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)

Autoimmune hepatitis (AIH) runs a variable clinical course. Slow disease progression or even spontaneous remissions can be observed and suggest that the autoimmune process can, at least to a certain extent, be controlled by regulatory elements of the patient's own immune system. In experimental autoimmune hepatitis (EAH) spontaneous recovery is regularly observed and associated with antigen-specific and antigen-nonspecific suppression. The aim of the current study was to search for similar immunoregulatory phenomena in patients with AIH. We examined T-cell reactivity to soluble human liver antigens in 11 patients with active autoimmune hepatitis and 30 patients with other liver diseases (chronic viral hepatitis, primary biliary cirrhosis, fatty liver). T-cell reactivity to liver antigens was almost exclusively confined to the AIH patients. In 9 of these 11 patients we were able to compare the T-cell response in active untreated disease, directly after initiation of immunosuppressive therapy and in remission, at which point T-cell reactivity was found to be markedly reduced. Addition of irradiated peripheral blood cells from the active disease phase or the remission phase to the responding cells taken before treatment showed that in eight of the nine patients there was marked suppression of the liver-specific T-cell response by cells from the remission phase. Study of the in vivo immune responsiveness by giving a tetanus toxoid booster immunization to nine patients with active untreated AIH as well as healthy controls and patients with other liver diseases showed that none of the patients with AIH showed a response to the tetanus immunization, whereas almost all the other patients showed marked responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for spontaneous immunosuppression in autoimmune hepatitis. 763 4

The aim of the present was to define prognosis and life expectancy in patients with chronic liver disease of different etiologies and to relate them to an age- and sex-matched normal population. After a follow-up of 15 years, life expectancy of 620 patients with chronic liver disease was retrospectively calculated and compared with an age- and sex-matched normal population. Among patients with cirrhosis, prognosis was dependent upon Child classification (P = 0.001). Patients with alcoholic cirrhosis and fatty liver disease were younger (P = 0.01) and had a lower life expectancy than patients with other causes of chronic liver disease (P = 0.004). Patients with hepatitis B and hepatitis C cirrhosis showed a comparable prognosis and a significantly lower life expectancy than the age- and sex-matched population. Cryptogenic and autoimmune liver diseases showed a comparable life expectancy but a significantly shorter life expectancy than the normal population. In patients with alpha 1-antitrypsin deficiency-associated cirrhosis, a high viral coinfection rate was found (P = 0.01). For patients with noncirrhotic hemochromatosis, prognosis was poorer than that for the age- and sex-matched population. In patients with asymptomatic primary biliary cirrhosis, chronic persistent hepatitis B, and alpha 1-antitrypsin deficiency without cirrhosis, life expectancy was equal to that of the normal population. Prognosis and life expectancy in chronic liver disease depend on stage, cause, and symptoms of chronic liver disease; age; and possibilities of treatment. In patients with hereditary liver disease, additional viral infection of alcohol abuse lead to a significant deterioration of life expectancy. Patients with alcoholic chronic liver disease have the poorest prognosis.
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PMID:Prognosis and life expectancy in chronic liver disease. 764 84

We developed a sensitive enzyme-linked immunosorbent assay (ELISA) for serum ornithine carbamoyltransferase (OCT) protein, and examined serum OCT concentrations in patients with various liver diseases. OCT concentrations were markedly elevated in cases of hepatic encephalopathy, 'acute on chronic', and those with the acute phase of acute hepatitis, moderately in chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, primary biliary cirrhosis, and slightly in those with a fatty liver. High percentages (92-98%) of patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma had higher than normal concentrations of serum OCT protein. There was a close correlation with aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and moderate correlations with those of mitochondrial AST, glutamate dehydrogenase and gamma-glutamyltranspeptidase. The OCT/ALT ratio was higher in patients with liver cirrhosis than in those with chronic hepatitis (p < 0.001), and was still higher in cases of hepatocellular carcinoma (p < 0.05). In 2 patients with 'acute on chronic' disease, OCT concentrations decreased similarly with or more rapidly than AST or ALT activities after admission. In 2 patients with hepatic encephalopathy, the OCT concentrations changed similarly with AST and ALT activities. This OCT ELISA system will aid in diagnosing various liver diseases and in the follow-up of the patients, and the OCT/ALT ratio may serve for a differential diagnosis of liver diseases.
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PMID:Clinical evaluation of serum ornithine carbamoyltransferase by enzyme-linked immunosorbent assay in patients with liver diseases. 778 67

Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.
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PMID:Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease. 786 97

