Portal hypertension in systemic mastocytosis.

We report the case of a 66-year-old male patient with portal hypertension related to systemic mastocytosis. The liver was enlarged; microscopic examination showed portal mast cell infiltration and fibrosis. Portal hypertension was evidenced by splenomegaly, esophageal varices, and increased wedged-free hepatic venous pressure gradient.

Lack of parallelism between microsomal enzyme induction and phenobarbital-induced hypercholeresis in the rat.

The relationship between microsomal enzyme induction and the increase in bile flow associated with phenobarbital administration was studied in rats in three experimental situations: examination of the time-course effect of a single dose of phenobarbital (8 mg/100 g body weight) on bile flow and hepatic cytochrome P-450 concentration; study of the influence of SKF 525-A (8 mg/100 g body weight) and cobaltous chloride (6 mg/100 g body weight/day for 3 days) on the phenobarbital-induced hypercholeresis. It was observed that: (a) the maximal increase in bile flow occurred 18 h after the single injection of phenobarbital, while the maximal increase in cytochrome P-450 occurred at 48 h; (b) in rats pretreated with phenobarbital for 3 days, SKF 525-A did not suppress the hypercholeresis due to phenobarbital, and (c) in rats treated with phenobarbital and cobaltous chloride, cytochrome P-450 concentration in the liver was not increased, while bile flow was increased to approximately the same extent as in animals treated with phenobarbital alone. These results further support the hypothesis that microsomal cytochrome P-450-dependent enzyme induction and increase in bile flow are two separate effects of phenobarbital.

Hypogammaglobulinemia with lymphoid nodular hyperplasia of the small bowel: endoscopic diagnosis of one case.

A 37-year-old man suffering from abdominal pain and diarrhea, was hospitalized because of abdominal discomfort. Gastroduodenal series showed multiple duodenal filling defects. Gastroduodenoscopic examination revealed numerous nodular lesions in the duodenum and biopsy specimen demonstrated nodular lymphoid hyperplasia.

Massive splenic infarction in cirrhosis: report of a case with spontaneous disappearance of hypersplenism.

A cirrhotic patient with massive splenic infarction is described. Celiac angiography showed normally opacified splenic artery and vein and a markedly enlarged spleen with large avascular zones. Splenic infarction was associated with the spontaneous disappearance of a syndrome of hypersplenism.