Psoriasis treatable with antibiotics if microbial theory true! PART 1

** Originally posted by abuabdallah **

It all started when i read the following article,

Psoriasis treatable with antibiotics if microbial theory true
Article from: Dermatology Times , June 1, 1999 , Guttman, Cheryl

New Orleans -- Ongoing research is focusing on developing proof for a hypothesis that there is a microbial source underlying the inflammatory response associated with psoriasis, E. William Rosenberg, M.D., said at the annual meeting of the American Academy of Dermatology.

"The concept that psoriasis is an autoimmune disease is advanced by many researchers in this field worldwide and is the basis for many existing and investigational agents that suppress the immune system. However, that hypothesis remains to be proven, and we are pursuing our own theory that it is microbial antigen that is driving T-cell stimulation in psoriasis. If our assumption is correct, then we believe that if we take the `ball away' with antibiotic therapy, the game will be over," said Dr. Rosenberg, professor of dermatology, University of Tennessee, Memphis.

The research efforts of Dr. Rosenberg and his colleagues are occurring on two fronts -- aiming to demonstrate and define the microbial antigen in skin and to evaluate the response of psoriasis patients to antimicrobial therapy.

He reported that he has now obtained IRB approval to begin an investigator IND study of clindamycin in the treatment of psoriasis. Patients with disease severe enough to warrant systemic treatment will be randomized to receive clindamycin 300 mg QID for 14 days or placebo. The study aims to enroll 40 patients aged 20 to 40 years and will exclude those with erythrodermic, pustular, scalp, and palmar-plantar psoriasis.

The study was prompted by the findings from a retrospective analysis Dr. Rosenberg performed examining responses among psoriasis patients who had been treated with clindamycin. He noted that of 53 patients who received clindamycin 300 mg QID for various periods, mostly in the range of 10 to 14 days, 58 percent had an excellent response. Further analyses revealed ageand gender-related differences in efficacy, with women faring better than men overall and patients aged 20 to 40 years old having higher response rates than both older and younger individuals.

Of particular interest, however, was the finding of a higher response rate among patients testing negative for the streptococcal carrier state compared with those who were positive, 71 percent vs. SO percent, respectively.

"Knowing that streptococcal infection can evoke psoriasis, we began using clindamycin with the intent of eradicating the strep carrier state. The observation that it was particularly effective in individuals who are negative for strep by culture or antiDNase-B suggests that there may be a different mechanism for clindamycin's efficacy in psoriasis patients," Dr. Rosenberg said.

In this regard, he postulated that micro-organisms in the gut may be the source of antigen involved in the development of psoriasis and that clindamycin's activity may reflect alteration of the intestinal microflora.

Dr. Rosenberg said if the autoimmune theory of psoriasis pathogenesis is incorrect, then treatment aimed at suppressing the immune system is not only an inappropriate way to treat psoriasis but hazardous as well.

"A group of Toronto rheumatologists have recently reported that the mortality rate among psoriatic arthritis patients is 1.5 times higher than expected in the general population.

These data raise real questions about treatment approaches based on the autoimmune concept.

WELL, COME ON NOW DR. ROSENBERG, can you give me evidence! Heres an article i found of great interest

Effort to Identify an Effective Treatment for Psoriasis Being Conducted by University of Tennessee Health Science Center Researchers

Memphis, TN (Insert Date) – The University of Tennessee Health Science Center is looking for volunteers to participate in a research study being conducted by the Departments of Preventive Medicine and Dermatology to determine how Bicillin L-A, a commonly used antimicrobial drug (a drug that destroys germs), affects the course of psoriasis.

The study drug, Bicillin L-A, is an antibiotic that has been in use in the USA for more than 30 years. Bicillin L-A is a long-acting form of penicillin. Following intramuscular administration, Bicillin L-A is slowly released from the injection site and transformed into penicillin in the human body. The drug is presently approved by the U.S. Food and Drug Administration (FDA) for the treatment of certain streptococcus infections (a group of disease causing organisms, commonly known as strep) but not specifically for psoriasis.

The reasons why an individual develops psoriasis are not completely understood but the factors that may provoke a flare-up have been extensively sought and well described in the medical literature. In the course of this research it has been established that psoriasis may be triggered or worsened by throat infections from disease causing organisms. As Bicillin L-A is active against these disease causing organisms, there are some observations that the drug may be effective in the treatment of psoriasis. To provide valid scientific evidence that Bicillin L-A is beneficial to psoriatic patients, it is necessary to perform a study in which the investigators will assess the improvement (if any) of the psoriasis skin conditions, comparing the study drug with an identical appearing inactive substance (known as placebo) that has no medical effect. Therefore, some individuals will receive the active drug (Bicillin L-A) and others will receive only the inactive substance (placebo). Because there is no animal model of psoriasis currently in use, it is necessary to enlist the help of persons who have active, hard-to-treat psoriasis in order to conduct such research.

Approximately 40 participants, aged 18-40, in good health, with psoriasis that does not improve with use of creams or ointments will take part in this study; 20 will receive Bicillin L-A and 20 will receive the placebo. Neither the doctor nor the volunteer participant will know whether the participant received the active drug or the placebo until after the study has been completed. Only in that way is it possible to be sure that the benefit observed, if any, was really due to Bicillin L-A.

All study procedures and tests will be performed at the University of Tennessee Health Science Center Department of Preventive Medicine Research Clinic office at 66 N. Pauline, Ste. 501, Memphis, TN 38105.

A participant’s involvement is about 4 months for clinic visits, then phone follow-up for 24 months. Preliminary studies suggest that a long-term course of Bicillin L-A, when successful, seems to provide a remission for chronic psoriasis.

The results of this study may benefit society by introducing a safe and cost-effective treatment for plaque-type psoriasis that cannot be further controlled by other psoriasis medications. This information could be helpful for finding the optimal treatment for other patients with psoriasis and contribute to the improvement of their quality of life.

Participants who complete the study will receive a total of $275 for the time required to participate in the entire study.

Principal Investigator for the Psoriasis Study is Elias Wm. Rosenberg, MD, and Co-Investigators are Robert Skinner, MD and Elizabeth Tolley, PhD. Anyone interested in participating in the Psoriasis research study should call the UTHSC Preventive Medicine Recruitment Department at (901) 448-8400

BUT DR. ROSENBERG, WHAT RESULTS HAVE U OBTAINED TO WARRANT FURTHER STUDIES?

Bicillin L-A vs Placebo for the Treatment of Chronic, Plaque-Type Psoriasis Unresponsive to Topical Medications

This study is currently recruiting participants.
Verified by University of Tennessee, January 2007

Sponsored by: University of Tennessee
Information provided by: University of Tennessee
ClinicalTrials.gov Identifier: NCT00427609

Purpose
The purpose of this study is to determine the efficacy fo Bicillin L-A, administered intramuscularly in a dose of 2.4 million units every three (3) weeks, for the treatment of chronic, plaque-type psoriasis unresponsive to topical medications or when other systemic therapies are contraindicated.

Condition Intervention Phase
Psoriasis
Drug: Bicillin L-A
Phase II



MedlinePlus related topics: Psoriasis


Drug Information available for: Penicillin G Penicillin G Benzathine Penicillin G Potassium Penicillin G Sodium Penicillin G, benzathine Penicillin G, procaine



U.S. FDA Resources

Study Type: Interventional
Study Design: Treatment, Randomized, Double-Blind, Placebo Control, Parallel Assignment, Efficacy Study


Official Title: Efficacy of Bicillin LA for the Treatment of Chronic, Plaque-Type Psoriasis Unresponsive to Topical Medications.



Further study details as provided by University of Tennessee:

Primary Outcome Measures:
A reduction of an individual's PASI by 75% after five (5) treatments of the active drug (Bicillin L-A). To demonstrate benefit comparable to the currently available biologicals, the response rate of Bicillin L-A must be at least 40%


Estimated Enrollment: 40


Detailed Description:
Psoriasis is a chronic, inflammatory skin disorder most commonly manifested by well-demarcated, erythematous and/or scaling plaques on the elbows, knees, scalp, and trunk. Psoriasis is a common disease with overall incidence of 1-3% of the general population. The estimated prevalence varies from 1-2%. There is significant geographical variability with the lowest incidence of the disease around the equator and increasing towards the poles.

