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HYPOPHYSEO‐ADRENOCORTICAL FUNCTION IN DIABETES MELLITUS
Author(s) -
Asfeldt V. H.
Publication year - 1972
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1972.tb00063.x
Subject(s) - medicine , endocrinology , diabetes mellitus , blood sugar , insulin , basal (medicine) , dexamethasone , circadian rhythm , ketonuria , fasting blood sugar
Earlier experiments have given conflicting information on the hypophyseo‐adrenal function in diabetic patients. Normal suppression of plasma corticosteroids with 1 mg of dexamethasone (1 mg‐DST) in stable, noninsulin‐treated diabetics has previously been reported. However, only a partial response was found during 1 mg‐DST in approximately one‐third of the juvenile, insulin‐treated diabetics, indicating a slight hypercorticism in these patients. The cause of this was presumed to be repeated small stress‐stimuli as a consequence of fluctuation in the blood sugar. The present study attempts to elucidate this supposition. In contrast to earlier investigation a normal circadian rhythm and normal baseline values of plasma corticosteroids were found in 19 insulin‐treated diabetics during “basal” conditions, but this does not exclude the presence of a slight hypercorticism in some of the patients. Plasma corticosteroids and blood sugar were determined during 96 “subjective” hypoglycaemic attacks in 73 insulin‐treated diabetics. Elevated valuse of plasma corticosteroids were found both in cases of normal and low values of blood sugar. In six insulin‐treated diabetics with hyperglycaemia and ketonuria (four without acidosis) elevated values of plasma corticosteroids were found. The results support the assumption that a fall in the blood sugar to low values and fluctuations in the blood sugar at normal or high levels can bring about increased hypophyseo‐adrenal activity, and that this might be the cause of a slight hypercorticism in some cases of juvenile, insulin‐treated diabetics. It is not known whether the presumed hypercorticism is a reversible condition or not.

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