October 18, 2018 at 1:56 pm #463102MazKeymaster
For the most part, scleroderma patients have favorable responses to long-term minocycline therapy. In general, minocycline alone can work to slow and halt progression in the first year of therapy, after which incremental reversals in disease symptoms commonly occur. In some instances, however, response to minocycline doesn’t occur in this first year, is slow or just not happening.
SD patients become disheartened and wonder why they just aren’t gaining any traction and, in these cases, if all the usual suspects are eliminated (e.g., dud generic brands), it is likely worth running some infection testing. It is possible that a different antibiotic protocol is indicated and this can depend on the type of infection the person is dealing with. A good example of this type of scenario is outlined in the following 2017 Danish case study of a woman in her 40s with swiftly-progressive, seropositive scleroderma who was put on a long-term (12-month) course of combination antibiotics, rifampin and clarithromycin, to treat an infection with a cell-walled microbe, called Mycobacterium intracellulare:
Mycobacterium intracellulare Infection Mimicking Progression of Scleroderma. Case Reports in Rheumatology, Volume 2017, Article ID 4029271, 3 pages.
Danish case report of a woman in her 40s with seropositive scleroderma (SD), exhibiting a positive ANA with nuclear speckled pattern, rheumatoid factor, and high titer anti-SSA antibodies. In addition, she had clearly identifiable disease features, including sclerodactyly, Raynaud’s phenomenon, abnormal nail fold capillary test, interstitial lung disease, esophageal dysmotility, and severe inflammatory skin and muscle fasciae changes. Failing several immunosuppressive treatments, it was found that her progressively worsening symptoms were being caused by the infection Mycobacterium intracellulare (M. intracellulare) in spite of normal immunoglobulin levels. This infection was discovered after she had received high-dose prednisolone that led to hospitalization for Listeria monocytogenes meningitis. After successful recovery from the meningitis, she was then administered a 12-month course of clarithromycin and rifampin combination oral antibiotic therapy for the M. intracellulare infection. This combination antibiotic protocol resulted in substantially significant improvements in her skin, arthritis, and fatigue, and her leg wounds also healed. These authors conclude that M. intracellulare was the cause of a severely-progressive case of SD and that this infection should be considered as a differential cause of disease in cases that are unresponsive to immunosuppressive therapies.
This case is highly notable, because quite often we hear the following common myths with regard to SD and AP:
1. “AP only works for seronegative SD.” As demonstrated in the above case, this seropositive SD patient exhibited all the clinical signs (including seropositivity) and symptoms of swiftly-progressive SD.
2. Or, “Minocycline is the only antibiotic that works for SD.” This clearly isn’t the case, as has been shared by numerous patients here (albeit these are considered anecdotal, unpublished, patient-reports) of SD patients being treated with different classes of antibiotics that have antimicrobial actions that are very different from tetracyclines. For e.g., in cases of tickborne disease-induced SD.
3. Or, “Minocycline only works for SD as a DMARD.” Again, not necessarily entirely true. If that was the case in all instances, then why would other classes of antibiotics also work for some cases of SD? E.g., penicillin for linear SD or Ciprofloxacin for lung and skin fibrosis?
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