Psoriasis is now considered an autoimmune disease mediated by activated T-cells, releasing proinflammatory cytokines, predominately TNF-a and IFN-y. The key role for T-cells in the pathogenesis of psoriasis was supported by reported beneficial effects of specific T cell targeted therapies including cyclosporin A and certain recently marketed immune response modifiers.

While disease pathogenesis is still not completely understood, the factors that may trigger or worsen psoriasis have been systematically studied and well described in the medical literature. Psychological stress, mechanical trauma to the skin, certain medications and Streptococcus strains are the most common disease triggers.

It was first reported in 1916 that the onset of psoriasis is often preceded by throat infections with hemolytic streptococci and the role of M-protein positive beta hemolytic streptococci in triggering guttate psoriasis has been confirmed in subsequent studies. Exacerbation of chronic plaque type psoriasis has been reported in association with tonsillitis in retrospective studies. Moreover, high frequency of remission after tonsillectomy or antibiotic treatment has been documented.

2 DERMATOLOGISTS IN INDIA HAVE COME TO THE SAME CONCLIUSION AND ARE DRIVING PSROASIS PATIENTS INTO REMISSION RIGHT NOW!

Dermatologists claim breakthrough in cure of psoriasis

Date:19/05/2006 URL: http://www.thehindu.com/2006/05/19/stories/2006051915100500.htm


Dr. V.N. Saxena and Dr. Jaideep Dogra identify a bacterium in the throat as a causative organism of the illness




JAIPUR: Two dermatologists of Jaipur have claimed a breakthrough in the cure of psoriasis, a skin disease causing red scaly patches that was previously thought to be a lifelong ailment, by identifying a bacterium in the throat as a causative organism of the illness.
The doctors have treated the patients of psoriasis by antibiotic drugs such as penicillin and azithromycin.
V.N. Saxena of the Department of Dermatology at Sawai Man Singh Medical College here and Jaideep Dogra of the Central Government Health Scheme in their evidence-based research have for the first time found a permanent cure for psoriasis for which only suppressive therapy was available so far.
The two doctors have stated that streptococci bacteria in the throat are responsible for causing acute psoriasis, which is found in approximately three per cent population around the world.
The remnants of streptococci left in the body following throat infection, possibly because of inadequate elimination by the immune system, cause psoriasis after a gap ranging from a few months to several years, according to their research.
The research, published in the European Journal of Dermatology recently, has found similarities between the psoriasis disorder after throat infection and rheumatic heart disease after rheumatic fever.
Dr. Dogra told The Hindu here on Thursday that when the therapy was initiated on the lines of treatment of rheumatic heart ailment, excellent clearing of lesions and patches was observed within a few weeks after injecting benzathine penicillin into the patients.
Those suffering from psoriasis have oval to round scaly patches of different sizes occurring mainly on the back of arms and scalp.
The lesion has silvery scales with reddish base and the disorder generally intensifies during winter. In some patients, joints and nails may also be affected.
Dr. Dogra said nearly 70 per cent of the psoriasis patients of all age groups develop the disease in a chronic form.
"When killed streptococcal material was injected in the skin of normal persons, psoriatic lesion developed at the site of injection and elsewhere in the body," he said, adding that experiments spanning two years concluded that streptococci was the cause of the illness.
A recent study by Richard D.R. Camp of the Department of Infection, Immunity and Inflammation in the University of Leicester, U.K., has also supported the work of the Jaipur doctors by concluding that "long-lived'' streptococci might be responsible for chronic psoriasis.
Prof. Saxena and Dr. JaideepDogra selected 30 histopathologically confirmed patients, including 20 men and 10 women, with chronic psoriasis for the study, and all of them responded positively to the treatment with none of them having had a relapse of disorder during the study period of two years, except for the development of a few small new lesions in the six patients during winter which were cleared on continuing the treatment.
© Copyright 2000 - 2008 The Hindu

WHAT THE HELL IS PSORIASIS!?

Psoriasis is a cutaneous inflammatory disorder characterized by epidermal keratinocyte hyperproliferation. Several theories have been proposed regarding the molecular nature and etiology of psoriasis. Factors that have been invoked to cause or promote psoriasis include genetic composition, immune functions, epithelial functions, proliferative and differentiation signals, and/or environmental factors. See Nickoloff et al. (2000) Exp Dermatol 9:359-375.

The disparate explanations offered by such theories have directed the development of accordingly different therapeutic strategies.

A prevailing view holds that skin disorders such as psoriasis can develop by an initial immune response to a microbial agent that subsequently evolves to a self-perpetuating auto-immune disease. Thus, a current strategy for therapeutic treatment of psoriasis comprises disruption or suppression of the immune response. In particular, drug design approaches are directed at disruption of various aspects of T-cell function, including mechanisms of recruitment, cell-cell interaction, and cytokine production. See Barker (1998) Hosp Med 59(7):530-533.

A second view holds that the psoriasis results from erroneous activation of an epithelial defence system. Such an abnormal defence response is characterized by the activity of superantigens and proinflammatory cytokines. This model asserts to explain the predominance of psoriasis in skin and the resemblance of psoriatic skin to bacterial infection and wound healing. In one aspect, genetic factors are implicated in abnormal epithelial responses to infectious and/or physicochemical skin insults.

A related perspective suggests that inappropriate keratinocyte proliferative and differentiation signals comprise the primary disorder of psoriasis. For example, psoriasis may result from misregulation of neutrophils, which are required for epithelial differentiation and keratinization. This developmental defect can occur in the absence of an infectious challenge.

Yet another model proposes that the interaction among epidermal factors (e.g., adhesion molecules), neuropeptides (e.g., nerve growth factor, Substance P), and T lymphocytes plays a causative role in the development of psoriasis.

Yet a model, and hence a therapy, that encompasses most, if not all, observations related to psoriasis remains undisclosed and unavailable in the art.

Dr. Rosenberg suggests that psoriasis is an immunologically mediated response of the epidermis to cope with microbial antigens of external or circulating form. Psoriasis is the result of a continuous and useful response of the skin to the presence of microbial antigen in the skin. This model reconciles several contrasting views summarized above, and, as will be evident from the disclosure herein, presents a novel approach for treating systemic and autoimmune diseases.

THE ABOVE STATEMENT MAKES SENCE!!!!!!!!!! PART 2 IS PROOF!

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** Originally posted by abuabdallah **

1: Br J Dermatol. 1976 Dec;95(6):603-6.Links

Bacterial flora in psoriasis.Aly R, Maibach HE, Mandel A.

The aerobic bacterial flora of psoriatic plaques, uninvolved skin and the anterior nares of forty psoriatic patients was studied. The incidence od Staphylococcus aureus was 30% in the anterior nares, 20% on the plaques and 13% on the uninvolved skin. S. aureus counts were 3 x 10(2)/cm2 on the plaques and 1-5 x 10/cm2 on the normal skin. The total bacterial counts were also higher on plaques (7-9 x 10(3)/cm2) than on normal skin (3-0 x 10(3)/cm2). The incidence of lipophilic diphtheroids was significantly lower on the plaques (4%) than the normal skin (30%). Eighty percent of the strains of S. aureus isolated from psoriatic patients were resistant to 10 units of penicillin. Because of increased desquamation, psoriatic skin is a public health hazard.

Dermatologica. 1978;157(1):21-7.Links

Bacteriology of psoriatic plaques.Singh G, Rao DJ.

