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Biomedical subjects

E Ferrannini

Publications and source records attributed to E Ferrannini.

282 records · Page 16Linked to original sources
PubMedDate not supplied

Marrow aplasia following colchicine treatment for gouty arthritis.

A 69-year-old man was given 8 mg of colchicine intravenously to treat an acute attack of gout. A maintenance dose of 2 mg/day of oral colchicine was then used to prevent recurrence. Three months later, the patient developed thrombocytopenia, followed by leukopenia and then by anemia at three and four months distance, respectively. The patient had shown no signs of acute toxicity with intravenous colchicine, but liver enzymes were raised after two months of oral treatment. The sequential involvement of the three blood precursor lines, in the order to their physiological half-lives, suggests direct toxicity, rather than idiosyncrasy, due to slow accumulation of the drug within target cells. The prophylactic use of colchicine, especially in the elderly, is questioned.

Aged↗
PubMedDate not supplied

Insulin resistance: a universal finding in diabetic states.

The mechanisms contributing to the impairment in glucose metabolism in non-insulin-dependent diabetes mellitus, insulin-dependent diabetes mellitus, and diabetic ketoacidosis are summarized in Table 2. Impaired insulin secretion is characteristic of patients with IDD and DKA. In contrast, insulin secretion in NIDD may be normal, increased, or decreased. Peripheral tissue resistance to the action of insulin is present in all three diabetic conditions; it is moderate in NIDD and IDD and severe in DKA. Basal hepatic glucose production in NIDD and IDD can be either normal or increased, and correlates closely with the fasting plasma glucose concentration. In DKA, HGP is elevated. Suppression of HGP by insulin is normal in NIDD and IDD but severely impaired in DKA. Hepatic glucose uptake following oral glucose is decreased in NIDD; hepatic uptake of ingested glucose has not been examined in IDD and DKA.

Adult↗
PubMedDate not supplied

Renal effects of insulin in man.

We review some of the effects that insulin exerts on glomerular and tubular functions. In healthy subjects, insulin has little or no effect on renal hemodynamics, glomerular filtration rate, or permeability to albumin. In patients with noninsulin-dependent diabetes, hyperinsulinemia selectively increases urinary albumin excretion. In vivo, euglycemic hyperinsulinemia is associated with reduced urinary sodium excretion both under conditions of forced and normal diuresis. Whether the principal site of this action is the proximal or distal tubule remains somewhat controversial. The effect, however, is not mediated by insulin-induced hypokalemia and antikaliuresis, as it is still observed when plasma potassium concentrations and urinary potassium excretion are maintained. Hyperglycemia potentiates insulin antinatriuresis through an effect on the proximal tubule (sodium-glucose cotransport). Insulin antinatriuresis is accompanied by a reduction in the urinary excretion of uric acid. Both the antinatriuretic and antiuricosuric effect of insulin are preserved in states of insulin resistance of glucose metabolism (obesity, diabetes, essential hypertension). Thus, in insulin resistant individuals compensatory hyperinsulinemia imposes a chronic antinatriuretic and antiuricosuric pressure on the kidney. This may provide an explantation for the clustering of insulin resistance with hypertension and hyperuricemia.

Animals↗