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)

A number of chronic hepatic lesions can result from adverse reactions to medicinal agents. Such lesions include a form of chronic active hepatitis; hepatic steatosis, phoepholipidosis and granulomatosis; several vascular lesions; two types of noncirrhotic portal hypertension; several types of cirrhosis and several neoplasms.
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PMID:Drug-induced chronic hepatic disease. 22 60

The large number of chemical agents administered for therapeutic or diagnostic purposes can produce various types of hepatic injury by several mechanism. Acute injury may be cytotoxic, cholestatic or mixed. Cytotoxic injury may consist of necrosis or steatosis. Cholestatic injury may be cholangiolitic (hepatocanalicular) or bland (canalicular). Chronic hepatic lesions caused by medicinal agents include chronic active hepatitis, steatosis, cirrhosis, fibrosis, hepatoportal sclerosis (non-cirrhotic portal hypertension), hepatic vein thrombosis, peliosis hepatis, adenoma, carcinoma, and angiosarcoma. There is a useful relationship between the type of hepatic injury and the chemical setting in which the drugs are employed. Some agents produce the liver damage because they are intrinsic (true, predictable) hepatotoxins. Other (non-predictable "hepatotoxins"), produce hepatic injury only in the rare and unusually susceptible individual (idiosyncratic injury). Hepatotoxic agents can be recognised by their dose-dependent and experimental reproducibility, properties which are not shared by agents which produce hepatic injury only in idiosyncratic hosts. Intrinsic hepatotoxins may be categorised as direct or indirect. Direct hepatotoxins injure the hepatocyte by direct physiochemical alteration and as a consequence produce metabolic defects. Indirect hepatotoxins selectively block metabolic pathways and, by producing a precise biochemical lesion, lead to structural changes. They may lead to hepatic steatosis or necrosis (cytotoxic indirect hepatotoxins) or block bile flow (cholestatic indirect hepatotoxins). Direct hepatotoxins are rarely encountered as drugs. Overdoses of some drugs and antineoplastic agents appear to be indirect cytotoxic hepatotoxins, and the C-17 alkylated anabolic and contraceptive steroids are indirect, cholestatic hepatotoxins. Idiosyncracy of the host is the mechanism for most types of drug-induced hepatic injury. It may reflect allergy to the drug or a metabolic aberration of the host permitting the production of hepatotoxic metabolites.
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PMID:Drug-induced liver disease. 35 64

Collagenisation of the space of Disse was systematically assessed to determine its relationship to the clinical and histological manifestations of chronic alcoholic liver disease. Ninety-four chronic alcoholics who had been submitted to biopsy were assessed by clinical manifestations of hepatic dysfunction and by a 17-parameter Combined Clinical and Laboratory Index (CCLI). Liver biopsies were scored for light (LM) and electron-microscopy (EM) abnormalities using a universal scoring system for both. Thirty-five patients with normal liver histology (LM) had an average collagen score of 0.6 +/- 0.1. Twelve cirrhotic patients and 29 with fatty liver, both groups with mild clinical manifestations, did not differ significantly. In 18 cirrhotic patients and five with fatty liver, both groups having severe clinical manifestations, the mean scores were 2.1 +/- 0.8 (P less than 0.02) and 2.5 +/- 0.6 (P less than 0.01) respectively. Collagenisation also correlated with CCLI (P less than 0.001), serum bilirubin (P less than 0.001), serum aspartate transferase (SGOT) (P less than 0.003), and clinical evidence of portal hypertension and histological changes of necrosis, inflammation, and terminal hepatic vein sclerosis. These results suggest that collagenisation of the Disse space may be important in the pathogenesis of alcoholic liver disease.
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PMID:Collagenisation of the Disse space in alcoholic liver disease. 48 62

Oral glucose tolerance tests (100 g glucose) and the intravenous tolbutamide test were carried out. The glucose tolerance was seen to be disordered even in acute infectious hepatitis, but returning to normal when cured. If chronic hepatitis develops, however, the proportion of manifest diabetes increases to 7.2% in chronic persistent hepatitis and to 16.3% in chronic progressive hepatitis, while 30% each have latent diabetes. The glucose tolerance is most impaired in fatty liver (stage III) and in active cirrhosis of the liver with portal hypertension, where more than half of all patients present manifest or latent diabetes. Conversely, glucose tolerance improves even in chronic hepatitis and in cirrhosis of the liver as the inflammatory activity subsides. The main cause for the development of "liver diabetes" is therefore likely to be the activity of the inflammatory process, the extent of portal hypertension, disorders of glucose regulation in the liver and the increased insulin inactivation in the cirrhotic liver.
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PMID:[Disorders of glucose tolerance in 2600 histologically confirmed acute and chronic liver patients (author's transl)]. 81 Jun 95