Qualitative and quantitative studies of cutaneous bacterial flora were carried out in psoriatic patients and normal healthy controls. In psoriatics, the flora isolated from the affected skin was compared with the flora of adjacent normal skin. No significant qualitative difference was observed. The total number of bacteria isolated from the psoriatic plaque was significantly higher than on the adjacent normal skin. Flora of normal skin of psoriatics when compared with the skin of healthy controls did not reveal any qualitative difference, but a statistically significant difference was observed in the total bacterial counts. The nasal carriage rate of Staphylococcus aureus in psoriatics was higher than the control groups.

1: J Am Acad Dermatol. 1986 May;14(5 Pt 1):761-4.Links

Use of rifampin with penicillin and erythromycin in the treatment of psoriasis. Preliminary report.Rosenberg EW, Noah PW, Zanolli MD, Skinner RB Jr, Bond MJ, Crutcher N.

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.

1: Acta Derm Venereol Suppl (Stockh). 1989;146:72-4; discussion 75.Links

Microbial associations of 167 patients with psoriasis.Rosenberg EW, Noah PW, Skinner RB Jr, Vander Zwaag R, West SK, Browder JF.
Department of Medicine (Dermatology), University of Tennessee College of Medicine, Memphis.

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.

1: Semin Dermatol. 1990 Dec;9(4):269-76.Links

The role of microorganisms in psoriasis.Noah PW.
Department of Medicine Dermatology, College of Medicine, University of Tennessee, Memphis 38163.

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.

1. Am Acad Dermatol. 1992 Mar;26(3 Pt 2):458-61.Links

A therapeutic trial of the use of penicillin V or erythromycin with or without rifampin in the treatment of psoriasis.
Vincent F, Ross JB, Dalton M, Wort AJ.

Department of Medicine, Faculty of Medicine, Dalhousie University, Halifax, N.S., Canada.
BACKGROUND: After the publication of an uncontrolled trial of nine patients with streptococcus-associated psoriasis who appeared to benefit from a course of oral penicillin or erythromycin with the addition of rifampin in the last 5 days, we wished to confirm or refute the validity of this observation. OBJECTIVE: Our purpose was to confirm the effectiveness of antibiotics in the treatment of streptococcus-associated psoriasis. METHODS: Twenty patients were placed randomly into two groups. One group was given penicillin or erythromycin for 14 days with a placebo added during the last 5 of the 14 days. The other group received the same medication with the addition of rifampin in the last 5 days. RESULTS: Although all the patients studied met the criteria of the reported preliminary study, we were unable to detect any evidence of improvement in their psoriasis. CONCLUSION: There was no apparent benefit for patients with streptococcus-associated psoriasis from a course of oral penicillin or erythromycin with the addition of rifampin in the last 5 days in a 14-day trial.


1: J Natl Med Assoc. 1994 Apr;86(4):305-10.Links

Microorganisms and psoriasis.Rosenberg EW, Noah PW, Skinner RB Jr.
Department of Dermatology, University of Tennessee College of Medicine, Memphis 38163.

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.

CONCLUSION

Do antibiotics offer a practical way to manage psoriasis? In our experience, a search for relevant microbes and treatment with antimicrobial drugs is a practical way to manage psoriasis. Recently, we reported results of antimicrobial treatment of 126 patients with
psoriasis, many of these problem cases referred by other physicians. Approximately 50% of our patients were completely or almost completely cleared of their diseases, another 30% markedly improved, and in about 20% the treatment failed. These results compare favorably with results achieved with other treatments including some with a substantial potential for harm.

Certainly, we think that a work-up and therapeutic trial of antimicrobial treatment should always be attempted before starting treatment with methotrexate, etretinate or
cyclosporin, and probably prior to the institution of psoralen-ultraviolet-light therapy.

Even for patients who can control their diseases topically with either corticosteroid or tars but who require almost continuous such applications, this kind of approach appears to offer significant potential benefit.

1: J Dermatol. 1994 Jun;21(6):375-81.Links

Psoriasis is a visible manifestation of the skin's defense against micro-organisms.
Rosenberg EW, Noah PW, Skinner RB Jr.
Department of Medicine (Dermatology), University of Tennessee College of Medicine, Memphis.

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.

1: Dermatol Clin. 1995 Oct;13(4):909-13.Links

Antimicrobial treatment of psoriasis.Skinner RB Jr, Rosenberg EW, Noah PW.
Department of Medicine, University of Tennessee, Memphis 38163, USA.

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.

1: Adv Exp Med Biol. 1997;418:157-9.Links

Microbial associations and response to antimicrobials seen in a psoriasis clinic.

Belew-Noah PW, Rosenberg WE, Zabriskie JB, Skinner RB Jr, Henson TH, Beard GB.
University of Tennessee, Memphis, USA.

INTRODUCTION

Microbial agents have often been reported in association with flares of psoriasis and psoriasis often clears when treated with antimicrobial agents or tonsillectomy. All patients seen at the University of Tennessee Psoriasis clinic are studied for evidence of relevant microorganisms. We report a survey of the microbial findings in 95 patients chosen at random from the 693 psoriasis patients seen during 1995.
RESULTS IN PSORIASIS

The most frequently seen organisms were streptococci of Lancefield groups A, B, C, D (Enterococcus) and G. Also Streptococcus sanguis, mitis and moribillorum; also Haemophilis, Moraxella, Klebsiella, Enterobacter, Eschericia, Proteus, Pseudomonas, Flavomonas, Acinetobacter, Bacillus, Candida, Malassezia and dermatophytes. Positive serological tests to group A streptococcal exoenzymes, Helicobacter and cytomegalovirus occured.

CONCLUSION

Antimicrobials evoking clearing in psoriasis were ketaconazole, fluconazole, itraconazole, nystatin, penicillin/rifampin, peniccilin G benzathine, loracarbef, amoxicillin, and sulfasalazine. A positive response to antimicrobials occured in 68 of 77 (88%) of patients.

1: Acta Derm Venereol Suppl (Stockh). 2000;(211):17-8.Links

Subclinical microbial infection in patients with chronic plaque psoriasis.
Bartenjev I, Rogl Butina M, Potocnik M.

Department of Dermatovenereology, University Medical Centre, 1525, Ljubljana, Slovenia.
Epidemiological evidence implicates bacterial infection as a common triggering stimulus for psoriasis. Recent studies suggest that continuing, subclinical streptococcal and staphylococcal infections might be responsible not only for relapse of acute guttate psoriasis but also for a new episode of chronic plaque psoriasis. In this study 195 patients suffering from a severe form of chronic plaque psoriasis hospitalized between 1996 and 1998 were examined. The presence of subclinical microbial infection of the upper respiratory tract was studied by the cultivation of pathogens from this area. Patients with other provoking factors, such as a positive history of taking any drugs that may exacerbate psoriasis, endocrine and metabolic factors, alcohol abuse, trauma, dental focus and clinically evident bacterial infection, were excluded. Subclinical streptococcal and/or staphylococcal infections were detected in 68% of tested patients and in only 11% of the control group. The results of this study indicate that subclinical bacterial infections of the upper respiratory tract may be an important factor in provoking a new relapse of chronic plaque psoriasis. Searching for, and eliminating, microbial infections could be of importance in the treatment of psoriasis.



1: Br J Dermatol. 2003 Sep;149(3):530-4.

Streptococcal throat infections and exacerbation of chronic plaque psoriasis: a prospective study.
Gudjonsson JE, Thorarinsson AM, Sigurgeirsson B, Kristinsson KG, Valdimarsson H.
Departments of Immunology, Dermatology and Microbiology, Landspitali University Hospital, Hringbraut, Reykjavik, Iceland.

