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I never thought about daily use of doxy and discussed with gp only the 3 days scheme. Can you tell me how is correct to start and to continue and is it okay to stay on the 3 days scheme?
The following is Dr. Brown’s way to start AP for RA (though if prescribed as a DMARD by a rheumatologist, it’s usually 100mg twice daily). If patients do well on just 100mg M-W-F without unbearable Herxing, the dose can be gradually increased to twice daily on the same days and, later to daily, if progress is slow. If initial herxing is rough-going, RAers tend to be better off staying on the low pulsed dose until herxing is passed and labs stabilize and start to improve.
See FAQ #15 copied below:
15. What is the difference between the Harvard Protocol and intermittent pulse dosing?
When the Minocycline in Rheumatoid Arthritis (MIRA) trials were run in the early 1990s, the dosing schedule used (100mg minocycline, administered twice daily) became known as the “Harvard Protocol.” It was dubbed this because one of the lead authors, Dr. David Trentham, was based at Beth Israel Deaconess Medical Center, a Harvard Medical School teaching hospital.
Dr. Brown mostly used low-dose, pulsed, intermittent antibiotic therapy and his protocols are still valid and used as models for treatment today by experienced AP doctors. Sometimes the intermittent pulsing method would be used with just one class of antibiotic, such as the tetracyclines, on just three days a week (e.g., M-W-F). On these days, minocycline or doxycycline would be administered once daily (e.g., 50mg or 100mg) and tetracycline would be pulsed twice daily (e.g., 250mg BID). At times, other complementary antibiotics (to increase the spectrum of activity) would be added on an alternate day, although Dr. Brown also used IV clindamycin in a five-day series at various intervals on a case-by-case basis. Pulsed dosing was recommended as a means of allowing the patient’s inflamed tissues time to recover between doses in order to limit the effects of a herx reaction and to prevent excessive oxidative tissue damage.
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