Ongoing research includes a Internet-based, phase II clinical trial of a succesful antibiotic therapy for sarcoidosis (at SarcInfo.com). Currently the study is supporting a cohort of nearly 200 sarcoidosis patients. Two papers have already been published describing the preliminary results:
Marshall TG, Marshall FE: Antibiotics in Sarcoidosis - Reflections on the First Year.
JOIMR 2003;1(3):2 http://www.joimr.org/phorum/read.php?f=2&i=38&t=38
Mangin M: Observations of Jarisch-Herxheimer Reaction in Sarcoidosis Patients.
JOIMR 2004;2(1):1 http://www.joimr.org/phorum/read.php?f=2&i=51&t=51
Ours is a Phase II observational study. Many of the patients in this cohort are Health Care workers (Physicians, Nurses and ex-Nurses), and thus are not necessarily representative of the patient population as a whole. Therapy was prescribed and monitored by the patients’ personal physicians. Since the recruitment and ongoing support was provided over the Internet, all patients needed to have a level of education sufficient to operate Internet-capable Computers.
These factors are all capable of introducing bias into the study results. Further bias could be introduced by the lack of a standardized results questionnaire (it was adjudged impractical to produce a standardized questionnaire which could meaningfully evaluate a heterogeneous cohort of Cutaneous, Cardiac, Pulmonary and Neuro-sarcoidosis patients).
To compensate for these biases, extreme care was taken to document adverse events, especially adverse outcomes, and correspondence was publicly logged and reviewed by both investigators.
Despite these reservations, the remission induced by this Antibiotic/ARB protocol was dramatic, and it is unlikely that any of these methodological limitations were sufficient to have skewed the study’s conclusions.
Anyone spot why the avoidance of Vit D?The Marshall Protocol (MP)[1,2] uses specific combinations of antibiotics in a pulsed regimen along with an angiotensin receptor blockade and avoidance of Vitamin D.
These pathogens then stimulate Nuclear-Factor-kappaB in the cytoplasm to release mRNA from the nucleus. This triggers a Th1 cytokine cascade. Additionally, the production of ACE (angiotensin converting enzyme) is stimulated which converts inert angiotensin I to usable angiotensin II, for which these pathogens have receptor sites. This excess angiotensin II allows the pathogens produce excess 1,25 D. This excess affects proteins in the macrophage cell walls, allowing bacteria to more easily traverse the cell outer membrane
Resonates with some of the MS / multiple pathogen "conspiracy" theories
After reading about your experiences, I started on David's treatment about 3 months ago. I must say that it has been a confusing period and sometimes it is hard to say whether you are really improving or you think that you are improving just because you want it so much. That is the reason why I haven’t been posting in the regimen section yet.
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