Adrian Reuben

Do bile acids reflux into the esophagus?: A study in normal subjects and patients with gastroesophageal reflux disease

To determine if bile acids reflux into the esophagus in patients with gastroesophageal reflux disease and in normal subjects during physiological gastroesophageal reflux episodes, esophageal aspiration and pH monitoring were performed simultaneously in 16 patients with gastroesophageal reflux disease and 8 normal subjects. Esophageal samples were collected for 30 min in the fasting state and for 3 h (as hourly samples) after the ingestion of a test meal (egg salad sandwich, peaches, and milk). Bile acids were assayed by a standard enzymatic assay and also by a sensitive and specific assay, liquid secondary ion mass spectrometry. Bile acids were not detected by enzymatic assay in any of the fasting samples. In 6 of the 8 normal subjects and 15 of the 16 patients with gastroesophageal reflux disease, bile acid-like reactivity was detected by the enzymatic assay in postprandial samples. However, bile acid-like reactivity was also found by enzymatic assay in aliquots of the homogenized test meal in concentration similar to the highest concentrations detected in esophageal aspirates. Bile acids were not detected by the liquid secondary ion mass spectrometry method in any of the fasting or postprandial esophageal aspirates (limit of detection greater than 2 microM). However, this assay accurately identified samples to which exogenous bile acids were added as controls. Our results suggest that bile acids did not reflux into the esophagus of patients with gastroesophageal reflux disease whom we studied and caution must be exercised in the use of enzymatic assay for bile acids in postprandial gastrointestinal fluids, as the commonly used hydroxysteroid dehydrogenase assay is not specific for bile acids alone.

Multiple focal nodular hyperplasia of the liver associated with hemihypertrophy and vascular malformations

A case of multiple focal nodular hyperplasia of the liver occurring in a 22-year-old woman with musculoskeletal hemihypertrophy and anomalous vascular supply to the liver is described. The patient had Klippel-Trénaunay-Weber syndrome and abdominal pain and tender massive hepatomegaly. Visceral angiography showed marked dilatation of the celiac axis and both the main trunk and peripheral branches of the hepatic artery. Large abdominal veins drained from the dome of the liver into the hepatic veins. The vascular anomalies were evident on contrast-enhanced computed tomography and magnetic resonance imaging. Multiple focal nodular hyperplasia was confirmed by laparoscopic liver biopsy. The findings in this patient support the concept that multiple focal nodular hyperplasia characteristically occurs in a syndromic form and is induced by an irregular arterial supply in the liver, with localized hyperfusion that leads to nodular areas of hepatocyte hyperproliferation.

Liver transplant rejection arteritis: Serial hepatic arteriography

Two liver transplant recipients underwent serial hepatic arteriography, demonstrating a severe, rapidly progressive arteritis involving the hilar hepatic arteries. Liver biopsies in these patients demonstrated ischemic necrosis as a prominent feature. The angiographic appearance and therapeutic implications of liver transplant rejection arteritis are presented.