Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within the framework of a prospective study on the course and prognosis of ulcerative colitis and Crohn's disease begun in 1968, serial blind needle biopsies of the liver were carried out for the early establishment of liver involvement. In 201 needle biopsies taken in 114 patients with ulcerative colitis, normal findings were observed in 51, fatty infiltration in 24, and accompanying inflammation in 23, fatty infiltration together with a mesenchymal reaction in 8, fatty liver in 6 and sclerosing cholangitis and granulomatous hepatitis in 1 patient each. Of 69 needle biopsies taken in 45 patients with Crohn's disease we established normal findings in 13, an insignificant accompanying inflammation in 19, fatty infiltration in 5, granulomatous hepatitis in 3, fatty liver in 2, fatty liver together with a mesenchymal reaction in 2 and serum hepatitis in 1. Laboratory tests (alkaline phosphatase, SGOT, SGPT, BSP excretion) are not particularly suitable as screening tests. The diagnostic yield of serial blind needle biopsies of the liver is low and, despite the low-risk nature of the method, often dispensable. Laparoscopy, or at least blind needle biopsy of the liver, should be retained for the further clarification of serious deviations of laboratory values from the normal range, or of suspicious palpation findings.
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PMID:[Hepatic reaction in ulcerative colitis and Crohn's disease (author's transl)]. 4 40

Transient bacteremia associated with percutaneous liver biopsy was studied by pour-plate blood cultures, which were obtained immediately before and after the procedure and 5, 10, 15, and 30 min later in 89 patients. Part of the liver tissue was also cultured in all patients. Histological diagnoses included hepatitis, cirrhosis, cholangitis, fatty liver, granulomata, metastatic liver disease, lymphoma, and miscellaneous disorders. All blood cultures obtained before liver biopsy were sterile. Bacteremia was demonstrable in 12 patients (13.48%). In most of these patients, blood cultures were positive for as long as 15 min after liver biopsy; all cultures were negative at 30 min. Among the bacteria associated with 12 episodes of bacteremia were Escherichia coli, Klebsiella, Bacteroides, enterococci, diphtheroids, Staphylococcus aureus, alpha-hemolytic Streptococcus, and Streptococcus pneumoniae. The patients with positive liver biopsies had a higher incidence of bacteremia (83.3%) than did the patients whose liver biopsies were sterile (8.r%); this difference is stastically significant (P smaller than 0.01). Thus, liver biopsy can be associated with transient bactermia.
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PMID:Transient bacteremia associated with percutaneous liver biopsy. 109 72

Clinically significant liver and biliary disorders occur in approximately 5 percent of persons with inflammatory bowel disease. The most common hepatobiliary disorders encountered in patients with inflammatory bowel disease are fatty liver, sclerosing cholangitis and gallstones. In addition, chronic hepatitis, cirrhosis, biliary cancer and amyloidosis sometimes occur. Family physicians should be alert for these gastrointestinal problems in patients with inflammatory bowel disease.
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PMID:Hepatobiliary complications of inflammatory bowel disease. 757 66

In a retrospective study of 1101 patients (302 men, 799 women; mean age 56,7 [19-88] years) with symptomatic cholelithiasis who had undergone elective cholecystectomy and intraoperative liver biopsy, histological examination revealed inflammatory changes in the gallbladder in 96.7%, chronic fibrotic cholecystitis in 94.5% and a severe form of cholecystitis in 8.8%. Clinically relevant changes in the liver parenchyma were present in 27.9%, most frequently intrahepatic cholangitis (21.8%). The latter was significantly more common in choledocholithiasis than in isolated cholecystolithiasis. 27 patients had signs of severe liver disease, namely viral hepatitis, cirrhosis or fatty liver. Since the gall-bladder in cholelithiasis is almost always inflamed, cholecystectomy is the treatment of choice. Not uncommonly liver biopsy will reveal clinically relevant changes in the liver parenchyma. This will be useful information, especially in the management of symptoms which persist postoperatively.
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PMID:[Histopathological changes of gallbladder and liver parenchyma in symptomatic cholelithiasis]. 850 22

