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Objective. Liver cholestatic enzymes and/or bilirubin occasionally occur in acute stroke and are usually, but not always, ascribed to comorbid conditions. We investigated the frequency and possible etiology of this phenomenon. Material and methods. Prospective evaluation of post- admission biochemical cholestasis of all patients hospitalized with acute stroke was conducted during a 21- month period. Results. Of 169 consecutive patients, 18 (10.7% ) developed cholestasis. In 7 of the patients (4.1% ; 4 M, 3 F, median age 70 years, range 57- 82 years) no apparent cause of cholestasis could be found, and they were further evaluated (Group A). These patients were compared with 21 randomly selected stroke patients without cholestasis, matched for age and gender, and who acted as controls (Group B). Group A patients were in a deeper coma than the controls (Glasgow Coma Scale 3.4 ± 0.8 versus 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). Cholestasis started on the 3rd- 6th day and lasted up to the 11th- 25th day, with maximum median levels of γ - GT and serum alkaline phosphatase (SAP) of up to 4.38 (range 2.33- 8.25) and 1.49 (range 0.63- 2.56) times the upper limit of normal, respectively. Serum alanine aminotransferase (ALAT), total and direct bilirubin increased in Group A but not in Group B. The common bile duct was significantly wider in Group A than in Group B (7.7 ± 0.5 versus 4.7 ± 0.6 mm, p < 0.001) and within Group A during and after cholestasis (7.7 ± 0.5 versus 4.7 ± 0.5 mm, p < 0.001). Conclusions. Transient cholestasis may occur in 4.1% of patients following acute stroke. Cholestasis is associated with deeper coma, autonomic and hypothalamic involvement and common bile duct dilatation without obstruction, possibly related to inordinate hypertonia of the sphincter of Oddi.
Objectives. Liver cholestatic enzymes and / or bilirubin occasionally occur in acute stroke and are usually, but not always, ascribed to comorbid conditions. We investigated the frequency and possible etiology of this phenomenon. Material and methods. Prospective evaluation of post-admission biochemical cholestasis Of all patients hospitalized with acute stroke was conducted during a 21-month period. Of 169 consecutive patients, 18 (10.7%) developed cholestasis. In 7 of the patients (4.1%; 4 M, 3 F, median age 70 years , range 57-82 years) no apparent cause of cholestasis could be found, and they were further evaluated (Group A). These patients were compared with 21 randomly selected stroke patients without cholestasis, matched for age and gender, and who acted as controls (Group B). Group A patients were in a deeper coma than the controls (Glasgow Coma Scale 3.4 ± 0.8 versus 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). Cholestasis started on the 3rd - 6th day and lasted up to the 11th - 25th day with maximum median levels of γ - GT and serum alkaline phosphatase (SAP) of up to 4.38 ( range 2.33- 8.25) and 1.49 (range 0.63- 2.56) times the upper limit of normal, respectively. Serum alanine aminotransferase (ALAT), total and direct bilirubin increased in Group A but not in Group B. The common bile in Group A than in Group B (7.7 ± 0.5 versus 4.7 ± 0.6 mm, p <0.001) and within Group A during and after cholestasis (7.7 ± 0.5 versus 4.7 ± 0.5 mm, p <0.001). Conclusions. Transient cholestasis may occur in 4.1% of patients following acute stroke. Cholestasis is associated with deeper coma, autonomic and hypothalamic involvement and common bile duct dilatation without obstruction, possibly related to inordinate hypertonia of the sphincter of Oddi.