1961
DOI: 10.1210/jcem-21-2-209
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Antithyroid Antibody in Juvenile Diabetics*

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1964
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Cited by 34 publications
(5 citation statements)
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“…The prevalence of antithyroid antibodies in diabetic patients has been variously reported as ranging from 8% to 22% (Pettit, Landing and Gest, 1961;Landing et al, 1963;Whittingham et al, 1971;Goldstein, Drash and Blizzard, 1970;MacCuish and Irvine, 1975. The demonstration of islet-cell antibodies in diabetics (Bottazzo, Florin-Christensen and Doniach, 1974) has led to the concept of distinct types of diabetes mellitus based on the presence or absence of autoimmune markers (MacCuish and Irvine, 1975).…”
Section: Discussionmentioning
confidence: 99%
“…The prevalence of antithyroid antibodies in diabetic patients has been variously reported as ranging from 8% to 22% (Pettit, Landing and Gest, 1961;Landing et al, 1963;Whittingham et al, 1971;Goldstein, Drash and Blizzard, 1970;MacCuish and Irvine, 1975. The demonstration of islet-cell antibodies in diabetics (Bottazzo, Florin-Christensen and Doniach, 1974) has led to the concept of distinct types of diabetes mellitus based on the presence or absence of autoimmune markers (MacCuish and Irvine, 1975).…”
Section: Discussionmentioning
confidence: 99%
“…There have been no previous reports on the association of vitiligo witli diabetes mellitus but in this survey we found a statistically significant association between these conditions. It is of interest that Unger et al, (1967) reported an increased incidence of gastric intrinsic factor antibody in diabetes mellitus and an increased incidence of thjroglobulin antibodies has also been described in juvenile diabetics (Petit et al, 1961). Carpenter (1964) has shown that diabetes mellitus is much more common in the idiopathic than in the tuberculous form of Addison's disease.…”
Section: Discussionmentioning
confidence: 99%
“…Various investigators have asserted that the prolonged administration of anterior pituitary extracts, purified growth hormone preparations, adrenocortical hormones, thyroid hormones, or glucose in quantities sufficient to maintain elevated blood glucose levels throughout most of the day, can induce a diabetic state by exhausting the insulin‐secreting cells (72). Hypoglycemia is probably the most potent stimulus to the secretion of human growth hormone (73)—a relationship which also suggests that a vicious cycle between excessive elaboration of both insulin and growth hormone may occur in diabetogenic hyperinsulinism. There is both direct and indirect evidence (e.g., inhibition of cortisone‐induced deposition of liver glycogen in starved rats by administration of puromycin and actinomycin) that cortisone exerts a regulatory effect on carbohydrate metabolism by its action on the cellular concentration of certain enzyme proteins which influence the rate of glycogen deposition in the liver, gluconeogenesis, and homeostasis of glucose concentration (74).…”
Section: Discussionmentioning
confidence: 99%