Over the past 30 years, liver transplantation has evolved from an experimental therapy to a routine procedure and most pathology textbooks have now a section dedicated to the pathology of liver transplant. Although there remain problems of biopsy interpretation due to the numerous post-transplant complications which can occur singly or in association, the major changes have been well characterized and are reviewed here, a particular attention being given to those features which are unique to or distinctive of the liver allograft. These include the outcome of donor fatty liver, reperfusion damage, massive haemorrhagic necrosis and the patterns of rejections, in particular the rarity and delayed onset of hyperacute rejection and the selective involvement of the small interlobular bile ducts and vascular endothelia in both acute and chronic graft rejection. "Functional" cholestasis with hepatocyte ballooning, cholangiolar cholestasis associated with sepsis and lesions of the larger bile ducts which may result from preservation, immune and/or ischaemic injury and closely resemble the changes observed in primary sclerosing cholangitis are also considered. Later in the post-transplant course, changes due to de novo or recurrent hepatitis have to be distinguished from those of late cellular rejection, protracted biliary complications, lymphoproliferative disorders, disease recurrence, in particular autoimmune chronic hepatitis, primary biliary cirrhosis and sclerosing cholangitis, differential diagnoses which often require interpretation of allograft changes in conjunction with all laboratory and clinical data available.
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PMID:Pathology and biopsy diagnosis of the transplanted liver. 860 Jun 91

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23

Alcoholic liver disease encompasses three main forms of liver injury: fatty change, alcoholic hepatitis and cirrhosis. However, there are many other types of injury, including perivenular fibrosis, venous occlusive lesions, microscopic cholangitis and chronic active hepatitis. The pathological spectrum is reviewed in this paper, and the contribution of other injurious agents to the pathological features is identified. Alcoholic liver disease can be mimicked by a variety of non-alcoholic liver diseases. However, features such as fatty liver with perivenular fibrosis, giant mitochondria, spotty hepatocyte necrosis, Mallory bodies, a micronodular pattern of cirrhosis, and iron deposition are strongly suggestive of an alcoholic aetiology. Correlation of clinical findings, and especially the alcohol history, and histopathological factors is necessary for the definitive diagnosis.
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PMID:Pathological spectrum of alcoholic liver disease. 897 50

A number of hepatobiliary tract and pancreatic disorders have been documented in patients with celiac disease. Some disorders have shared immunological or genetic factors, including chronic hepatitis, primary biliary cirrhosis and sclerosing cholangitis. Other hepatic or pancreatic pathological changes in celiac disease have been documented with severe malnutrition and malabsorption, including hepatic steatosis and pancreatic insufficiency, sometimes with pancreatic calcification. Finally, celiac disease may be associated with other very rare hepatic complications, such as hepatic T cell lymphoma.
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PMID:Hepatobiliary tract and pancreatic disorders in celiac disease. 911 4

Unexplained liver test abnormalities are frequent in patients with Turner's syndrome. This cohort study was performed to clarify the histopathologic features, causes, and long-term outcome of liver involvement in these patients. Thirty patients with persistently abnormal liver test results were followed-up for 8.8 +/- 5.2 years. Liver specimens were available in 27 patients. Marked architectural changes were present in 10 patients, including nodular regenerative hyperplasia in six, multiple focal nodular hyperplasia in two, and cirrhosis in two patients. These changes frequently were associated with obliterative portal venopathy lesions and with aortic malformations. There was mild to moderate portal fibrosis in 15 of the 17 other patients, inflammatory infiltrates in nine patients, and nonalcoholic fatty liver disease in 11 patients. Bile duct alterations resembling small duct sclerosing cholangitis were observed in 21 patients (with or without architectural changes). There was no viral, alcoholic, autoimmune, or drug-induced liver damage. Portal hypertension was observed in four patients with marked architectural changes, including three in whom refractory ascites or recurrent variceal bleeding developed, one of whom underwent transplantation. None of the patients without marked architectural changes experienced progressive or decompensated liver disease. There was no evidence of liver toxicity from estrogen replacement therapy. In conclusion, the main causes of liver involvement in Turner's syndrome are vascular disorders, probably of a congenital origin, and nonalcoholic fatty liver disease. In patients with vascular disorders, severe liver disease requiring liver transplantation may develop. Estrogen therapy does not appear to be pathogenically implicated.
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PMID:Vascular involvement of the liver in Turner's syndrome. 1475 43