BACKGROUND: Guttate psoriasis has a well-known association with streptococcal throat infections but the effects of these infections in patients with chronic psoriasis remains to be evaluated in a prospective study. OBJECTIVES: To determine whether streptococcal throat infections are more common in and can cause exacerbation in patients with chronic psoriasis. METHODS: Two hundred and eight patients with chronic plaque psoriasis and 116 unrelated age-matched household controls were followed for 1 year. At recruitment all patients were examined, their disease severity scored and throat swabs taken. Patients and corresponding controls were then re-examined and tested for streptococcal colonization whenever they reported sore throat or exacerbation of their psoriasis during the study period. RESULTS: The psoriasis patients reported sore throat significantly more often than controls (61 of 208 vs. three of 116, P < 0.0001), and beta-haemolytic streptococci of Lancefield groups A, C and G (M protein-positive streptococci) were more often cultured from the patients than the controls (19 of 208 vs. one of 116, P = 0.003). A significant exacerbation of psoriasis (P = 0.004) was observed only if streptococci were isolated and the patients were assessed 4 days or later after the onset of sore throat. No difference was observed between groups A, C or G streptococci in this respect. CONCLUSIONS: This study confirms anecdotal and retrospective reports that streptococcal throat infections can cause exacerbation of chronic plaque psoriasis. It is concluded that psoriasis patients should be encouraged to report sore throat to their physician and that early treatment of streptococcal throat infections might be beneficial in psoriasis. A controlled trial for assessing potential benefits of tonsillectomy in patients with severe psoriasis should also be considered.

Rifampicin is effective in the treatment of psoriasis with and without concurrent streptococcal infection
Source: Inpharma, Volume 1, Number 1530, 2006-03-25 , pp. 7-7(1)
Publisher: Adis International

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** Originally posted by abuabdallah **

Continued


1: J Dermatolog Treat. 2006;17(1):18-23.

Old drug--new indication. Rifampicin in psoriasis.
Tsankov N, Grozdev I, Kkzandjieva J.
Department of Dermatology and Venereology, Medical Faculty, Sofia, Bulgaria. Tsankn@ns.medfac.acad.bg

BACKGROUND: The efficacy of traditional systemic therapies for psoriasis is limited by various side effects, toxicity, drug-drug interactions, and the need for frequent laboratory monitoring. In animal models, rifampicin causes immunosuppression and in conventional doses it suppresses the T-cell function. OBJECTIVE: To show that rifampicin has a therapeutic effect in eruptive psoriasis and to try to explain its mode of action. Materials and methods: A total of 76 patients (34 men and 42 women, aged between 12 and 68 years) with eruptive psoriasis were enrolled in the study. They were divided into two groups according to the evidence of a concomitant streptococcal infection. Rifampicin was administered orally in a 600 mg daily dosage for at least 60 days. Only emollients were given for topical therapy. RESULTS: A statistical (chi-squared test) analysis was done and it could be concluded that improvement in the two groups was statistically indistinguishable (p = 0.892), while comparison with the control group showed a significant difference (p = 0.00082). CONCLUSION: The results express that there is no statistically significant difference between the treating groups and the effect of rifampicin could not be related only to its antimicrobial properties. Its therapeutic effect most probably is due to its immunosuppressive properties.


1: Skinmed. 2006 Mar-Apr;5(2):72-9; quiz 80-1.

Skin basement membrane zone: a depository for circulating microbial antigen evoking psoriasis and autoimmunity.
Noah PW, Handorf CR, Skinner RB Jr, Mandrell TD, Rosenberg EW.
Department of Medicine (Dermatology) and Preventive Medicine, University of Tennessee, Memphis, TN 38104-7514, USA.

BACKGROUND: Elevated levels of antibody to streptococcal exoenzymes have been found in patients with psoriasis or psoriatic arthritis. Research on the role of streptococcal antigen in psoriasis has been hampered by a potential molecular mimicry between streptococcal epitopes and human epidermal keratin. OBJECTIVE AND METHODS: Evidence of microbial product was sought in skin biopsies of psoriasis patients thought clinically to have either streptococcal carrier state or gastrointestinal candidal colonization. A polyclonal antibody to streptococcal-derived exoenzymes unlikely to share antigenic structures with normal human skin, and an anticandidal antibody, were used with linked streptavidin biotin amplification stain. RESULTS: The predicted microbial product appeared heavily in lesional epidermis, but unexpectedly also as a thin deposit along the skin basement membrane zone (SBMZ) of apparently unaffected skin. Staining was negative for nonpsoriatic subjects. CONCLUSIONS: The findings support a direct effect of microbial antigen in psoriasis. They also suggest an important role for SBMZ as a very large adhesive surface in the first step of a process of percutaneous epidermal
elimination of foreign antigens and microbial toxins. The many autoimmune phenomena seen so often at the SBMZ are probably a physiologic part of this important immune function. Efforts to enhance the adhesive properties of SBMZ should be exploitable for both diagnostic and therapeutic benefit

1: J Coll Physicians Surg Pak. 2007 Dec;17(12):717-20.Links

1: PLoS ONE. 2008 Jul 23;3(7):e2719.

Substantial alterations of the cutaneous bacterial biota in psoriatic lesions.
Gao Z, Tseng CH, Strober BE, Pei Z, Blaser MJ.
Department of Medicine, New York University School of Medicine, New York, New York, United States of America.

For psoriasis, an idiopathic inflammatory disorder of the skin, the microbial biota has not been defined using cultivation-independent methods. We used broad-range 16S rDNA PCR for archaea and bacteria to examine the microbiota of normal and psoriatic skin. From 6 patients, 19 cutaneous samples (13 from diseased skin and 6 from normal skin) were obtained. Extracted DNA was subjected to the broad range PCR, and 1,925 cloned products were compared with 2,038 products previously reported from healthy persons. Using 98% sequence identity as a species boundary, 1,841 (95.6%) clones were similar to known bacterial 16S rDNA, representing 6 phyla, 86 genera, or 189 species-level operational taxonomic unit (SLOTU); 84 (4.4%) clones with <98% identity probably represented novel species. The most abundant and diverse phylum populating the psoriatic lesions was Firmicutes (46.2%), significantly (P<0.001) overrepresented, compared to the samples from uninvolved skin of the patients (39.0%) and healthy persons (24.4%). In contrast, Actinobacteria, the most prevalent and diverse phylum in normal skin samples from both healthy persons (47.6%) and the patients (47.8%), was significantly (P<0.01) underrepresented in the psoriatic lesion samples (37.3%). Representation of Propionibacterium species were lower in the psoriatic lesions (2.9+/-5.5%) than from normal persons (21.1+/-18.2%; P<0.001), whereas normal skin from the psoriatic patients showed intermediate levels (12.3+/-21.6%). We conclude that psoriasis is associated with substantial alteration in the composition and representation of the cutaneous bacterial biota.

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** Originally posted by abuabdallah **

In summary DR. Rosenberg has and continues to "CURE" people with antibiotics

WELL I KEEP READING ABOUT DR. HENG, i sent off for her treatment and I got this,

Oral:


Keflex - Cefalexin

or appropriate antibiotic for the bacterial superinfection until clear (usually in 4 months, longer for palms and soles). If skin cultures are positive for MRSA infection (methicillin resistant Staphylococcus aureus infection, other appropriate antibiotics may be necessary.


Diflucan (Nystatin is safer?) -

200 mg once a week for scalp and groin until clear (usually 4 months for the scalp, about 2 months for groin and axilla).



Topical:



Scalp: Ketoconazole shampoo 2% at night.

Curcumin application after bath.


Face and Flexural: Ketoconazole cream 2%

mixed with triamcinolone cream 0.1% once or twice a day. Curcumin application after bath.


Trunk and Limbs: Ketoconazole cream 2%

mixed with clobetasol cream 0.05% morning and noon.
Curcumin application after bath


ANTIBIOTICS AND ANTIFUNGALS!!!!! WHY!?!?!?!??!!

MICROBIAL ASSOCIATIONS AND RESPONSE TO ANTIMICROBIALS SEEN IN A PSORIASIS CLINIC
Patricia W. Belew-Noah, William E. Rosenberg, John B. Zabriskie, Robert B. Skinner, Terri H. Hansen, Gwen B. Bernard

Streptococci and the Host: Proceedings of the XIIIth Lancefield International Symposium Held in Paris, France, September 16-20, 1996 By Thea Horaud Published by Springer, 1997 ISBN 0306456036, 9780306456039 1064 pages


“Antimicrobials evoking clearing in psoriasis......”