We report the free, acyl-, and total carnitine contents of 49 clinically healthy volunteers and 167 chronic alcoholics with various clinically and/or anatomopathologically identified degrees of hepatic affection. There was a gradual upward trend in carnitine levels as the degree of hepatic affection increased. In cirrhotic patients, both free and acylcarnitine levels were significantly higher than normal, but there was no systematic hypercarnitinemia in other stages of alcoholism; on the contrary, noncirrhotic alcoholic patients accounted for 82.6% of all hypocarnitinemia cases. Hypercarnitinemia among cirrhotic alcoholics was due chiefly to increased free carnitine concentrations. Acylcarnitine levels in patients with hepatic steatosis were significantly higher than those in normal subjects (P less than 0.001), but there were no other statistically significant differences in either acyl- or free carnitine levels between normals on the one hand and, on the other, patients with hepatic steatosis, alcoholic hepatitis, slight hepatopathy, or chronic hepatopathy without portal hypertension.
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PMID:Free carnitine and acylcarnitine levels in sera of alcoholics. 239 Feb 92

For the detection of mild liver disease (acute viral hepatitis, chronic persistent hepatitis, fatty liver) serum bile acids levels have not proved to be superior to transaminases or other common liver tests with almost similar sensitivity and/or specificity. Indeed it has been possible to show in patients with compensated cirrhosis of the liver that the serum bile acids concentration is related to the degree of intrahepatic shunts and that there was a significant relationship between the fasting serum bile acids and the intrinsic clearance of ICG. Measurement of serum bile acids appear to be more sensitive for detection of cirrhosis than commonly used tests. The elevation of bile acids concentration in cirrhotic patients is thought to result from a reduced hepatic clearance and/or from portosystemic shunting. In order to determine the role of serum bile acid estimation in the indirect assessment of portal hypertension, fasting and two-hour postprandial serum bile acids concentration were measured in 36 patients with liver cirrhosis, classified according to Child-Pugh's criteria. Real time ultrasonography, esophagogastroscopy and static liver scintigraphy of the liver were carried out in all patients. The size of esophageal varices, the portal vein and its related structure, the nuclear criteria were graded according to the common methods. Between the clinical findings, splenomegaly, was noted and graded, though the size of spleen does not correlate well with the level of portal pressure. In our patients a good correlation (p less than 0.001) existed between the two hour postprandial bile acids concentration and ultrasonographic findings of portal hypertension. Fasting serum bile acids (SBA) were significantly higher in severe than in mild liver cirrhosis according to Pugh's criteria (p less than 0.001). In conclusion we think that SBA concentrations have a great prognostic value in assessment of major complications (upper gastrointestinal hemorrhage particularly). The reduced liver blood flow, for intra-and extrahepatic porto-systemic shuntings, is probably the main cause of reduced hepatic clearance of bile acids.
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PMID:[Serum concentration of bile acids and portal hypertension in cirrhotic patients. Possible correlations]. 264 42

From June, 1969 to February, 1987, distal splenorenal shunt was carried out on 78 patients with esophagogastric varices. The operations were urgent in 9, elective in 40, and prophylactic in 29 patients. There were 52 males and 26 females. Age ranged from 16 to 76 years with an average of 53 years. Thirty-seven patients were alcoholics. Hepatitis B surface antigen was positive in only 15.5%. The causes of portal hypertension were cirrhosis of the liver in 67, chronic hepatitis in 5, idiopathic portal hypertension in 4, primary biliary cirrhosis in 1, and fatty liver in 1 patient. Fifty-two patients were in Child's class A, 18 in class B, and 8 in class C. Emergency shunts were performed only when conservative therapy had failed to stop variceal bleeding. Prophylactic operations were done in patients having Child's class A or class B liver disease and risky varices, in varices larger than 5 mm in diameter and/or varices with red color signs such as cherry red spots. Forty-two patients underwent the original Warren shunt, but the remaining 36 had modified distal splenorenal shunt with expanded polytetrafluoroethylene interposition. The operative mortality rates were 11.1% in the emergency group, 2.5% in the elective group, and 3.4% in the prophylactic group. The overall operative and hospital death rates were 3.8% and 7.7%, respectively. The patency rate was 94.1% and the incidence of rebleeding from esophageal varices was 3.8%. Hepatic encephalopathy, although mild to moderate in degree, was observed in 14.7% of 75 patients excluding 3 operative deaths.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Appraisal of distal splenorenal shunt in the treatment of esophageal varices: an analysis of prophylactic, emergency, and elective shunts. 278 85

