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)

The appearance of perivenular fibrosis on liver biopsy reflects the beginning of the fibrotic process that ultimately results in liver cirrhosis. To examine whether the fibrogenic activity can be detected by blood tests, we evaluated whole antibody radioimmunoassay (RIA) of procollagen type III N-terminal peptides (P-III-P), RIA of these peptides using Fab fragments (Fab-P-III-P), and RIA of the laminin P1 peptide in alcoholics within 1 week of alcohol abstinence. The Fab-P-III-P levels in subjects with perivenular fibrosis were significantly higher than those in patients with simple fatty liver. Values in 63% of subjects with perivenular fibrosis exceeded the upper limit of the fatty liver group. Patients with simple fatty liver had significantly lower values than nonalcoholic controls. Serum levels of P-III-P and laminin were elevated in patients with alcoholic hepatitis and correlated well with the degree of inflammation. With abstinence, Fab-P-III-P levels increased in all alcoholics. P-III-P values increased in patients with normal P-III-P values on admission. By contrast, the values of laminin decreased during abstinence. Therefore, to interpret serum levels of Fab-P-III-P, P-III-P, and laminin, the duration of abstinence must be taken into consideration. P-III-P, Fab-P-III-P and laminin measurements in the serum within 1 week of abstinence can contribute to the detection of alcoholic liver disease and the determination of its stage.
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PMID:Serum procollagen type III N-terminal peptides and laminin P1 peptide in alcoholic liver disease. 330 95

About 90 per cent of morbidly obese patients show histological abnormalities of the liver. One third of patients have fatty change involving more than 50 per cent of hepatocytes. Fatty liver disease can be divided into four histological groups: Fatty liver, fatty hepatitis, fatty liver with portal fibrosis, and cirrhosis. Most patients show only fatty change. Alcohol, drugs, diabetes, poor nutrition, and weight-reducing surgery contribute to progressive liver damage, but morbid obesity alone may lead to severe disease showing all the features of alcoholic hepatitis and may end in cirrhosis and liver failure. The accumulation of fat alone is unlikely to be the stimulus to inflammation and fibrosis. Only one fifth of patients have complaints that arise from the liver. The development of severe fatty liver disease may also be asymptomatic and rarely shows the florid picture associated with alcoholic hepatitis. There is poor correlation of liver function test results with morphology in obesity. ALT levels exceeding twice the normal limit have some predictive value for histological grades of severity, but they are present in few patients. Pericentral and pericellular fibrosis in prebypass liver biopsies may be an important prognostic lesion for the development of fatty hepatitis and cirrhosis. In contrast with the frequent progression to massive fatty change, inflammation and fibrosis after bypass surgery, weight loss by low-calorie dieting, or starvation is accompanied by improvement in fatty change and return of liver function tests to normal.
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PMID:Fatty liver disease in morbid obesity. 331 4

To study the profile of alcoholic liver disease in India, 144 consecutive, histologically diagnosed patients were prospectively studied. The patients were divided into those having alcoholic fatty liver (AFL) (Gr. I, n = 32), alcoholic hepatitis (AH) (Gr. II, n = 42) and alcoholic cirrhosis (AC) (Gr. III, n = 70) on the basis of their histological findings. All the patients were males, those with fatty liver being younger than those with cirrhosis. The amount of alcohol consumed by patients with AFL, AH and AC was not significantly different. Similarly, the duration of alcohol consumption was not significantly different between the three groups of patients. The clinical features of the patients were quite similar to those reported from the West, except that AH was relatively milder in our patients. Intake of poor quality country liquor was quite common (60%), but its use was not found to be associated with more severe liver injury as compared with the use of good quality foreign varieties of liquor.
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PMID:Profile of alcoholic liver disease in an Indian hospital. A prospective analysis. 339 62

