Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous cholelithiasis was found in seven owl monkeys (Aotus spp.) at necropsy. There were four male and three female animals. Antemortem clinicopathologic findings included weight loss, anemia, increased alanine aminotransferase and gamma glutamyl transpeptidase, and hyperbilirubinemia in several animals. Choleliths ranged in size from sand-like particles to 5 mm in diameter. Gallstones from five animals were analyzed by accepted analytical methods. Results showed the gallstones to be composed primarily of cholesterol (89%). The gallbladder was histologically normal in all cases examined. The etiopathogenesis of cholelithiasis in the owl monkey is unknown.
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PMID:Cholelithiasis in owl monkeys: seven cases. 217 29

In a double-blind controlled study of ursodeoxycholic acid (400 and 800 mg/day) and chenodeoxycholic acid (375 and 750 mg/day), in comparison with placebo, ursodeoxycholic acid was significantly more effective than chenodeoxycholic acid in dissolving gallstones after 12 mo of treatment. Although there continued to be better dissolution during ursodeoxycholic acid treatment (dissolution complete in 30% and partial in another 30% of the patients) than during chenodeoxycholic acid treatment (dissolution complete in 7% and partial in 40%) at 24 mo, this difference between the treatment groups was no longer statistically significant. The incidence of floating stones was significantly higher in the patients who dissolved their stones than in those who did not (p less than 0.001). The three failures of dissolution of floating stones during bile acid treatment were associated with chenodeoxycholic acid therapy--two of them with the 750-mg and the third with the 375-mg doses. Gallstone dissolution with ursodeoxycholic acid occurred in spite of a rise in biliary cholesterol saturation, which was consistent with a nonmicellar mechanism of cholelitholysis. Furthermore, more than threefold serum elevations of L-alanine aminotransferase were observed only during chenodeoxycholic acid therapy. They occurred in 2 patients treated with 375 and 750 mg/day, respectively. The enzyme levels normalized after discontinuation of chenodeoxycholic acid and have remained normal for 13 and 8 mo, respectively, after the institution of treatment with 800 mg/day of ursodeoxycholic acid. There was no correlation between the liver tests and biliary levels of lithocholic acid. Of all the symptoms studied, only constipation showed changes that approached statistical significance (p = 0.0681). There was a significant improvement of constipation in the combined chenodeoxycholic acid groups when they were compared with the combined ursodeoxycholic acid groups. The total bile acid pool expanded significantly in both the chenodeoxycholic acid and in the 800-mg ursodeoxycholic acid treatment groups. The marked increases of biliary ursodeoxycholic acid and chenodeoxycholic acid, respectively, indicated compliance with the treatment in all but 1 bile acid-treated patient. Neither serum triglycerides nor serum cholesterol showed significant changes in any of the treatment groups. The study shows that ursodeoxycholic acid dissolves gallstones faster and with fewer side effects than chenodeoxycholic acid. The results of the study are also consistent with the view that ursodeoxycholic acid is cholelitholytic at a lower dose than is chenodeoxycholic acid.
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PMID:Comparative efficacy and side effects of ursodeoxycholic and chenodeoxycholic acids in dissolving gallstones. A double-blind controlled study. 635 26

Periodical ultrasonic findings were taken up to 1 year after operation in 207 gastric cancer patients and generation of gallstones after gastrectomy was examined. Abnormal ultrasonic findings were observed frequently in cases with advanced cancer and cases which received anticancer drugs, but operative procedures, reconstruction procedures and the degree of removal of lymph nodes did not significantly affect ultrasonic findings. Gallstone findings were observed from 3 months after operation. Among 18 of 135 cases (13.3%) with gallstone findings observed 12 months after operation, 10 had shifted from biliary debris and sludges to gallstones. In 53 cases which were able to be observed periodically from the preoperative period, 9 (17.0%) of gall stones were observed after 12 months, and 7 had shifted from biliary debris and sludges. In cases with abnormal ultrasonic findings, the serum GOT levels on day 1 and day 7, and GPT levels on day 1, day 7, and day 14 were significantly higher than the preoperative values. Hepatic dysfunction of the early postoperative stage and generation of biliary debris and sludges may play an important role in gallstone formation, and anticancer drugs after gastrectomy may have an aid of gallstone formation.
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PMID:[Ultrasonic findings of the cholecyst and biliary tract after gastrectomy]. 832 Nov 82

In previously published studies ursodeoxycholic acid (UDCA) showed beneficial effect on the course of chronic hepatitis. We investigated the effect of UDCA on the course of acute viral hepatitis in a prospective double-blind study. Seventy-eight consecutive patients were randomly assigned either to the UDCA group or to placebo. At 12 months of follow-up 76 patients were available for the final assessment. The analysis of all cases and of the patients with hepatitis B (n = 59) showed a comparable rate of decline of the alanine aminotransferase and other liver function tests in the treatment group and in the placebo group. However, the elevation of alanine aminotransferase persisted more frequently in the placebo group (all cases, p = 0.05; hepatitis B group, p = 0.03). Persistence of the hepatitis B virus infection, measured by the presence of hepatitis B early antigen and hepatitis B virus DNA (polymerase chain reaction and hybridization) at 12 months of follow-up, was observed in I of 33 patients in the UDCA group and in 6 of 25 patients in the placebo group (p = 0.02). Gallstones detected by entry ultrasound dissolved in four of eight cases in the UDCA group and in none of six in the placebo group. We conclude that UDCA has a beneficial effect on the course of the acute viral hepatitis. It may enhance the clearance of the hepatitis B virus and thus prevent the development of chronic hepatitis.
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PMID:Effect of ursodeoxycholic acid in acute viral hepatitis. 1019 13

Gallstones are the commonest cause of acute pancreatitis in developed countries. There is now a considerable evidence base consolidated by a series of systematic reviews, meta-analyses and guidelines that has established a clear algorithm for diagnosis and management. In the majority of patients the combination of ultrasonography and serum alanine transaminase > or = 60 iu/l < or = 48 hours of symptoms will identify gallstones as the cause. The simplest method of severity assessment is a high level of serum C-reactive protein (> 150 mg/l up to 72 hours after symptoms). In mild disease, all fit patients must undergo laparoscopic cholecystectomy with intraoperative cholangiography or if not fit for surgery then endoscopic sphincterotomy during the same admission to prevent further attacks. All patients with severe disease should undergo endoscopic sphincterotomy in less than 72 hours. Patients with > 30% necrosis should undergo fine needle aspiration for bacteriology. Necrosectomy is indicated for infected necrosis or sterile necrosis if there are persisting clinically significant symptoms. There is increasing evidence for the use of minimally invasive pancreatic necrosectomy. Enteral nutrition should be instituted whenever possible but antibiotics should be reserved for patients with proven sepsis. The presence of fungal infection requires active anti-fungal therapy. Patients with severe disease should undergo cholecystectomy at a later stage. Patients who have undergone necrosectomy require long-term follow-up because of delayed complications.
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PMID:Algorithm for the diagnosis and treatment of acute biliary pancreatitis. 1611 Oct 94