Alcoholic hepatic steatosis, considered for a long time as a reversible "harmless" disease, is now re-evaluated according to the concept of cirrhosis without cell necrosis and inflammation. The study of 166 biopsies from alcoholic hepatic steatosis has demonstrated the presence of fibrotic process in 25 (15%) of the cases. Histologic and electron microscopic examination have supplied data on the distribution of this fibrosis (perivenous, perisinusoidal and extensive) as well as on the cells involved in collagen synthesis; myofibroblasts, fat storing cells (Ito cells) and the hepatocyte itself. Peritoneoscopy revealed aspects of incipient portal hypertension in some of the cases. Follow-up in time with reiteration of morphologic exploration at intervals of 2 to 3 years has shown the possible evolution toward cirrhosis in cases of steatosis with fibrosis when ethanol consumption is continued. Detection of early fibrosis, in patients with alcoholic steatosis, by means of morphologic or biochemical methods would be necessary for its therapeutic implication: possible reversibility by abstinence from alcohol and antifibrogenic therapy.
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PMID:Hepatic fibrosis in alcoholic steatosis. Morphologic aspects and evolutive tendencies. 338 76

The liver in an infant or child is as liable to the same pathologies afflicting the adult liver but with certain differences in prevalence and causes. Genetic disorders are more likely to present in the paediatric age group where many involve metabolic processes such as galactosemia, phenylketonuria, glycogen storage disease and others. Many of these present in the newborn period. However, neoplasms and hamartomas also present in the newborn period, such as congenital neuroblastoma with an enormously enlarged liver, hepatoblastoma and haemangioma. The latter may present with intractable cardiac failure as a result of considerable shunting of blood. Acquired liver lesions often present in the newborn period or early infancy and this includes hepatitis and biliary atresia. The difficulties in the differentiation of the two lesions will be discussed together with the management of biliary atresia. As the child grows older, Reyes encephalopathy with microvesicular fat in the liver is not uncommon. The pathophysiology of Reyes encephalopathy as seen locally will be described. The choledochal cyst with direct (Caroli's disease) or indirect effect on the liver will be described. Problems of childhood portal hypertension as well as congenital hepatic fibrosis will be described. Hemosiderosis of the liver is chiefly seen in homozygous beta-thalassaemia patients who have been kept alive with repeated blood transfusions. Amoebic and pyogenic hepatitis, fatty liver due to protein malnutrition, biliary ascariasis, etc, which are common in tropical and subtropical countries are rarely seen now in Singapore children.
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PMID:Paediatric liver disorders in Singapore. 346 38

Portal hypertension, widely recognized as a complication of cirrhosis, may also develop as an intrahepatic consequence of numerous hepatic disorders in the absence of cirrhosis. When gastrointestinal bleeding occurs in such cases, ruptured esophageal varices must be considered. Among chronic liver diseases, some, such as schistosomiasis, are commonly associated with portal hypertension and its complications. In others, including tuberculosis, amyloidosis, and polycystic disease, well-documented portal hypertension has been reported in only a small minority of cases. Nevertheless, because of the ever-present possibility of variceal hemorrhage whenever portal hypertension occurs, clinicians should be aware of these disorders. Acute conditions associated with noncirrhotic intrahepatic portal hypertension include acute (and particularly fulminant) viral or drug-induced hepatitis, acute alcoholic hepatitis, acute veno-occlusive disease, and acute fatty liver of pregnancy. Portal hypertension may be reversible following recovery in these settings. Particular attention is called to the increasing frequency of acute veno-occlusive disease on bone marrow transplant units, presumably as a complication of high-dose chemo- and radiotherapy.
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PMID:Noncirrhotic intrahepatic portal hypertension. 354 26


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