Autoantibodies to smooth muscle (ASMA), and to actin which is a major determinant of such reactivity, were measured in the serum of 94 patients with three defined categories of alcoholic liver disease, fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, and in controls matched individually by age and sex with the patients. Autoantibody to monomeric G-actin was detected by an ELISA and autoantibody to polymeric F-actin by immunofluorescence staining of fibroblast stress fibers in cultured cells. Values for the ELISA were expressed as a percentage of the value for a strongly reactive standard serum. The mean value for antibody to G-actin in 40 patients with alcoholic cirrhosis (70 +/- 33%) was significantly greater than that for the matched controls (28 +/- 18%), but the mean value for the 30 patients with alcoholic hepatitis (46 +/- 16%) and the 24 with fatty liver (42 +/- 24%) did not differ significantly from the controls. High levels of reactivity with G-actin correlated significantly with HLA B7. ASMA was demonstrable to low titer in 11 of the 94 sera, and positive ASMA reactions by immunofluorescence correlated with high binding values to G-actin in the ELISA. Antibody to F-actin was found in only one serum and no controls. Thus in different liver diseases the reactivity of antibodies to monomeric G-actin and polymeric F-actin may differ, presumably because of specificity for different determinants of the actin molecule. Reactivity to G-actin may distinguish a group of alcoholic subjects in whom a predisposition to autoimmune reactivity is one of the determinants of progression of liver damage to cirrhosis.
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PMID:Antibody to G-actin in different categories of alcoholic liver disease: quantification by an ELISA and significance for alcoholic cirrhosis. 385 90

Pathogenetic associations between benign hepatic tumours and liver damage were studied in an autopsy series of 91 males with high incidence of alcoholism. Information on the consumption of alcohol was obtained by interviewing a family member or a close friend of the deceased. The reported use of alcohol correlated well with the increase of fatty and fibrotic changes and with the occurrence of liver cirrhosis, alcoholic hepatitis or pancreatitis. Benign bile duct tumours (bile duct adenomas and von Meyenburg's complexes) (n = 26) were associated with the occurrence of bridging (P less than 0.0005) and periportal (P less than 0.025) fibrosis of the liver and, independently from these, with chronic pancreatitis (P less than 0.05) and with non-parasitic liver cysts (n = 14) (P less than 0.01). The weight of the liver was greater (P less than 0.01) in males with focal nodular hyperplasia (n = 3). Cavernous hemangioma (n = 19) occurred independently of the parameters studied. None of the tumours showed significant correlation to liver cirrhosis, alcoholic hepatitis, fatty liver or diseases of the gallbladder. The results are in line with observations on the reactive nature and connections to fibropolycystic liver disease of benign bile duct tumours in laboratory animals and in man. Their presence in human liver specimens should be taken into account as a sign of liver damage, in this study related to heavy use of alcohol or to chronic inflammation of the pancreas.
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PMID:Benign bile duct tumours, non-parasitic liver cysts and liver damage in males. 395 Mar 64

Infraclinical myocardial lesions were searched for in patients with various types of liver disease due to chronic alcoholic intoxication. During a single procedure, a transjugular liver and right endoventricular biopsy and hemodynamic evaluation were performed in 26 patients without clinical evidence of cardiac involvement. Patients were classified into 5 groups: I, no liver disease (n = 4); II, fatty liver (n = 7); III, acute alcoholic hepatitis (n = 3); IV, cirrhosis (n = 7); V, cirrhosis with alcoholic hepatitis (n = 5). The study also included the determination of the serum thiamine level, a 24 h non-stop EKG recording and a M mode echocardiography. The cardiac-thoracic ratio, the EKG and Holter monitoring were normal. The serum thiamine levels decreased regularly from group I to group V, but there was no significant difference between patients with cirrhosis (group IV and V) and the others (group I to III). The same findings applied to the echocardiographic data. At rest, hemodynamic data were normal in all patients. Various degrees of myocardial lesions were present in 86 p. 100 of the cases. They included: cellular hypertrophy, contraction bands, interstitial fibrosis, fibroblastic infiltrate, perinuclear, cellular and or interstitial edema. Although frequent, these lesions were moderate and not specific. No correlation was found between the myocardial lesions and the type of liver disease. Myocardial lesions without cardiac manifestations have therefore been observed in vivo in nearly all patients with chronic alcoholic intoxication. These lesions were not correlated with the stage of alcoholic liver disease.
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PMID:[Latent myocardiopathy in chronic alcoholic patients with or without hepatic involvement]. 399 13