In early hepatic fibrosis, increased amounts of type III collagen are deposited. Persistently high serum concentrations of aminoterminal type III procollagen propeptide (PIIIP) correlate with the activity of the fibrogenic process. Another index for the detection of fibrosis, the PGA index, combines the prothrombin time, gamma-glutamyl transpeptidase activity, and serum apolipoprotein A1 concentration (the latter falls with progressive fibrosis). We compared PIIIP measurements and PGA index in patients with various histological forms of alcoholic liver disease (104), primary biliary cirrhosis (38), and chronic B virus hepatitis (27), and in healthy age-matched controls (30). The ability of each test to identify correctly patients with fibrosis or cirrhosis was assessed with receiver operating curves. The PGA index was much higher in all groups of patients with alcoholic liver disease than in controls (p < 0.0001). PIIIP concentrations were also substantially higher than in controls (p < 0.05 for fatty liver, p < 0.0001 for all other groups), especially in the group with alcoholic hepatitis and cirrhosis. For the detection of cirrhosis the PGA was 91% sensitive and 81% specific and the PIIIP concentration was 94% sensitive and 81% specific. The two tests combined had 85% sensitivity, but 93% specificity. Among patients with primary biliary cirrhosis, both PGA index and PIIIP concentration correlated well with the severity of the disease, determined by the Mayo score (r = 0.72 and 0.66 respectively). The combined tests were 96% sensitive for the detection of fibrosis. All patients with chronic B virus hepatitis had raised PGA and PIIIP values in comparison with controls (p < 0.0001) but there were no differences between subgroups. Substantially raised PIIIP concentrations thus identify the subgroup of alcoholic patients with both hepatitis and cirrhosis. The combination of PGA index and PIIIP concentration may be useful for targeting treatment with antifibrotic drugs and to reduce the need for liver biopsy.
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PMID:Comparison of serum procollagen III peptide concentrations and PGA index for assessment of hepatic fibrosis. 790 68

Autonomic neuropathy has been evaluated by various cardiovascular bedside tests in 172 patients with chronic alcoholism (36 alcoholics without liver disease, 50 patients with fatty liver and 86 with cirrhosis), in 21 patients with HBsAg-positive chronic liver disease, in 14 patients with primary biliary cirrhosis, in 14 patients with cirrhosis of other origin and in 86 healthy controls. Parasympathetic integrity was evaluated by beat-to-beat variation during deep breathing, Valsalva manoeuvre and standing up, sympathetic function by blood pressure response to standing and to sustained handgrip test. Autonomic reflex damage was found in all groups examined. Patients with alcoholic cirrhosis exhibited the most severe alterations. Our results suggest, that chronic hepatopathy itself presents a pathogenetic factor of autonomic neuropathy. Autonomic failure has to be considered as a possible cause of symptoms in liver diseases with all its prognostic consequences.
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PMID:[Autonomic neuropathy in chronic liver diseases]. 846 64

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

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

In hematoxylin and eosin (H and E) stained sections from liver biopsies, the destruction of bile ducts in the portal triads is regarded as an important histologic parameter in the diagnosis of primary biliary cirrhosis (PBC). In contrast, the bile ducts are not destroyed by chronic inflammation in chronic active hepatitis (CAH). Nevertheless, the differential histologic diagnosis between PBC and virus or autoinmune-induced chronic active hepatitis (CAH), is very difficult in 15% of cases. That difficulty is mainly due to the impossibility of identifying bile ducts in the portal triads with marked lymphocytic infiltration. In this investigation we report that bile ducts may be specifically stained by anti-human cytokeratin 7 (CK7). Sections from 16 liver biopsies (PBC = 6, CAH = 6 and fatty liver (FL) = 4) were stained with H and E and CK7. The results in H and E stained sections indicated that the mean number of bile ducts found in PBC was was 0.56 (range 0-2), in CAH 0.67 (range 1-3), and in FL 0.56 (range 1-3). In parallel CK7 stained sections, the mean number of bile ducts in PBC was 5.33 (range 2-35), in CAH 3.44 (range 4-18), and in FL 1.39 (range 2-6). The difference between H and E and CK7 stained sections was significant (p < 0.001) in all 3 groups. In the light of these preliminary results, it would appear that Cytokeratin 7 may be the stain of choice to detect bile ducts, an important parameter to histologically differentiate between PBC and CAH, as well as to classify PBC into its different stages.
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PMID:The detection of bile ducts in liver biopsies by cytokeratin 7. 962

Many subjects with cryptogenic cirrhosis have underlying nonalcoholic steatohepatitis (NASH). The natural history of NASH-related cryptogenic cirrhosis after orthotopic liver transplantation (OLT) is not well defined. A primarily retrospective study of patients with the clinical histological phenotype of NASH-related cirrhosis undergoing OLT was performed. Data were compared with 2 sets of age- and weight-matched controls with (1) primary biliary cirrhosis or primary sclerosing cholangitis or (2) alcoholic liver disease. After OLT, all patients were managed by a standard immunosuppressive protocol. Liver biopsies were performed at 6 and 12 months after OLT and at 1- to 2-year intervals thereafter, as well as when liver enzyme levels were elevated enough to warrant diagnostic biopsy. Twenty-seven subjects with cryptogenic cirrhosis and a clinical histological phenotype of NASH and 3 patients with a long-standing diagnosis of NASH before OLT were included. The 30-day perioperative mortality was 1 in 30 patients. During a median follow-up of 3.5 +/- 2.7 years, 2 additional patients died of sepsis. There was a time-dependent increase in the risk for allograft steatosis that approached 100% by 5 years compared with only an approximately 25% incidence of steatosis in the control groups (P <.009, log-rank test). On multivariate analysis, only the cumulative steroid dose correlated with time to development of allograft steatosis. Three patients developed histological progression from hepatic steatosis to steatohepatitis. Of these, 1 patient developed progressive fibrosis. Four patients experienced at least 1 episode of acute cellular rejection; however, no patient developed chronic rejection or graft failure. In conclusion, nonalcoholic fatty liver disease occurs frequently after OLT in patients with the phenotype of NASH-related cirrhosis. Despite the frequent histological recurrence of disease, clinical outcomes are similar to those of other groups of patients undergoing OLT.
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PMID:Development of nonalcoholic fatty liver disease after orthotopic liver transplantation for cryptogenic cirrhosis. 1130 98


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