HIV caregivers face many challenges following initiation of ART. The development of jaundice is uncommon but worrisome. In this case, two distinct and contrasting episodes of jaundice were observed. In the first instance, isolated elevation of the indirect bilirubin without elevation of the alkaline phosphatase was noted. The normal PT and serum aminotransferase levels indicate the absence of intrinsic liver dysfunction. Elevations in the indirect bilirubin may result from either impaired uptake/conjugation or excess production. The latter, usually from acquired hemolysis, may be a complication of an occult NHL. A work-up for this AIDS-related malignancy was not initiated since the caregivers recognized jaundice as a complication of IDV, which inhibits UDP-glucuronyl transferase and produces a Gilbert's-like syndrome. Physicians can expect to encounter this syndrome even more frequently with ATV. Experienced patients given RTV-boosted ATV have experienced elevations of unconjugated hyper-bilirubinemia in up to 45 percent of cases in clinical trials. However, such elevations do not reflect liver dysfunction and symptomatic jaundice requiring dosage reduction that occurred infrequently (7 to 8 percent of study patients). Counseling patients about this syndrome may promote adherence and prevent self-directed interruptions of ATV that compromise efficacy. The second case of jaundice provides a more formidable diagnostic challenge. The triad of LFT abnormalities (mild elevation of aminotransferases, normal PT, and marked cholestatic jaundice) implies an acute process that is mildly toxic to hepatocytes without affecting their synthetic function. The subacute nature of the patient's cholestatic jaundice suggests either intrahepatic infiltrative disease of the liver or extrahepatic obstruction of the biliary tree, most likely due to the patient's relatively modest level of pain and lack of fever. Despite LFT abnormalities occurring 17 months after a switch in his ART, cumulative drug-related toxicities must still be considered. Ritonavir can produce significant elevations in the AST/ALT, especially with pre-existing chronic liver disease as with hepatitis C virus coinfection. The NRTIs can produce hepatic steatosis, a result of mitochondrial toxicity and impaired fatty acid oxidation. However, jaundice and cholestasis are not typical of the latter syndrome. With a negative contrast CT that excludes parenchymal liver disease, investigation of the biliary tree to assess the presence of AIDS-related cholangitis was the next step. Performing a sphincterotomy or stent placement, and obtaining brushings or biopsy specimens to determine the extent of extrahepatic obstruction may help define a pathogen and be life-saving. The negative results of the ERCP justify the final diagnostic step, a liver biopsy to evaluate microscopic infiltrative disease that might not have been detected on contrast abdominal CT. Examples might include granulomatous disease (MAC), fungal etiologies (histoplasmosis), carcinomatosis (lymphoma, hepatoma, cholangiocarcinoma), and microvascular disease (bacillary angiomatosis). The failure to observe granulomatous inflammation in the liver does not exclude MAC infection, as MAC may involve other peri-aortic or mesenteric lymph nodes. This form of IRIS is unlikely given the abdominal CT findings, lack of systemic complaints, and extended persistence of liver aminotransferases. The nonspecific results of the liver biopsy are a common outcome in advanced AIDS patients with elevated alkaline phosphatase levels. Despite not having identified a pathogen, the biopsy establishes chronic liver disease and prompts re-evaluation and change of treatment to NFV. The subsequent normalization of the patient's aminotransferase levels suggests a prior adverse effect of LPV/r in the setting of unexplained, chronic liver disease. Most importantly, this case highlights the importance of HIV caregivers to review ART for safety when noting chronic liver dysfunction. Patients need to be counseled to minimize acetaminophen use, to consume alcohol in moderation, and to avoid behavior with risk for hepatitis C. Finally, all HIV patients should receive appropriate vaccination against hepatitis A and B if serology shows lack of protective immunity.
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PMID:Clinical vignette in antiretroviral therapy: jaundice. 1498 14


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