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clinmed/2002080004v1 (August 22, 2002)
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Remission in Sarcoidosis

Trevor G. Marshall, and Frances E. Marshall

The granulomatous inflammation of Sarcoidosis is triggered by one or more microbes behaving in a non-infectious fashion in a genetically predisposed individual. Once started, the inflammation is fed and nurtured by the secosteroid hormone 1,25-dihydroxyvitamin D. Lipopolysaccharide from gram-negative bacteria living in the inflamed tissues causes macrophages to extra-renally convert 25-hydroxyvitamin D into 1,25-dihydroxyvitamin D. Once this hormone builds to a concentration sufficient to catalyze the formation of granuloma, its production is also fueled by the Gamma Interferon produced within those granuloma. The inflammatory cycle can be interdicted by removing 25-hydroxyvitamin D, thus removing the fuel for the extra-renal production of the secosteroid. This can be achieved by isolating the patient from sunlight and removing all sources of Vitamin D from the diet. Minocin can reduce the bacterial activity. Remission is observed as a gradual decrease in the amount of extra-renal 1,25-dihydroxyvitamin D being produced within the granulomatous biochemistry. A clinician can follow this process by tracking the D-Ratio, serum 1,25-dihydroxyvitamin D to serum 25-hydroxyvitamin D. Although the D-Ratio will often reach 4.5 in active sarcoidosis, 1.25 is the normal mean. When this D-Ratio has fallen to within the normal range we have an indication that the secosteroid is again being regulated within the kidneys and that remission has been achieved.

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Remission in Sarcoidosis
Jan Lewis
ClinMed NetPrints, 1 Apr 2003 [Full text]
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