Last update:
21-Sep-2006

OBJECTIVE At the acute phase of cerebrovascular accidents a rise in liver cholestatic enzymes and/or bilirubin are occasionally observed, usually ascribed to co-morbid conditions. This study investigated the frequency and possible etiology of this phenomenon.

METHOD Prospective evaluation for post-admission biochemical cholestasis of all patients hospitalized with acute stroke during a 21-month period.

RESULTS Of 169 consecutive patients, 18 (10.7%) developed increased levels of serum alkaline phosphatase (SAP) and γ-glutamyltranspeptidase (γ- GT). In 7 (4.1%; 4 males, 3 females; median age 70, range 57-82 years), no cause for cholestasis could be found, and they were further evaluated (group A). They were compared to 21 of the remaining patients without cholestasis, matched for age and sex (group B). Group A patients were in deeper coma than control cases (Glasgow Coma Scale 3.4±0.8 vs 1.9±0.7, P<0.001), associated with severe autonomic and hypothalamic involvement, while no such manifestations were present in group B (P<0.001). In group A patients, γ-GT and SAP increased from the 3rd-6th day to the 11th-25th day of hospitalization, median levels reaching 4.38 (range 2.33-8.25) and 1.49 (range 0.63-2.56) times the upper limit of normal, respectively. Serum ALT, total and direct bilirubin also increased in group A but not in group B. The common bile duct was significantly wider in group A than in group B (mean 7.7±0.5 vs 4.7±0.6 mm, P<0.001), without apparent obstruction.

CONCLUSIONS Transient cholestasis may occur in 4.1% of patients following acute stroke. It is associated with deeper coma, autonomic and hypothalamic involvement and common bile duct dilatation without obstruction. Its exact nature is still not understood, but it may be due to inordinate hypertony of the sphincter of Oddi.

Key words: Catecholamines, Cerebrovascular accident, Cholestasis.