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)

Cholesterol, triglyceride, free fatty acid, and phospholipid concentrations were measured in 33 brain, liver, and adipose tissue samples obtained from 17 children who died of an acute encephalopathy associated with liver dysfunction and hyperammonemia (hyperammonemic encephalopathy). Eleven patients had Reye's syndrome, three had acute "toxic" encephalopathy (without fatty liver), two had glycogen storage disease type 1, and one had congenital hyperammonemia type 2. Hepatic triglyceride concentrations were markedly increased in Reye's syndrome, but varied from normal to increased concentrations in other hyperammonemic encephalopathies. In contrast, the acute encephalopathy could not be differentiated on the basis of clinical, laboratory, or pathologic features and the brain lipid profiles were remarkably similar among all patients studied.
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PMID:Tissue lipids in hyperammonemic encephalopathies of childhood. 692 60

A case of acute fatty liver of pregnancy is presented. This case is characterized by many of the reported diagnostic features of AFLP, including the abrupt onset of symptoms with progressive liver failure, coagulopathy and encephalopathy, during the third trimester of pregnancy. Autopsy findings confirmed the diagnosis. The literature is reviewed, emphasizing the clinical and laboratory features helpful in the diagnosis of this entity.
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PMID:Acute fatty liver of pregnancy. Case report and review of the literature. 801 96

The liver has a central role in the metabolism of many drugs, since this organ is the main site of biotransformation of endo- and xenobiotics. Water-soluble drugs have a small volume of distribution and can be eliminated unchanged in the urine. By contrast, lipid-soluble drugs have a larger volume of distribution and require conversion to water-soluble metabolites for their elimination in urine or bile. The liver with its specific receptors, transporters and enzymes is responsible for the uptake, transformation and excretion of the lipophilic drugs. While most of the drugs are transformed into stable metabolites, other drugs form reactive, potentially toxic, metabolites producing liver cell damage. Liver injury caused by drugs may mimic almost any kind of liver disease. Clinical findings are gastrointestinal symptoms with nausea, vomiting and abdominal pain, cholestatic liver injury with jaundice and pruritus of severe inflammatory and cirrhotic liver damage with signs of liver failure, encephalopathy and cerebral edema. The morphological changes vary from hepatitis, cholestasis, fatty liver, granulomatous hepatitis, peri-/portal inflammation, to fibrosis with cirrhotic alterations and vascular lesions and tumors. The most commonly used drugs causing severe liver injury are discussed in detail. These are anabolics, oral contraceptives, antituberculous and antifungal agents, nonsteroidal anti-inflammatory drugs, ring substituted amphetamins ("designer drugs"), antiarrhythmics and antibiotics.
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PMID:[Liver damage caused by drugs]. 1041 44

Malnutrition and micronutrient deficiencies are common in patients with liver diseases. The pathogenesis of protein-energy malnutrition in cirrhosis involves many factors, including poor oral intake, malabsorption, and metabolic abnormalities similar to stress. Encephalopathy may complicate cirrhosis but is usually not caused by diet. Protein restriction is only necessary in rare patients with refractory encephalopathy. The use of branched-chain amino-acid solutions is not supported by the literature. Chronic liver diseases without cirrhosis are not usually associated with protein-energy malnutrition, but vitamin and mineral deficiencies are common, especially with significant cholestasis. Fatty liver may result from excessive triglyceride uptake and production by the liver or by a secretory defect. Therapy for fatty liver depends on its cause. Chronic total parenteral nutrition may induce fatty liver and inflammation especially in patients with short-bowel syndrome. Deficiency of choline in parenteral nutrition has been proposed as the mechanism for liver disease. Acute liver diseases such as fulminant hepatic failure or alcoholic hepatitis are considered hypercatabolic diseases and thus require prompt nutritional intervention with a high-calorie enteral or parenteral formula. In fulminant hepatic failure, low-protein, fluid-restricted formulas are recommended.
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PMID:Nutrition and liver diseases. 1098 Sep 70

Reye's syndrome (RS), a condition characterized by encephalopathy and fatty liver, is associated with aspirin use and carries a poor prognosis. The majority of patients with RS are children and adolescents. We report a case of RS in an adult.
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PMID:Reye's syndrome in an adult: a case report. 1106 Oct 22

Acute fatty liver of pregnancy is a rare disease which may be letal if diagnosis is missed. The pathogenesis is not completely clear, but there is some evidence that some cases have been associated with a genetic deficiency of fatty acid beta-oxidation. Other predisposing factors include primiparity, multiple pregnancy, male fetal sex and pre-eclampsia. Clinical presentation and laboratory findings are often unspecific. Increasing serum aminotransferases are characteristic in the early stage of the disease. Liver biopsy establishes the diagnosis and typically shows microvesicular, centrilobular fatty changes of hepatocytes. Differential diagnosis includes the HELLP-Syndrome, cholestasis of pregnancy, pre-eclampsia and viral or drug induced hepatitis. Without adequate treatment liver failure with coagulopathy and encephalopathy may develop. Two cases of acute fatty liver in pregnancy in an early stage are presented. Clinical and histopathological findings as well as diagnostic and therapeutic procedures are discussed.
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PMID:[Acute fatty liver in pregnancy: clinical and histopathological course. Case report]. 1188 62

