Glucose intolerance in patients with chronic inflammatory diseases is normalized by glucocorticoids.
Nine of 16 patients with inflammatory connective tissue diseases (rheumatoid arthritis, polymyalgia rheumatica, scleroderma and mixed connective tissue disease) had glucose intolerance defined a a K-rate less than one but a normal early insulin response to intravenous glucose loading. The degree of the impaired glucose handling was related to the degree of inflammatory activity as defined by acute phase reactants. Glucocorticoid therapy induced within three days an improved and normalized glucose tolerance and an augmented early insulin response (p less than 0.001). The glucocorticoid effect was still present up to six months of ongoing therapy. It is suggested that glucose intolerance in chronic inflammation is a consequence of a peripheral insulin antagonism and an inhibition of insulin secretion. This inhibition may be mediated directly or indirectly by inflammatory cell products and may be sensitive to glucocorticoids.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D003240:Connective Tissue Diseases / Q000097:blood* / Q000188:drug therapy; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D008297:Male; D008875:Middle Aged; D011111:Polymyalgia Rheumatica / Q000097:blood; D011239:Prednisolone / Q000627:therapeutic use*; D012595:Scleroderma, Systemic / Q000097:blood
D001786:Blood Glucose; D011239:Prednisolone