Venlafaxine-induced cholestatic hepatitis: case report and review of literature.

Venlafaxine is a widely used antidepressant with relatively low occurrence of adverse side effects. Increasing evidence suggests that venlafaxine may cause severe liver damage. Until now, 10 cases of venlafaxine-related liver injuries have been reported. We describe a case of a 39-year-old woman who developed cholestatic hepatitis after intake of venlafaxine. The patient had taken low-dose venlafaxine (75 mg/d) for 2.5 years. Three months before admission to the hospital, the venlafaxine dosage had been increased to 300 mg/d because of severe depression. Laboratory findings revealed elevated serum transaminases (aspartate aminotransferase 1033 U/L; alanine aminotransferase 2063 U/L), alkaline phosphatase (274 U/L), γ-glutamyltransferase (284 U/L), and serum bilirubin (4.6 mg/dL). Liver biopsy showed cholestatic hepatitis predominantly involving zone 3 of hepatic acini and a mixed portal inflammatory infiltrate along with eosinophils. Symptoms rapidly resolved after cessation of venlafaxine and administration of corticosteroid. The present paper describes detailed clinicohistopathologic characteristics of venlafaxine-associated cholestatic hepatitis and provides a comprehensive summary of prior case reports.

Glucagon-like peptide 1 induces natriuresis in healthy subjects and in insulin-resistant obese men.

Glucagon-like peptide-1-(7-36)-amide (GLP-1) is involved in satiety control and glucose homeostasis. Animal studies suggest a physiological role for GLP-1 in water and salt homeostasis. This study's aim was to define the effects of GLP-1 on water and sodium excretion in both healthy and obese men. Fifteen healthy subjects and 16 obese men (mean body mass index, 36 kg/m2) were examined in a double-blind, placebo-controlled, crossover study to demonstrate the effects of a 3-h infusion of GLP-1 on urinary sodium excretion, urinary output, and the glomerular filtration rate after an i.v. 9.9-g salt load. Infusion of GLP-1 evoked a dose-dependent increase in urinary sodium excretion in healthy subjects (from 74 +/- 8 to 143 +/- 18 mmol/180 min, P = 0.0013). In obese men, there was a significant increase in urinary sodium excretion (from 59 to 96 mmol/180 min, P = 0.015), a decrease in urinary H+ secretion (from 1.1 to 0.3 pmol/180 min, P = 0.013), and a 6% decrease in the glomerular filtration rate (from 151 +/- 8 to 142 +/- 8 ml/min, P = 0.022). Intravenous infusions of GLP-1 enhance sodium excretion, reduce H+ secretion, and reduce glomerular hyperfiltration in obese men. These findings suggest an action at the proximal renal tubule and a potential renoprotective effect.