Ultrasound demonstration of portosystemic collaterals in cirrhosis and portal hypertension.
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Biomedical subjects
Publications and source records attributed to L I Goldstein.
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Amebic abscess of the liver has protean manifestations that often resemble causes of an acute surgical abdomen. Patients presenting at University of California, Los Angeles Hospital with acute abdominal injuries who underwent exploratory laparotomy and subsequently were found to have an amebic hepatic abscess were studied. There are various clinical symptoms of amebic hepatic abscess as well as problems of differentiating this pathologic entity from an acute surgical abdomen. Most patients with amebic hepatic abscess that mimics an acute abdomen present as acute cholecystitis or acute appendicitis. All patients recovered uneventfully once the diagnosis was made and appropriate therapy instituted. The salient features of the history, physical examination and laboratory data that can identify the amebic abscess were analyzed. The key to correct diagnosis is cognizance of the condition.
In 143 jaundiced patients, ultrasound demonstrated the extrahepatic biliary system in 38% of those with medical and 74% of those with surgical jaundice. The size of the extrahepatic biliary system indicated that surgical was best differentiated from medical jaundice when 5 mm served as the upper normal limit for the common hepatic or common bile duct in patients without prior biliary surgery. Half of those patients with prior biliary bypass surgery had nondiagnostic sonograms. In 22% of the jaundiced patients, no additional imaging procedures were performed before definitive therapy. The role of ultrasound in evaluating jaundiced patients is discussed.
Hepatotoxicity, in association with intravenous oxacillin therapy, is described and documented for the first time by liver biopsy in an illicit drug user suffering from acute staphylococcal endocarditis. Mild gastrointestinal symptomatology, fever, eosinophilia and abnormal liver enzyme abnormalities were noted. Liver biopsy showed features consistent with a drug-induced hepatic injury. Cessation of therpy led to rapid reversal of clinical and biochemical changes and on further observation no evidence of chronic hepatic dysfunction was noted. A brief review of oxacillin hepatic injury is presented.
Gray-scale ultrasonography (GSU) and thin-needle cholangiography (TNC) were performed in 35 consecutive patients with unexplained jaundice. The status of the biliary tree was correctly assessed by GSU in 33 of 35 cases (94%); in two patients technical difficulty prevented definitive assessment. Neither false-positive nor false-negative results were encountered. There were no discrepancies between the results of GSU and TNC. We conclude that GSU provides a safe, highly reliable method of assessing the jaundiced patient and should be the preferred initial procedure in the diagnostic evaluation of patients with jaundice when the major differential lies between the medical and surgical types. If GSU does not demonstrate a dilated biliary system, TNC is unnecessary, and other diagnostic studies should be undertaken.
Thin needle cholangiography (TNC) was performed in 50 patients with obstructive jaundice or jaundice of obscure origin. The purpose of this study was to assess the diagnostic accuracy and safety of this procedure. TNC was performed by the technique described by Redeker et al. using the Chiba needle (JAMA 231:386, 1975). Obstructed ducts were successfully demonstrated in 100% of cases (29/29). Non-obstructed ducts were opacified in 12/21 (57%). Overall success was 82% (41/50). Two septic complications occurred. It is concluded that 1) TNC is a highly reliable, easy to perform and safe procedure in the evaluation of the jaundiced patient; 2) Accurate demonstration of the biliary anatomy by TNC provided important information which often in (10/50 = 20%) led to a change in diagnosis, avoidance of unnecessary procedures, and shortening of hospitalization; 3) Failure to visualize patients with non-dilated biliary ducts occurred with advanced chronic liver disease or fatty liver.