Acute fatty liver of pregnancy is an uncommon, potentially fatal disorder. Between 1998 and 2000, two patients with acute fatty liver of pregnancy presented at the Christian Medical College Hospital, Vellore. Both patients were in the thirty-sixth week of pregnancy. jaundice and encephalopathy were the predominant symptoms. Both the mothers died after they delivered a stillborn Infant each. The maternal deaths were due to multiorgan failure and/or postpartum haemorrhage and sepsis. The route of delivery was vaginal in both the patients. Extrahepatic and metabolic complications in both cases Included renal failure, sepsis, hypoglycaemia, disseminated intravascular coagulation and gastrointestinal bleeding. Liver biopsy done in both patients was consistent with the diagnosis of acute fatty liver of pregnancy. To the best of our knowledge, this is the first report from India on acute fatty liver of pregnancy.
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PMID:Acute fatty liver of pregnancy: a report of two cases. 1254 67

We report the case of a 26-year-old second gravida in the third trimester of pregnancy who presented with a history of nausea, repeated vomiting and jaundice. The patient was diagnosed as acute fatty liver of pregnancy. After delivery, the condition of the patient progressed to grade IV encephalopathy and did not improve despite all intensive clinical management measures. After 3 days in grade IV encephalopathy, the patient was infused 3 x 10(8) human foetal hepatocytes. The patient's level of consciousness started improving after 24 hours of foetal hepatocyte transfusion and she recovered completely within 7 days.
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PMID:Peritoneal transplantation of human fetal hepatocytes for the treatment of acute fatty liver of pregnancy: a case report. 1568 63

The introduction of highly active antiretroviral therapy (HAART) for treatment of human immunodeficiency virus (HIV) infection has led to substantial reduction in morbidity and near-complete suppression of HIV-1 replication. But since HAART is unlikely to eradicate HIV-1, antiviral therapy may be required a lifelong, leading to an increase in attention on the long-term safety of HAART. A major toxicity of HAART is the mitochondrial toxicity. Mitochondrial toxicity becomes apparent particularly over the medium-term to long-term therapy and is attributed to treatment with nucleoside reverse transcriptase inhibitors (NRTIs), leading to a wide range of severe adverse events in HIV-infected patients. These include lactic acidosis, hepatic steatosis, neuropathy, (cardio-) myopathy, pancreatitis, and probably lipodystrophy. Furthermore, lactic acidosis and encephalopathy have been reported in children exposed in-utero and/or postnatally to NRTIs. Mitochondrial toxicity could pose a major threat to long-term success of HIV-therapy, and is of great concern for children exposed in-utero and/or postnatally to NRTIs. Therefore, investigation of mitochondrial toxicity of new compounds or new combinations is of growing interest for the clinical application of antiretroviral agents. However, at present no standardized and validated screening model system exists for the investigation of NRTI-induced mitochondrial toxicity. There is a need for the generation of a relevant in vitro assay system that can assess the mitochondrial toxicity in early preclinical development. This paper gives an overview of cell culture models currently used for the investigation of NRTI-induced mitochondrial toxicity and discusses the relevance and suitability of these models for prediction of clinical toxicity.
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PMID:Cell culture models for the investigation of NRTI-induced mitochondrial toxicity. Relevance for the prediction of clinical toxicity. 1640 76

Abnormal liver tests occur in 3%-5% of pregnancies, with many potential causes, including coincidental liver disease (most commonly viral hepatitis or gallstones) and underlying chronic liver disease. However, most liver dysfunction in pregnancy is pregnancy-related and caused by 1 of the 5 liver diseases unique to the pregnant state: these fall into 2 main categories depending on their association with or without preeclampsia. The preeclampsia-associated liver diseases are preeclampsia itself, the hemolysis (H), elevated liver tests (EL), and low platelet count (LP) (HELLP) syndrome, and acute fatty liver of pregnancy. Hyperemesis gravidarum and intrahepatic cholestasis of pregnancy have no relationship to preeclampsia. Although still enigmatic, there have been recent interesting advances in understanding of these unique pregnancy-related liver diseases. Hyperemesis gravidarum is intractable, dehydrating vomiting in the first trimester of pregnancy; 50% of patients with this condition have liver dysfunction. Intrahepatic cholestasis of pregnancy is pruritus and elevated bile acids in the second half of pregnancy, accompanied by high levels of aminotransferases and mild jaundice. Maternal management is symptomatic with ursodeoxycholic acid; for the fetus, however, this is a high-risk pregnancy requiring close fetal monitoring and early delivery. Severe preeclampsia itself is the commonest cause of hepatic tenderness and liver dysfunction in pregnancy, and 2%-12% of cases are further complicated by hemolysis (H), elevated liver tests (EL), and low platelet count (LP)-the HELLP syndrome. Immediate delivery is the only definitive therapy, but many maternal complications can occur, including abruptio placentae, renal failure, subcapsular hematomas, and hepatic rupture. Acute fatty liver of pregnancy is a sudden catastrophic illness occurring almost exclusively in the third trimester; microvesicular fatty infiltration of hepatocytes causes acute liver failure with coagulopathy and encephalopathy. Early diagnosis and immediate delivery are essential for maternal and fetal survival.
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PMID:Liver disease in pregnancy. 1826 10


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