** 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 participants 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
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
Drug: Bicillin L-A
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
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!