Amoxicillin (INN) or amoxycillin (BAN) is a moderate-spectrum, bacteriolytic, β-lactam antibiotic used to treat bacterial infections caused by susceptible microorganisms.

Fluconazole (INN) (pronounced /fluː'kɒnəzoʊl/) is a triazole antifungal drug used in the treatment and prevention of superficial and systemic fungal infections.(Diflucan or Trican)

Ketoconazole is a synthetic antifungal drug used to prevent and treat skin and fungal infections, especially in immunocompromised patients such as those with AIDS. Ketoconazole is sold commercially as an anti-dandruff shampoo, branded Nizoral, by Janssen Pharmaceutica.

Nystatin is a polyene antifungal drug to which many molds and yeast infections are sensitive, including Candida spp. Nystatin has some toxicity associated with it when given intravenously, but it is not absorbed across intact skin or mucous membranes. It is considered a relatively safe drug for treating oral or gastrointestinal fungal infections.

Penicillin (sometimes abbreviated PCN or pen) is a group of Beta-lactam antibiotics used in the treatment of bacterial infections caused by susceptible, usually Gram-positive, organisms.

Rifampicin (INN) (pronounced /rɪ'fæmpəsɪn/) or rifampin (USAN) is a bactericidal antibiotic drug of the rifamycin group.[1] It is a semisynthetic compound derived from Amycolatopsis rifamycinica (formerly known as Amycolatopsis mediterranei and Streptomyces mediterranei).

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** Originally posted by abuabdallah **

WHERES THE PROOF!?!?!?!?

1: Arch Dermatol. 1984 Apr;120(4):435-6.Links
Oral nystatin in the treatment of psoriasis.
Crutcher N, Rosenberg EW, Belew PW, Skinner RB Jr, Eaglstein NF, Baker SM.
4 cases of long term, bodily psoriasis (10-25 years) were cured with oral nystatin within several months

1. Am J Med Sci. 1986 Feb;291(2):75-80.Links

Ketoconazole's inhibition of fungal antigen-induced thymidine uptake by lymphocytes from patients with psoriasis. Alford RH, Vire CG, Cartwright BB, King LE Jr.

Ketoconazole, an oral antifungal imidazole, has been effective in some refractory cases of psoriasis, particularly those with scalp involvement, perhaps because of suppression of Pityrosporum ovale. To assess an ancillary immunologically mediated role for ketoconazole, its effects were evaluated on psoriatic patients' lymphocyte function. Ketoconazole in vitro markedly inhibited Pityrosporum antigen-induced lymphocyte blastogenesis as indicated by impairment of cellular tritiated thymidine uptake. Ketoconazole likewise inhibited lymphocyte uptake of other pyrimidine nucleosides by both normal and psoriatic lymphocytes. Neither imidazole or an investigational triazole antifungal (Bay n7133) inhibited the uptake. Thus, ketoconazole potentially could affect psoriasis in seborrheic areas of skin by a direct antifungal action or indirectly by suppressing fungal antigen-induced lymphocyte-mediated immune responses affecting the skin.

Mycoses. 1990 Jan;33(1):29-32.Links

Studies on the yeast flora in patients suffering from psoriasis capillitii or seborrhoic dermatitis of the scalp.
Senff H, Bothe C, Busacker J, Reinel D.
Universitäts-Hautklinik Essen, Germany FR.

In 65 patients with scalp psoriasis or seborrhoic dermatitis of the scalp, stool specimens, tongue swabs and scalp scales were examined for yeasts. The stool specimens showed in 70.8% of the patient group massive and in 7.7% moderate yeast colonization. Yeasts were found in 47.7% of the tongue cultures and in 12.5% of the scalp scales. Candida albicans was the predominant pathogen in the faeces and on the tongue. In comparison with a control group, frequency of yeasts in faeces and on the tongue in patients with psoriasis capillitii and seborrhoic dermatitis of the scalp could be shown to be significantly higher

1. Mycoses 1990 Feb; 33(2):90-4.

Fungal flora of human faeces in psoriasis and atopic dermatitis.
Buslau M, Menzel I, Holzmann H

Faeces samples taken from 343 patients with psoriasis and 581 patients with atopic dermatitis were subjected to mycological examination. Yeasts were detected in 68% of the psoriatics and in 70% of the patients with atopic dermatitis but in only 54% of the controls (n = 50). Qualitative analysis revealed a predominance of Candida albicans. Non-pathogenic yeasts constituted only 1% in each of these groups. Of the hyphomycetes, Geotrichum candidum occurred in 22% of the psoriatics, in 10% of the atopic dermatitis patients and in 3% of the controls. Aspergillus species were found in 1% of the patients but not in the controls. Stool samples collected on three consecutive days from 141 patients were examined for yeasts. Qualitative correlation between all three samples was shown in 95% of the patients and quantitative correlation in 38%. Deviations were mainly of exponential magnitude. Germ cell concentration of 10(4) cells per ml and above were measured in 38% of the psoriatics and in 28% of the atopic dermatitis patients but in only 22% of the test subjects with healthy skin. There was no correlation between the concentration levels of yeasts in the faeces and the extent of psoriasis or atopic dermatitis.


1: Br J Dermatol. 1993 Feb;128(2):143-50.Links

Antiproliferative effects on keratinocytes of a range of clinically used drugs with calmodulin antagonist activity.
Mac Neil S, Dawson RA, Crocker G, Tucker WF, Bittiner B, Singleton JG, Hunter T, Tierney DF.
Department of Medicine, Northern General Hospital, Sheffield, U.K.

Thirty-two drugs, including some in use for a variety of clinical disorders, were examined for their ability to inhibit calmodulin activity in vitro. From these, 10 drugs were selected for their inhibition of calmodulin activity and examined for their ability to inhibit proliferation of rapidly dividing human keratinocytes. A significant correlation between antiproliferative activity and calmodulin antagonist potency was found. Of these drugs there were several, including miconazole, dequalinium chloride, bromocriptine and tamoxifen, whose use is well established and well documented. The potential use of these drugs (and others identified in this way) as antipsoriatic agents is discussed.


1: Rocz Akad Med Bialymst. 1997;42(1):236-40.Links

Effect of topical miconazole in plaque psoriasis.
Niczyporuk W, Krajewska-Kułak E.
Department of Dermatology, Venerology Medical Academy of Białystok.

The aim of this study was the assessment of efficacy and tolerance of topical miconazole in plaque psoriasis. 9 patients aged 23-63 years with diagnosis of plaque psoriasis were enrolled. 2% miconazole cream was applied twice daily from 7 to 12 weeks (under occlusive dressing to obtain optimal penetration of the drug) in the plaque with a minimum diameter of 5 cm. In most patients clinical improvement of the topical miconazole treatment was observed.


1: Mycoses. 1997;40 Suppl 1:22-8.Links

Mycoses in patients with psoriasis or atopic dermatitis
Henseler T, Tausch I.
Universität-Hautklinik Kiel, BR Deutschland.

Both, psoriasis and atopic dermatitis are multifactorial diseases with an unknown pathogenesis. To elucidate the influence of fungal infections in the onset or recurrence of those inflammatory skin disease we determined the frequencies of Candida and dermatophyte infections of the skin and orointestinal tract concomitantly seen in patients with psoriasis or atopic dermatitis. We analyzed the files of more than 40,000 in-patients of the Department of Dermatology, Kiel. Sex- and age-adjusted relative risk were calculated. The results demonstrate that patients with psoriasis (N = 3006) presented with a decreased rate of tinea. This was significant for tinea corporis (RR = 0.13, p < 0.01). Candida infections of the skin were seen more often in psoriasis patients compared to controls. Differentiating between Type I (early onset) and Type II (late onset) psoriasis only Type I psoriasis patients presented with decreased dermatophyte infections and increased Candida colonization of the intestinum. However, patients with Type II psoriasis demonstrated an increased rate of candidosis cutis and candidosis oris as compared to controls. Patients with atopic dermatitis (N = 1808) displayed a decreased overall incidence of tinea and Candida infections. Furthermore, in patients with atopic dermatitis a Candida colonization of the orointestinal tract was found elevated (RR = 1.51, p < 0.01), whereas tinea corporis (RR = 0.24, p < 0.01) and candidosis cutis (RR = 0.30, p < 0.001) was found decreased compared to controls. Our results show that the influence of fungal infections on the two skin diseases investigated is not as strong as often considered. The increased relative risk in patients with atopic dermatitis to present with Candida colonization in the digestive tract or vice versa may contribute to the pathogenesis of atopic dermatitis.