Serum selenium was evaluated in relation to hepatic structure and function in 46 alcoholics with diagnostic liver biopsy classified into 4 groups by hepatic histology. Their serum selenium concentration varied from 12 to 88 micrograms/l and was lower (p less than 0.001) in all groups of alcoholics, ie patients with normal liver (53.0 +/- 20.7 micrograms/l, mean +/- SD), fatty liver (55.8 +/- 21.2 micrograms/l), alcoholic hepatitis (46.0 +/- 14.1 micrograms/l), and cirrhosis (41.1 +/- 12.8 micrograms/l), than in 25 healthy controls (88.7 +/- 11.0 micrograms/l). Serum selenium level was related to the severity of liver disease, and most reduced in subjects with decompensated alcoholic cirrhosis. Their serum selenium level (29.2 +/- 13.7 micrograms/l) was below (p less than 0.05) that obtained in alcoholics with normal liver and fatty liver respectively. Both inadequate dietary selenium intake and alcohol-induced changes in hepatic structure and function may have contributed to the decrease of serum selenium in the subjects studied.
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PMID:Decreased serum selenium in alcoholics as related to liver structure and function. 401 64

An enzyme-linked immunosorbent assay was developed to detect insoluble liver cell membrane antigen (LMAg) which gives rise to serum LMA (anti-LM) in HBsAg-negative patients. The optical density (OD) ratio of the average LMAg level of normal subjects was less than 1.2. In HBsAg-positive cases, high LMAg levels (OD ratio greater than 2.4) were noted in 8 of 8 patients with acute hepatitis (AH), 3 of 8 with chronic persistent hepatitis (CPH), 5 of 10 with moderate chronic aggressive hepatitis (CAH), 7 of 10 severe CAH and 4 of 8 with liver cirrhosis (LC). In HBsAg-negative cases, however, high LMAg levels were noted in only 6 of 8 patients with AH, 1 of 10 with CPH, 1 of 10 with moderate CAH, 1 of of 10 with severe CAH, 0 of 8 with LC, 0 of 8 with fatty liver and 5 of 10 with alcoholic hepatitis. In micro-immunodiffusion experiments, intensively absorbed rabbit anti-rat LM precipitated two organ-specific components of rat liver homogenate, one of which was identical to liver specific protein (LSP). In immunohistochemical demonstrations of LMAg and LSP, anti-LM, prepared from the serum of a HBsAg-negative CAH patient, bound to both human and rat acetone-fixed liver cell membranes, but not to those of human or rat kidneys. Absorbed rabbit anti-rat LM also bound to liver cell membranes, but absorbed anti-rat LSP lacked organ-specificity when assayed with the immunofluorescence technique using acetone-fixed liver sections. In conclusion, the appearance of serum LMAg was associated with high-SGPT patients and HBsAg-positive CAH patients.
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PMID:Detection and clinical significance of acetone-insoluble liver cell membrane antigen in sera of patients with chronic active liver diseases. 404 Apr 88

Histopathological analysis for 94 Japanese alcoholic patients revealed alcoholic hepatitis 11%, chronic hepatitis 14%, fatty liver 16%, alcoholic liver fibrosis 22% and liver cirrhosis 31%. Alcoholic hyaline was found in only 30% of the cases of alcoholic hepatitis. Alcoholic liver fibrosis (without any findings except fibrosis and steatosis) was distinct from other type of diseases. Chronic hepatitis in alcoholics was mostly chronic active hepatitis (77%), whereas only 35% was chronic active hepatitis in nonalcoholics. Histologically typical alcoholic liver cirrhosis was uncommon.
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PMID:Characteristic features of liver disease in Japanese alcoholics. 407 6

Using a leucocyte migration inhibition test sensitisation to Mallory bodies (alcoholic hyalin) was found in a statistically significant 41% of 17 patients with alcoholic hepatitis. Patients with alcohol-induced fatty liver and cirrhosis did not demonstrate sensitisation. Mallory bodies are a characteristic feature of alcohol-induced liver damage, and immunological sensitisation to them might lead to liver cell death and cell progression of the hepatitis process.
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PMID:Sensitisation to Mallory bodies (alcoholic hyalin) in alcoholic hepatitis. 616 47


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