The effects of chenodeoxycholic (CDC), 750 mg. per day, phenobarbital (PB), 90 or 180 mg., combined (CDC + PB), and placebo on biliary lipid composition and on the rate-limiting enzymes of hepatic cholesterol synthesis (HMG-CoA reductase) and bile acid synthesis (cholesterol 7alpha-hydroxylase) were studied. Percutaneous liver biopsies were performed after 6 months of therapy in 4 patients from each group participating in a double-blind study of gallstone dissolution. The enzyme activities were also assayed in liver obtained at laparotomy in 7 untreated gallstone patients and 4 without gallstones. 7alpha,12alpha-Dihydroxycholest-4-en-3-one-12alpha-hydroxylase, an enzyme leading to cholic acid synthesis, was determined in 4 untreated gallstone patients and 4 without gallstones. Untreated gallstone patients had 35 per cent greater HMG-CoA reductase (p less than 0.01), 37 per cent less 7alpha-hydroxylase (p less than 0.01), and 40 per cent less 12alpha-hydroxylase (p less than 0.01) than patients without gallstones. CDC, PB, and both increased biliary CDC and decreased the lithogenic index significantly (p less than 0.01) but saturated bile persisted with PB. CDC decreased HMG-CoA reductase 40 per cent (p less than 0.01) and 7alpha-hydroxylase 47 per cent (p less than 0.01). PB increased HMG-CoA reductase 112 per cent (p less than 0.01) and 7alpha-hydroxylase 20 per cent (p less than 0.01). The combination of CDC and PB increased HMGCoA reductase 40 per cent (p less than 0.01) and had no effect on 7alpha-hydroxylase. In conclusion, CDC induced desaturation of bile while decreasing HMG-CoA reductase and increasing CDC in bile. PB reduced the saturation less effectively than CDC; it increased 7alpha-hydroxylase but also increased HMG-CoA reductase.
Cholesterol saturation of bile has a primary role in the pathogenesis of gallstone formation. Predisposing factors should be considered. The characteristic features of biliary colic are important to keep in mind, as well as the fact that a history of fatty food intolerance is not of value in the diagnosis of gallstones. The technique of endoscopic retrograde cholangiography is useful for the diagnosis of bile duct stones in jaundiced patients and in patients with a strong clinical history, but in whom findings on oral and intravenous cholangiograms are within normal limits. Improved techniques of operative cholangiography to diminish the incidence of retained gallstones have been developed. Also, choledochoscopy provides a remarkable technique for diagnosis and choledocholithotomy. The dissolution of gallstones with chenodeoxycholic acid is an experimental procedure. This bile acid is thought to act by increasing the chenodeoxycholic acid pool size and decreasing cholesterol synthesis and secretion, thereby reversing the defects responsible for gallstone formation.
In a controlled trial, 36 patients with asymptomatic radiolucent gallstones were treated with chenodeoxycholic acid, 750 mg per day, phenobarbital, 180 mg per day, combination of both drugs, and placebo. After one year, chenodeoxycholic acid, phenobarbital and the combination, but not placebo, significantly decreased biliary cholesterol saturation. The effect was significantly greater with chenodeoxycholic acid and the combination than with phenobarbital. Gallstones size decreased more than 50 per cent in nine of 20 patients receiving chenodeoxycholic acid, either alone or combined with phenobarbital, but in no patient receiving only phenobarbital or placebo. Gallstones disappeared completely in tow patients. Abnormalities in liver-function tests in thriee of 36 patients and in five of 16 liver biopsies, occured with equal frequency in the four treatment groups. Thus, after one year, phenobarbital alone was ineffective in gallstone dissolution. Chenodeoxycholic acid alone or combined with phenobarbital, however, offered a partially effective and safe treatment for asymptomatic radiolucent gallstones.
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UNLABELLED: The effects of feeding chenodeoxycholic acid (CDC) on biliary lipid composition, on the rate-limiting enzymes of hepatic cholesterol and bile acid synthesis, and on hepatic cholesterol and bile acids were determined in hamsters. The goals were to study the mechanism and duration of the cholesterol desaturation action of CDC. Administration of CDC for 30 days significantly increased the biliary bile acid and lecithin to cholesterol ratio and the percentage of CDC in bile (p less than 0.01). These effects persisted for 20 days after discontinuing CDC (p less than 0.01) and were no longer evident at 30 days. HMG CoA reductase and 7 alpha-hydroxylase activities were significantly reduced by CDC (p less than 0.01). After discontinuing CDC, these effects persisted for 10 days at which time HMG CoA reductase was still decreased by 50 per cent (p less than 0.01) and 7 alpha-hydroxylase by only 12 per cent (p less than 0.01) and were no longer evident by 20 days. Hepatic cholesterol did not change, while hepatic CDC was significantly elevated throughout the experiment. CONCLUSIONS: (1) CDC has a salutory effect on biliary lipid composition while causing an increase of exogenous CDC in bile and a decrease of endogenous cholesterol synthesis. (2) The persistence of decreased cholesterol synthesis and of improved biliary lipid composistion after discontinuing CDC provides a rationale for studying this in man and then testing intermittent CDC regimes for gallstone dissolution.
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