1: Mycoses. 2001 May;44(3-4):77-81.Links

Incidence of Candida in psoriasis--a study on the fungal flora of psoriatic patients.
Waldman A, Gilhar A, Duek L, Berdicevsky I.
Department of Microbiology, Rappaport Institute, Faculty of Medicine, Technion, Institute of Technology, Haifa, Israel.

The presence of Candida albicans and other Candida species in saliva and faeces of 50 psoriatic patients compared with a control group of 50 healthy donors was examined quantitatively. The quantity of Candida in saliva and faeces of the psoriatics proved to be significantly higher than in the controls. Candida was detected in 78% of the saliva samples of the psoriatics but in only 50% of the controls, and in the faeces samples in 72% of the psoriatics, but in only 46% of the controls. Qualitative analysis revealed a predominance of Candida albicans (saliva, 77%; faeces, 64%) and Candida rugosa (saliva, 28%; faeces, 28%). We did not find a correlation between the severity of the psoriasis according to the Psoriasis Area and Severity Index and the amount of Candida in the saliva or in the faeces. Our results reinforce the hypothesis that C. albicans is one of the triggers to both exacerbation and persistence of psoriasis. We propose that in psoriatics with a significant quantity of Candida in faeces, an antifungal treatment should be considered as an adjuvant treatment of psoriasis.

HERES A DOCTOR WHO CLAIMS NYSTATIN IS THE ANSWER ALONE TO PSORIASIS!

Eczema, psoriasis, Chronic Rashes, and their relationship to Candida albicans

This page is based on Dr. Bruce Semon's clinical experience and research. This page discusses how yeast can affect skin conditions, including psoriasis, eczema, and rashes. For detailed explanations, including an more case studies, and how you can treat these skin conditions--we recommend that you read An Extraordinary Power to Heal.

Dr. Semon is available to see patients and for consultation. For more information about his medical practice, call 1-877-332-7899, or click here.


The following is a description of a woman with severe generalized itching whose symptoms were treated by safe effective therapy of a change of food choices described in our books An Extraordinary Power to Heal and Feast Without Yeast:4 Stages to Better Health and the non-absorbed anti-yeast medicine nystatin. I explain how to take nystatin in An Extraordinary Power to Heal. After the case, a brief explanation of why this treatment works is presented. I explain how yeast causes skin problems and how you can treat it thoroughly in An Extraordinary Power to Heal.


A case of severe generalized itching treated with anti-yeast therapy

Joan, 54, came to me and told me she had generalized itchiness on her neck, arms and chest. This itchiness went back to her childhood and had worsened four years previously. She had had eczema as a child. At the time of the visit she also had itchy eyes and eyelids. She had scaling of her scalp at the back, and inflammation of the skin of her elbows, upper chest and at the waistline of her back. She had seborrhea (fatty secretions on the skin). She was using a tar shampoo to control scaling. She had low energy, but this had improved some. She had been tried on homeopathy for one year but nothing had helped the itchy skin. Four years previously she had received a small amount of nystatin and some itching on her back had cleared. In addition she had hay fever and fibrous breasts. She was having hot flashes. She had used oral contraceptive pills in her late thirties and she had used antibiotics throughout her life. She was not taking any medications.


Joan started nystatin and the anti-yeast diet.


She came back three weeks later and said that she was taking 1/2 tsp. of nystatin three times a day. She complained of itching at the hairline of her neck and face. Her eyes were better. Her hot flashes had disappeared. She stated that her energy level was much improved. However, her scalp was still flaking. I observed that the inflammation of the skin of her elbows was nearly resolved and her eyes were not swollen.


She came back three weeks later and noted that her energy was still good. The itching on her body was better, but her neck and face were still bothersome. The scalp was less itchy. She could have sex more easily. Energy was still good. Her face appeared clear to me.

She came back three weeks later and reported that she was feeling much better. She still had a little itchiness in the morning, but it was mild. She stated that she felt 95% better overall. She noted that her itchiness would recur if she ate the wrong foods. Her hot flashes had come back, but they were not as often or as intense. In a later appointment she stated that the hot flashes would reoccur when the itchiness recurred.

I followed this patient for another five years. Joan found that her symptoms of itchiness would come back if she ate the wrong foods, such as vinegar or malt. The problem would disappear if she went back on the diet and continued to take nystatin. Otherwise she was free of her itching.
!

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** Originally posted by abuabdallah **

Explanation

Eczema, psoriasis and chronic rashes plague many people. They can be treated successfully with anti-yeast treatment including dietary change and using the anti-yeast medication nystatin.

The diet for Candida problems consists of removing fermented foods from the diet. The worst offenders are alcoholic beverages and non-alcoholic beer, vinegar, barley malt, chocolate, pickles, and aged cheese. I explain the diet very thoroughly, including how to implement the diet for children, in An Extraordinary Power to Heal and Feast Without Yeast:4 Stages to Better Health. Feast Without Yeast has more than 225 recipes that are easy to make and taste great! Our new cookbook, Extraordinary Foods for the Everyday Kitchen contains more than 125 additional new, original recipes and more than 60 menus to help you plan meals.

To understand how the yeast Candida albicans causes skin problems such as eczema and psoriasis, first a brief overview of the body's immune system and its interaction with Candida will be presented.

The best way to look at the immune system is to understand that the immune system has both defensive and offensive weapons. The main defensive weapon is inflammation. Inflammation is like putting up a wall, a hot wall, which makes it difficult for invading foreign microorganisms to get through. Inflammation will occur anytime the immune system contacts a foreign invader. But as you know the inflammation is painful. Along with the inflammation, should come the offensive weapons which kill the foreign invader. The problem is that Candida has many tricks to evade the offensive weapons of the body's immune system.

Candida is a very difficult organism for the body's immune system to clear.

Why?

Candida has a number of tricks to evade the body's immune system. One of these tricks is to change its outside. The immune system recognizes the outside receptors of the invading organism and then sends out signals to start an immune response. Some of the immune responders then look for cells with those receptors. Candida albicans can change the receptors which it is displaying, making it difficult for the body's immune cells to react appropriately. In essence, Candida albicans is a moving target, which changes its form.

The most important thing to know about Candida is that Candida albicans can make factors which suppress the immune response to itself. These factors can be found in the circulation of people with significant Candida infections. When these factors are purified and placed in cultures of immune cells, these immune cells do not develop the responses to Candida which they are supposed to develop. In other words, Candida can make factors, which prevent the body from reacting to and killing the Candida. These factors prevent the total eradication of Candida from the body.

The Candida can suppress the offensive weapons of the body's immune system. But the inflammation will still be generated because when the immune system detects a foreign invader, there will always be inflammation. The problem is that the foreign invader, the Candida, is not going away, because the immune system's offensive weapons are suppressed. The inflammation will remain and inflammation is painful and on the skin is not attractive.

Let us look at some research on Candida and skin.


Candida and disorders of the skin

Out of all the Candida related disorders, research on psoriasis has come the closest to showing that Candida causes psoriasis. Researchers have actually shown that Candida causes all the changes in the skin characteristic of psoriasis (1). When Candida is injected into the skin of an experimental animal, the skin lesions of psoriasis, including scaling and thickening, develop. The authors of this study suggest that the scaling is a defense against the Candida (1). For some complicated reasons of experimental design, the authors stop short of saying Candida is the cause of psoriasis.

Is Candida found on normal skin? Candida may be found on normal skin, especially in skin folds (1A). Candida is much more likely to be found on skin after antibiotic use, after steroid use or in people with skin disorders (1B).

