treatments. The animal model of psoriasis was effectively treated by bimolane, both systemically and topically, and also by parenteral methotrexate and topical betamethasone valerate. The time course of bimolane's effect with this model was different from methotrexate's suggesting the possibility of a different mode of action. Because bimolane, like razoxane, is an ethylene diamino tetraacetate acid (EDTA) derivative, it is possible that its effects on this reaction relate to its chelating properties and that inhibition of complement activation is important to its mode of action.

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The microflora of 297 psoriasis patients was extensively examined. Throat, urine, and skin surfaces from scalp, ears, chest, face, axillary, submammary, umbilical, upper back, inguinal crease, gluteal-fold, perirectal, vaginal, pubis, penis, scrotal, leg, hands, feet, finger, and toenail areas were cultured for aerobic bacteria, yeast, and dermatophytes. Antibody levels to streptococcal enzymes were performed (streptolysin-O, DNAse-B, hyaluronidase, STREPTOZYME). Giemsa smears and KOH preparations were also used to determine yeast and dermatophyte presence. Associated organisms thought to provoke a psoriatic attack were as follows: streptococcal groups A, B, C, D, F, G, S viridans, S pneumoniae; Klebsiella pneumoniae, oxytoca; Escherichia coli; Enterobacter cloacae, E aerogenes, E agglomerans; Proteus mirabilis, P vulgaris; Citrobacter freundii, C diversus; Morganella morganii; Pseudomonas aeruginosa, P maltiphilia, P putida; Serratia marcescens; Acinetobacter calbio aceticus, A luoffi; Flavobacterium specie; CDC groups Ve-1, Ve-2, E-o2; Bacillus subtilis, cereus; Staphylococcus aureus; Candida albicans, C parapsilosis; Torulopsis, glabrata; Rhodotorula and dermatophytes. One or more antistreptococal enzyme tests was positive in 50% of patients. Titers to hepatitis E were elevated in one patient and to HIV in two patients.

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Plasma from 16 patients with psoriasis and 12 healthy control subjects were measured for iC3b, C4d, and Bb fragments generated by complement activation. Plasma concentrations for iC3b, C4d, and Bb fragments were found to be significantly increased in the patients with psoriasis. The highest concentrations of these complement activation fragments were seen in patients with erythrodermic pustular psoriasis, psoriatic arthritis, and Reiter's syndrome. The serum concentrations of complement components and regulatory proteins were normal or elevated in almost all samples.

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Phenotype frequencies for the complement proteins Bf (factor B), C4A and C4B were performed in a sample of 49 Caucasian patients with psoriasis followed in Memphis, Tennessee. The genes for these proteins are located in the major histocompatibility complex between the HLA-B and HLA-DR loci. Bf phenotype frequency did not differ significantly for the patients as compared to regional controls. The C4*A6 allele was present in 26.6% of the patients as compared to 5.4% of the controls, p less than 0.001, relative risk = 4.93. The C4*A6 allele is known to be in linkage disequilibrium with the HLA B17 allele and produces a functionally defective gene product. The role, if any, of C4*A6 in the pathogenesis of psoriasis is uncertain.

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Microbial findings were analyzed from a group of 167 patients with psoriasis in an attempt to discover specific associations. Positive findings include associations between Malassezia ovalis and scalp/ear/face psoriasis and between bacteria and bodyfold, nailfold, and gluteal/rectal psoriasis.

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Phenotype frequencies for the complement proteins C4A, C4B, Bf (factor B) and C3 were performed for 49 Caucasian patients with psoriasis. The C4*A6 allele was present in 26.6% of the patients as compared to 5.4% of healthy regional Caucasian controls, p less than 0.001, relative risk = 6.28. The C4*A6 allele is known to be in linkage disequilibrium with the HLA B17 allele and to produce a non-functional gene product when it occurs with the B17 allele. HLA B17 is known to be associated with psoriasis in many Caucasian populations. Additional findings in the present study were a significant reduction in the C4B*2 allele frequency, a non-significant increase in the Bf*F allele frequency and no difference for Bf or C3 phenotype frequencies in the patients with psoriasis as compared to the controls.

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The addition of 5 days of rifampin therapy to a 10- or 14-day course of penicillin or erythromycin therapy has been shown to reduce greatly the rate of chronic streptococcal carriage. The empiric use of rifampin in combination with penicillin or erythromycin in nine of nine patients with streptococcal-associated psoriasis appeared to coincide with a marked improvement in their skin.

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The rhino mouse, an experimental model for systemic lupus erythematosus, was found to have murine leukemia virus particles present in the skin. Immunoperoxidase studies with anti-type C virus antibody indicated viral antigen presence in the sebaceous cells and surrounding follicular cysts of the dermis. Electron microscope studies show virus particles, both type C extracellularly and type A intracellularly, around follicular cysts. Virus particle was labeled with specific ferritin-conjugated antitype C virus antibody.

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Thirty-seven patients with seborrheic dermatitis were treated topically with a 2% ketoconazole cream or its vehicle control in a double-blind study. The subjects were studied for numbers of Malassezia ovalis (Pityrosporum ovale) cells in their scalp scale; changes in numbers of yeast cells and morphology of M. ovalis were tabulated along with clinical assessment of improvement. The 2% ketoconazole cream, but not the placebo cream, reduced the numbers of viable yeast cells on the scalp. The clinical effect of 2% ketoconazole cream was good (75%-95% improvement) or better in eighteen of twenty subjects; the placebo cream produced good results in only three of seventeen subjects treated. Results of this study are consistent with the view that M. ovalis plays a central role in the pathogenesis of seborrheic dermatitis.

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