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We report a case of spontaneous Yersinia enterocolitica peritonitis revealing idiopathic hemochromatosis in a 62-yr-old man with fever and diarrhea. Blood and stool cultures were repeatedly negative, but Yersinia enterocolitica serotype 9 was isolated from ascitic fluid and serum agglutinins against this organism were positive at a dilution of 1:2560. Moreover, a serum Brucella agglutination test was positive at a dilution of 1:320. Antibiotic therapy with doxycycline led to a rapid clinical improvement, with disappearance of the organism in the ascitic fluid. This case suggests that Yersinia enterocolitica infection must be suspected in any febrile abdominal syndrome occurring in patients with iron overload, such as thalassemia major or idiopathic hemochromatosis.

We report on the observation of a 26-year-old woman with portal vein obstruction, diagnosed at the age of 3, and liver iron overload. Celiac and superior mesenteric angiography showed large and multiple venous collaterals between the portal and caval systems. Liver biopsy demonstrated, on Perl's staining, an important hemosiderin deposition, confirmed by an increased hepatic iron concentration (15.6 mumol/100 mg dry weight). No other histologic abnormality was found. This report suggests that large spontaneous portosystemic shunting may stimulate hepatic iron deposition in an otherwise normal liver. This mechanism could, at least in part, explain the significant hepatic siderosis observed in some cirrhotic patients.

The authors describe a slight but significant increase in the serum levels of indirect-reacting bilirubin in gallstone patients after 3 and 6 mo of treatment with chenodeoxycholic acid. A return to pretreatment values was noted at 9 mo. The mechanism of this abnormality remains unclear. Two explanations are theoretically possible: a subclinical hemolysis or a modification of the hepatic transport and/or the conjugation of bilirubin.

• We encountered a case of primary biliary cirrhosis in a nonalcoholic man who had been operated on for idiopathic retroperitoneal fibrosis 20 years previously. Chronic pancreatitis was also detected on endoscopic retrograde examination. After several episodes of digestive bleeding due to ruptured esophageal varixes, the patient died of massive hemorrhage. Postmortem examination showed stage 3 primary biliary cirrhosis and a thick retroperitoneal fibrous plaque, consisting of densely fibrotic areas of collagen with rare vessels and mononuclear cells. We suggest that idiopathic retroperitoneal fibrosis may be a new autoimmune disorder associated with primary biliary cirrhosis and that primary biliary cirrhosis is a potential cause of portal hypertension, cholestasis, or both in the course of idiopathic retroperitoneal fibrosis. (Arch Intern Med1985;145:2124-2125)