To compare the efficacy of endoscopic paravariceal sclerotherapy and oral propranolol in the prevention of recurrent upper gastrointestinal bleeding, 78 cirrhotic patients were randomly assigned to either treatment after an endoscopically proven bleed from esophageal varices. After randomization, but before treatment had been started, a total of eight patients had to be withdrawn from the study due to early rebleeding (requiring emergency sclerotherapy) or violations of the protocol. Among the 70 patients analyzed (36 sclerotherapy, 34 propranolol), both treatment groups were comparable with respect to demographic, clinical and laboratory data. The groups also did not differ with respect to continued alcohol intake. Sclerotherapy was performed twice weekly using 1% polidocanol as the sclerosing agent until the varices were eradicated or well-covered by fibrous tissue. Propranolol was given twice daily at a dose reducing the resting heart rate by 25% (60 to 320 mg per day; mean +/- SD = 161 +/- 80 mg per day). Patients were followed for up to 2 years with visits at 3 monthly intervals (mean follow-up = sclerotherapy, 14 months; propranolol, 9.2 months). Life table analysis of patients without rebleeding from nonvariceal sites revealed a tendency in favor of propranolol; however, the difference did not reach statistical significance. No significant difference was observed between sclerotherapy and propranolol in the proportion of patients rebleeding from esophageal varices or from all sources of upper gastrointestinal bleeding. Furthermore, survival was similar in both treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

Hepatocellular carcinoma in type I glycogen storage disease.

Patients suffering from Type I glycogen storage disease frequently develop hepatic tumors. Some of these were classified as carcinoma, with the majority of tumors representing benign adenomata. However, no evidence exists of malignant transformation of adenomata in these patients. Here, we describe the occurrence of a hepatocellular carcinoma in the adenomata-bearing liver of the elder of two sisters suffering from Type I glycogen storage disease at the age of 20 years, 6 years after the diagnosis had been made. Surprisingly, alpha-fetoprotein levels were normal throughout the entire course of this patient, whereas the younger sister had elevated levels despite the absence of malignant lesions. Thus, the clinical significance of alpha-fetoprotein remains unclear in both cases. Nocturnal feeding, although performed continuously over the 6 years after the diagnosis, had obviously failed to prevent the development of hepatic tumors in both patients.

Adult↗

PubMedDate not supplied

Feedback regulation of bile acid synthesis in the rat by dietary vs. intravenous cholate or taurocholate.

The regulation of bile acid synthesis was studied (i) in intact or colectomized rats receiving cholate or taurocholate as a dietary supplement and (ii) in experiments using chow-fed animals with a graded intravenous or intraduodenal taurocholate infusion. After the 2-week diet period a bile fistula was established and rates of taurocholate, tauromuricholate and taurochenodeoxycholate secretion were quantitated by high-performance liquid chromatography. During the infusion experiments taurocholate production was calculated from the difference in specific activity of [14C]taurocholate between infusate and bile, whereas tauromuricholate and taurochenodeoxycholate synthesis was derived directly from their secretion rates after pool depletion. Both the 0.5% cholate and taurocholate diet suppressed tauromuricholate and taurochenodeoxycholate secretion nearly totally, but only cholate led to a prolonged inhibition taurocholate synthesis. The diets stimulated total bile acid secretion and expanded the total bile acid pool size 2- to 3-fold, but they also prompted a dramatic increase in the biliary secretion of taurodeoxycholate. In contrast, colectomized animals did not secrete taurodeoxycholate following the cholate diet and, despite a comparable increase in bile acid pool size, tauromuricholate and taurochenodeoxycholate secretion was inhibited to a lesser extent. In addition, the rate of bile acid secretion and synthesis was significantly enhanced when compared to that of intact rats. To determine whether taurocholate affected bile acid synthesis directly, the bile acid was infused intravenously or intraduodenally at varying rates up to 300 mumoles per kg per hr for 54 hr, i.e. a rate exceeding normal total bile acid secretion in these acute bile fistula animals nearly 3-fold.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

[Hormonal regulation of lipogenesis. Hyperinsulinism in prediabetes and obesity].

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Adipose Tissue↗

PubMedDate not supplied

Potency of biosynthetic human insulin determined in vitro.

Biosynthetic human insulin (BHI) obtained from separately synthesized A- and B-chains by recombinant DNA technology with Escherichia coli fermentation was compared with human and pork insulin of high purity in vitro. Applying four biologic tests (glucose oxidation and glucose incorporation into the lipids by rat epididymal fat pads, inhibition of lipolysis, and ATP depletion of isolated fat cells) and three receptor assays (binding competition with human fat cells, IM-9 lymphocytes, and rat liver cell plasma membranes), we could not discern significant differences of the half-maximum response by these seven methods. The only variance occurred with the ATP-depletion assay. This method disclosed 10% greater maximum reversion of isoproterenol-induced ATP depletion by BHI when compared with pork insulin.

Adenosine Triphosphate↗

PubMedDate not supplied

Hyperlipidemia in acute pancreatitis. Relationship with etiology, onset, and severity of the disease.

Serum lipid (triglycerides and cholesterol) concentrations were studied in 49 patients with acute pancreatitis (AP). The aims of the study were to investigate the prevalence of hyperlipidemia (HL) in patients with AP according to etiology and to evaluate whether HL precedes or is a consequence of AP. Moreover, we analyzed the relationship between HL and the development of pancreatic necrosis. At admission, 23 patients (47%) had HL: 9 of 19 patients with alcoholic pancreatitis, 5 of 18 patients with biliary pancreatitis, and 9 of 12 patients with AP of miscellaneous etiologies (p less than 0.05). Severe HL (serum triglycerides greater than 20 mmol/L) was observed in five patients. Serum lipid levels in patients with AP and HL decreased markedly during the first 72 h of evolution, but remained slightly above the upper normal limit in most of them after 15 d. The prevalence of HL was similar in edematous and necrotizing pancreatitis. Necrotizing pancreatitis was significantly associated with the presence of hypertriglyceridemia in conjunction with hypercholesterolemia (p less than 0.05). The observations that a) hyperlipidemia is an early event in acute pancreatitis, (b) serum lipid values decrease during the acute phase of the disease, (c) hyperlipidemia has a different prevalence in different etiologies, and (d) high serum lipid levels are not always associated to pancreatic necrosis suggest that HL is a preexistent metabolic abnormality with respect to AP. On the other hand, HL may play a role in aggravating AP.

Acute Disease↗