Nephrogenic diabetes insipidus in a lethargic lithium-treated patient

We report on a patient who developed severe lithium-induced nephrogenic diabetes insipidus (NDI) and neurotoxicity, despite recommended serum lithium levels. Hydrochlorothiazide and indomethacin appeared effective antipolyuric drugs, which led to a normalization of serum osmolality. After re-initiating lithium therapy, with lithium levels around 0.3 mmol/l, recurrence of NDI or neurotoxicity was not observed, despite discontinuation of indomethacin and hydrochlorothiazide. Together with hypothyroidism, NDI and neurotoxicity must be considered in lethargic lithium-treated patients

Plasma adiponectin is modestly decreased during 24-hour insulin infusion but not after inhibition of lipolysis by Acipimox

Objective. Plasma adiponectin is associated with insulin resistance and atherosclerosis. Adiponectin expression in adipose tissue is up-regulated by peroxisome proliferator-activated receptor (PPAR)-gamma agonist treatment and its plasma level may be affected by insulin. We tested the hypothesis that prolonged exogenous insulin infusion decreases plasma adiponectin, and examined whether a possible effect of insulin on plasma adiponectin is attributable to inhibition of lipolysis. Material and methods. The effect of insulin infusion on plasma adiponectin ( Linco enzyme-linked immunosorbent assay) was evaluated during a 24-h moderately hyperinsulinemic clamp (8.3 mu U kg(-1) s(-1)) in 8 male type 2 diabetic patients and in 8 healthy men. On a separate day, acipimox ( 250 mg/4 h for 24 h) was administered to inhibit lipolysis. Insulin and acipimox were administered in random order with 1 week between study days. Results. In type 2 diabetic patients, insulin infusion decreased plasma adiponectin from 7.74 +/- 2.53 mg/ l to 6.76 +/- 2.41 mg/ l after 24 h (

Acquired APC resistance in neurosurgical patients may not be a risk factor for postoperative deep vein thrombosis

Acquired resistance to activated protein C has been reported during oral contraception and pregnancy. Its thrombogenic potential was studied in 41 neurosurgical patients who were enrolled in the placebo group of a thromboprophylaxis trial, Normalized activated protein C sensitivity ratio (nAPC-SR), clotting activity of factors V and VIII, and levels of protein C antigen were measured prior to and at days 3 and 7 after surgery. Bilateral venography was done in all patients at days 8-10 to demonstrate deep vein thrombosis. A lowered nAPC-SR was found in 76% (baseline), 80% (day 3), and 88% (day 7) of patients. It was inversely related to factor VIII clotting activity (p = .0003) and protein C antigen, (p = .02). Deep vein thrombosis was demonstrated in 30% of patients with a normal nAPC-SR and in 23% of patients with a lowered nAPC-SR. Pulmonary embolism was not observed. Multivariate analysis did not identify a lowered nAPC-SR as a thrombotic risk factor, in contrast with gender (women, p = .02) and Quetelet index (greater than or equal to 25 kg/m(2), p = .006). Our data provide no evidence that acquired activated protein C resistance, frequently found in neurosurgical patients, contributes to their high risk of postoperative deep vein thrombosis