You might legitimately ask why researchers could have this major finding that Candida can cause psoriasis and yet ignore this result and subject psoriasis sufferers to coal tar, steroids and methotrexate. I actually do not know for sure why researchers would not wish to follow up their finding. One reason I would imagine is that the relationship between the Candida on the skin and the Candida in the gut is not generally appreciated. Cells which are fighting Candida in the gut can circulate and start fighting yeast whereever these cells find yeast. One place these cells might find yeast is on the skin. If one takes a narrow view and only looks at skin, one will miss this relationship. The other main problem is that researchers do not know how to clear the Candida from the gut for any length of time, so even if they did appreciate the relationship between the Candida in the gut and the Candida on the skin, they would not know how to clear the gut of yeast. Unfortunately as long as there are immune cells fighting yeast in the gut, there will be immune cells looking for yeast on the skin.

When the immune cells come into contact with Candida on the skin, the same observations of the immune system being unable to clear Candida completely all apply. The Candida suppresses the immune system's offensive weapons on the skin as it does elsewhere in the body, so inflammation can be prolonged on the skin as it is elsewhere. If the inflammation occurs in the hair follicles, acne can result. If the inflammation is spread more generally, we can see eczema. When the inflammation becomes even worse, we see psoriasis. Psoriasis is the body's immune system fighting Candida on the skin and the immune system is unable to win so the inflammation, a defensive weapon persists.

Itching is a painful sensation that something must be removed from the skin and if there is no other way, one scratches. Your body would love to remove the Candida. Candida is one of the main causes of persistent itching.

Treatment

The way to reverse these skin problems is to clear the yeast from the intestinal tract. Then the yeast is no longer a target for the body's immune system. Once the immune system's cells are no longer fighting yeast in the intestinal tract, they no longer circulate to find yeast on the skin. Once the yeast is gone from the intestinal tract, the yeast induced inflammations on the skin clear up.

The way to clear intestinal yeast is to change food choices to exclude foods which help intestinal yeast grow. The diet contains many foods which help yeast. To treat yeast these foods must be removed from the diet. For example, malt contains growth factors for yeast. Vinegar contains chemicals which kill bacteria and at the same time, leave the yeast alone. These dietary choices are described in our cookbook Feast Without Yeast. Changing food choices in this way helps skin conditions.

The second step is to take the anti-yeast drug nystatin. This drug is not absorbed and kills the yeast living in the intestinal tract. Nystatin does not work well without changing the diet to exclude foods which help yeast. Yeast chemicals can kill bacteria and will clear space for the yeast to grow again. If these yeast chemicals are left in the diet, nystatin will not do much good because the yeast keeps growing back. Once the proper food choices are in place, nystatin can kill the yeast and people feel better.

Fortunately, because nystatin is not absorbed, nystatin causes no side effects except for a little nausea. No harmful side effects have ever been caused by the use of nystatin. Therefore there is no risk to this therapy.

I have found in clinical practice that symptoms of major skin problems are reduced within one to two weeks of starting diet and nystatin and by six weeks of diet and nystatin therapy there are significant reductions in inflammation from chronic eczema and psoriasis.


Footnotes:


(1) Sohnle, P. G. and C. H. Kirkpatrick. Epidermal Proliferation in the defense against experimental cutaneous candidiasis. The Journal of Investigative Dermatology. 70:13033, 1978.

(1A) Candida may be found on normal skin, especially in skin folds.

Schaller, M., Schackert, C., Korting, H. C., Januschke, E., and B. Hube. Invasion of Candida albicans correlates with expression of secreted aspartic proteinases during experimental infection of human epidermis. Journal of Investigative Dermatology. 114(4):712-7, 2000.

(1B) Candida albicans may be found on the skin in cases of dermatomycoses and this finding is more likely if antibiotics or steroids have been used or diabetes is present.

Abu-Elteen, K. H. Incidence and distribution of Candida species isolated from human skin in Jordan. Mycoses, 42(4):311-7, 1999. An Extraordinary Power to Heal (2003) gives you detailed instructions, day by day and week by week, about how to eliminate toxic foods from your diets. We give you the recipes and menus to do this in Extraordinary Foods for the Everyday Kitchen (2003) and Feast Without Yeast(1999).


Yeas doctors are CURING people with NYSTATIN,

Dr. M. Heng is CURING people with curcumin, antifungals, and antibitocs!!!!!


I CANT LIVE LIKE THIS ANYMORE, id rather be dead

I just got back from another doctors appointmetn and didnt get any antifungals or antibiotics, I GOT REFFERED to a dermatologist,

SOOOO ill continue to GET WORSE, i have to wait 3 months for a dermatologist, STEROIDS HAVE MADE MY PSORIASIS WORSE!! IN FACT, i didtn have MAJOR psoriasis untill i started treating MINOR psoriasis with steroids.

I hate my ugly lizard body, my ugly crusted face, if im not helped i wont live like this anymore, its not fair....

I HAVE NOTHING TO LIVE FOR, I lost my job, my family is dead (mostly) my love left me, Im broke and cant afford treatments anyways,

If i were to ever decide ive had enough id leave note that blames psoriasis 100%,

Myabe that would create awareness?

So i have 6 months left.... hope is running low if microbial treatment of psoriasis isnt an option for me

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** Originally posted by DottieD **

Hi abuabdallah -
thanks so much for posting all this information. It's more than I can digest at one sitting, but certainly will stimulate some thought and study.

There has been some recent discussion on this board of whether gut bacteria endotoxins getting into the body might be involved in p, and some of this info seems to go along with that possibility.
DottieD

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** Originally posted by Fidge **

I tried Dr. Heng's treatment. The only problem is my doctor refuses to give me the oral keflex, not because he has a valid reason, he's one of those docs that just says "i don't believe in that." and that's it. So, i'm trying to find a doctor who is more open to ideas. Also, my doc has a tendency to try and push specific drugs on me, he's always giving me samples of dovonex and others.

I am however doing the topical treatments she gave me of clobet and ketoderm and i find that it has cleared me about 80% but it doesn't keep them away permanently.

As for the no drinking, that is difficult because I'm in my 20's and in social situations it is just a thing we do, but I am doing it sparingly and on weekends.

I'm seeing a new derm on Monday and hopefully can get into the PUVA treatment center, so maybe that will give me more perm. treatment.

What other oral medications would you suggest in lieu of keflex?

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** Originally posted by abuabdallah **

It seems for me (female 43) that at the onset of my psoriasis, usually in the months when the heat has to start coming on in New England, that my skin starts to ache and feel really dry. Also at the onset I get a terrible sore throat right out of the blue. Sometimes I can catch it before it gets really bad but sometimes I wake up and my throat is blocked and it feels like I swallowed a new copper penny back there. It is horrible. My only help for years has been penicilin. I take 250mg penicillin tablets twice a day, one in morning and one at night and it seems to heal it. Sometimes when it is bad it takes 4 pills. After that the pain and swollenness is GONE! But I have to tell you, my doctor can't understand it and neither can I but all I know is that it has helped me and saved me trip after trip after trip to try for a strep culture only to find a negative test. So, if this is of any help to anyone...great. The onset is generally only one or two small spots and put the Dex..????cream on them and they go away or diminish in a week or so, but the sore throats are unbearable.

Would you look at that......

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** Originally posted by grannyfranny **

I don't know why derms are so resistant to trying antibiotics,,,,money,,,,maybe?
I am in remission with Keflex and some dietary supplements.

Doxycycline is another antibiotic that has worked.

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** Originally posted by abuabdallah **

I don't know why derms are so resistant to trying antibiotics,,,,money,,,,maybe?
I am in remission with Keflex and some dietary supplements.

Doxycycline is another antibiotic that has worked.

Quick question, i was meaning you ask, my other strep related thread has your AMAZING MIRACULOUS RECOVERY pics, I was meaning to ask you...

How did you go about receiveing Keflex in the first place?

Did you discover it worked by accident while treating a different issue?

Did you have skin cultures done?

If not, Any kind of tests to confirm/deny colonization of staph/and or strep?

Even though there are studies that it works with or without strep present, hmmmm,

Well, i shared all of the info i know, so at least people know im not some off the wall weirdo whos saying crazy things for no reason,

But i think killing yeast, and bacteria is the way to go about getting a remission of significant cleanance and or improvement! :)

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** Originally posted by grannyfranny **

abuabdallah,
I had been taking Enbrel, MTX and Soriatane. I have the pustular psoriasis on hands and feet. Messing with my immune system was too much. I got a staph infection in my finger. I had to have emergency surgery and was put on Ancef by IV. Ancef is in the same family of drugs as Keflex. While in the hospital my hands cleared and my feet got much better. I had to come home and continue Ancef by IV for 6 weeks. By then my feet were much better. My doc switched me to Keflex for 6 weeks. By then my feet were so much better I went to my derm and he kept me on Keflex and I am still taking it. I have not had any problem staying on Keflex this long,it was 3 years in August.
I take 500mg 3xdaily.
I hope your doc will let you try this. It might take 3 months or more to see if it is going to help.

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** Originally posted by abuabdallah **

I tried Dr. Heng's treatment. The only problem is my doctor refuses to give me the oral keflex, not because he has a valid reason, he's one of those docs that just says "i don't believe in that." and that's it. So, i'm trying to find a doctor who is more open to ideas. Also, my doc has a tendency to try and push specific drugs on me, he's always giving me samples of dovonex and others.

I am however doing the topical treatments she gave me of clobet and ketoderm and i find that it has cleared me about 80% but it doesn't keep them away permanently.

As for the no drinking, that is difficult because I'm in my 20's and in social situations it is just a thing we do, but I am doing it sparingly and on weekends.

I'm seeing a new derm on Monday and hopefully can get into the PUVA treatment center, so maybe that will give me more perm. treatment.

What other oral medications would you suggest in lieu of keflex?

I AM EXACTLY IN THE SAME BOAT AS YOU 100%, MY DOCTOR HAS THE EXACT SAME ATTITUDE.......

Instead of keflex??? im not sure.....

ID DEFINETLY START BARNEYS foruma, vit d-ibuprohen, etc, there is a thread where you can see how well its worked,

it HAS ACTUALLY helped me, also commercial tanning beds are said to offer some relief, keep us posted~!!!!!

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** Originally posted by abuabdallah **

abuabdallah,
I had been taking Enbrel, MTX and Soriatane. I have the pustular psoriasis on hands and feet. Messing with my immune system was too much. I got a staph infection in my finger. I had to have emergency surgery and was put on Ancef by IV. Ancef is in the same family of drugs as Keflex. While in the hospital my hands cleared and my feet got much better. I had to come home and continue Ancef by IV for 6 weeks. By then my feet were much better. My doc switched me to Keflex for 6 weeks. By then my feet were so much better I went to my derm and he kept me on Keflex and I am still taking it. I have not had any problem staying on Keflex this long,it was 3 years in August.
I take 500mg 3xdaily.
I hope your doc will let you try this. It might take 3 months or more to see if it is going to help.

CONGRATS!! thats amazing! I pray he does let me do this, i need to find more research on the value of antibiotics in psortiasis with or without strep

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** Originally posted by MadCat **

Sorry I had to give up on your postings...........far too long.

Just a note about antibiotics - taking too many or taking too many over a long period of time can cause other potential detrimental health issues.

Anyway each to their own.

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** Originally posted by abuabdallah **

Sorry I had to give up on your postings...........far too long.

Just a note about antibiotics - taking too many or taking too many over a long period of time can cause other potential detrimental health issues.

Anyway each to their own.

Sorry for the long post, if you didnt read all of it no worries, its just evidence supporting the theory that psoriasis is driven by your immunes systems response to yeast/bacteria, there are studies and testimonial that suggest if this is true, psoriasis can be cured! :)

Since antimicrobial treatment of psoriasis compares favorlably to the results that may or may not be obtained through "conventional" methods, it may be a reasonable course of treatment given the alternatives.

I only say "reasonable" because as you mentioned TAKING TOO MUCH OF ANYTHING over a long period of time can cause other potential health issues,

Taking even alittle methodextrate, or at least 6 months worth may be more detremental to ones health than antibiotics for 3 YEARS!!

I have a friend who was on methodextrate for 1 year and his liver is now shot.

Like you said, each to thier own

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** Originally posted by grannyfranny **

I had 3 doctors tell me that taking Keflex long term was not a problem. If I ever need another antibiotic there are many others they can use. I have been healthier since taking Keflex. I feel better than when I was in my 30-40's. I'm 69 now. And NO side affects.

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** Originally posted by subtlecheetah **

A concern with antibiotic use, especially long-term, is that it kills both disease-causing and beneficial bacteria.


Long-Term Antibiotic Use Affects 'Good' Gut Bacteria
Study finds up to 30% of beneficial species, strains are significantly affected

HealthDay

By Robert Preidt

Wednesday, November 19, 2008

HealthDay news imageWEDNESDAY, Nov. 19 (HealthDay News) -- Antibiotic treatment, especially when prolonged or repeated, may have a negative impact on beneficial bacteria that live in the gut, according to a new study.

Gut bacteria play helpful roles in various aspects of human nutrition, metabolism and immune responses, experts note.

Researchers focused on the widely-used antibiotic ciprofloxacin, prescribed for a number of bacteria-caused conditions, including urinary tract infections. It has been believed that ciprofloxacin causes only modest harm to beneficial bacteria in the body.

In this study, Stanford University's Dr. David Relman and colleagues catalogued bacteria in the feces of volunteers being treated with ciprofloxacin and identified more than 5,600 different bacterial species and strains. However, while the patients were taking the antibiotic, the overall abundance of about 30 percent of the bacterial species and strains was significantly affected, the researchers found.

The effects of the antibiotic on gut bacteria varied greatly between individuals, with two volunteers showing a strong reduction in bacteria diversity. The study also found that once antibiotic treatment was completed, it took up to four weeks for most strains of gut bacteria to return to pre-treatment levels.

None of the study participants reported signs of gut-related problems during fluctuation of their gut bacteria populations.

While the findings, published online this week in the journal PLoS Biology, reveal aspects of resiliency in gut bacteria, they also suggest that antibiotic treatment may have long-lasting effects on overall health that could go unnoticed, the researchers concluded.

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** Originally posted by sharka **

Have you ever taken the candida questionaire?

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** Originally posted by abuabdallah **

Id say its a good thing to supplement ones diet with probiotics to replace good gut bacteria,

Ive seen and heard many more studies suggesting long term use is ok, id go as far as saying that eating a chocolate bar everyday would cause the same effect to someones gut bacteria, lol,

questions u must ask yourself, who FUNDED THIS STUDY?

How many people participated in this study!?

Also, antibiotics (-) effect on gut bacteria varied greatly among volunteers,

ALSO, only 2 had a (-) effect suggesting this study was too small to make any conclusive conlclusion!

Have you ever taken the candida questionaire?

Hey sharka, ive taken the candida test, im off the charts, im full of candida, and my spit is like pancake syrup, have u?

CANDIDA and yeasts, and bacterias are not good! Research shows evidence they play a mahor role in psoriasis, the proofs in the pudding!

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** Originally posted by grannyfranny **

I did EVERYTHING for 42 years. This is the only thing that has ever helped me. I do take a probiotic. My doc monitors me,,,,,she does blood work every 3 months and checks with me to to see if anything is wrong. I feel better about this med than I did with Enbrel, MTX and Soriatane, Prednisone or any other steroid. Those are the ones that put me in the hospital.

I did not make this decision lightly. It was sit in a wheelchair and do nothing or take this med and be able to run and play with my grandchildren and do other things. I have had them here for the last 2 summers and go take care of them when they have days off from school. We just came home from Thanksgiving and will leave on the 16th for Christmas.

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