Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypocalcemic crisis developed in a patient with acute alcoholic fatty liver. In addition to jaundice and marked hepatomegaly, the patient presented with hypocalcemic crisis associated with hypomagnesemia, low plasma 1,25(OH)2-vitamin D and undetectable plasma parathyroid hormone (PTH) concentration. Subsequent computerized tomographic scan and liver biopsy showed the presence of severe fatty liver. With the improvement of liver function, the serum calcium level increased, and was accompanied by normalization of plasma PTH, serum magnesium, and plasma 1,25(OH)2-vitamin D levels. Serial ethylenediaminetetraacetic acid infusion tests demonstrated the reversal of the impaired PTH secretion. Thus, hypocalcemic crisis in this patient appeared to result from transient hypoparathyroidism induced by magnesium deficiency.
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PMID:Hypocalcemic crisis in alcoholic fatty liver: transient hypoparathyroidism due to magnesium deficiency. 311 39

Sixty-seven cases of alcoholic liver disease were histologically classified into 4 groups: alcoholic liver cirrhosis (ALC), alcoholic hepatitis (AH), alcoholic liver fibrosis (ALF) and alcoholic fatty liver (AFL). They were statistically reclassified by the likelihood method using age, total alcohol intake, hepatomegaly and 12 liver function tests. A score table for likely diagnosis was constructed from the incidences of each range. The cases were re-evaluated using the score table, with an overall correct diagnosis rate of 73%. The best combination of 5 parameters included the indocyanine green plasma disappearance rate, total alcohol intake, cholesterol, choline esterase and glutamic oxaloacetic transaminase/glutamic pyruvic transaminase ratio. A correct diagnosis rate of 75% was attained using these 5 parameters, and 94% of patients were correctly diagnosed by the first or the second likelihood diagnosis. Differential diagnosis of alcoholic liver diseases was easily and confidently obtained with the likelihood score table.
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PMID:Comparative diagnosis of alcoholic liver diseases by multivariate and histological analysis. 398 78

A study of 510 patients in Scotland and northeastern England with histological evidence of alcohol-induced liver disease showed no difference in the age of presentation between males and females. Single men and widowed females were particularly susceptible to alcoholic liver disease. The social class distribution was similar to the population in general. Women were more reluctant to volunteer a history of alcoholism than men, they had a higher incidence of previous psychiatric illness (usually due to alcohol abuse) and they developed liver disease at lower consumption thresholds of alcohol than men. Patients under 40 years of age were more likely to have alcoholic fatty liver and less likely to have active cirrhosis than those over 40. Most often, the presenting symptoms were non-specific and tended to be related to the gastrointestinal system, particularly in women. Five per cent of patients were asymptomatic and 14% came to hospital for conditions other than alcoholic liver disease. Important clues to asymptomatic alcoholic liver disease included hepatomegaly, clubbing of the fingers and abnormal liver function tests. Gastro-oesophageal varices accounted for 40% of instances of haemorrhage and the mortality from upper gastrointestinal bleeding was 17%. Anaemia was the most common haematological abnormality. Alcoholic hepatitis was observed more frequently in the Glasgow area then elsewhere.
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PMID:Alcoholic liver disease in Scotland and northeastern England: presenting features in 510 patients. 660 94

The term 'non-alcoholic fatty liver disease' (NAFLD) includes cases with steatosis alone and those with non-alcoholic steatohepatitis (NASH). Usually there are no signs or symptoms, sometimes fatigue or pain, and apart from hepatomegaly the condition is revealed by abnormal liver biochemistry or by abdominal ultrasound. Most cases are associated with overweight or diabetes. Liver enzymes are usually elevated, especially GGT, ASAT and ALAT. Other conditions, including alcohol abuse and autoimmune hepatitis, have to be excluded. The diagnosis of steatosis can be made with ultrasound or CT scan. A liver biopsy is often needed to exclude other disease and to assess inflammation and fibrosis. Cirrhosis can develop. NAFLD is usually caused by two 'hits': the 'first hit' is peripheral insulin resistance, causing steatosis. The 'second hit' is caused by reactive oxygen species, inducing vicious cycles leading to inflammation. Weight loss, metformin or thiazolidinediones can improve NAFLD by increasing insulin sensitivity. Radical scavengers such as vitamin E, betaine and perhaps also urodeoxycholic acid may improve the hepatitis component. Further studies on treatment are needed.
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PMID:Non-alcoholic fatty liver disease: a brief review. 1569 51

Non-alcoholic steatohepatitis (NASH) represents only a part of a wide spectrum of non-alcoholic fatty liver disease (NAFLD) and its prevalence is only 2 - 3% in the general population. Obesity, diabetes, hyperlipidemia and female sex are important risk factors for NASH. Two hit theory describes very well the pathogenesis of NASH wherein hepatic steatosis, the first hit is followed up by the second hit, one of which may be reactive oxygen species. Mitochondria is the main source of reactive oxygen species which may trigger steatohepatitis by lipid peroxidation, cytokine induction or induction of fas-ligand. Insulin resistance syndrome is the only metabolic syndrome that has been consistently associated with NASH. The diagnosis rests on the hallmark histological features and rigorous exclusion of significant alcohol consumption. Most patients are asymptomatic, have mild-to-moderate elevations of serum aminotransferase levels, clinical hepatomegaly and features of fatty liver on imaging. Liver biopsy is essential for positive diagnosis and prognostication of NASH. Histologically, fat deposition is typically macrovesicular and inflammation of steatohepatitis is predominantly lobular. Neutrophilic cells in lobular inflammatory infilterate are a distinguishing feature of steatohepatitis and differentiate it from other chronic hepatitis. The pattern of collagen deposition is perivenular & peri-sinusoidal spaces in zone 3. NASH is a progressive disease in more than one in four and has spontaneous regression in less than one in six. Therapy options include weight reduction in obese, good control in diabetics and exercise. Ursodeoxycholic acid has membrane stabilizing, cytoprotective and immunological effect and normalizes raised transaminases. Liver transplantation has been done in NASH but transplanted liver shows re-development in more than two thirds. Many more therapies are in the pipeline and show promise for the future.
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PMID:Non-alcoholic steatohepatitis. 1592 3

The anti-arrhythmic agent amiodarone (AD) is associated with numerous adverse effects, but serious liver disease is rare. The improved safety of administration of daily low doses of AD has already been established and this regimen is used for long-term medication. Nevertheless, asymptomatic continuous liver injury by AD may increase the risk of step-wise progression of non-alcoholic fatty liver disease. We present an autopsy case of AD-induced liver cirrhosis in a patient who had been treated with a low dose of AD (200 mg/d) daily for 84 mo. The patient was a 85-year-old male with a history of ischemic heart disease. Seven years after initiation of treatment with AD, he was admitted with cardiac congestion. The total dose of AD was 528 g. Mild elevation of serum aminotransferase and hepatomegaly were present. Liver biopsy specimens revealed cirrhosis, and under electron microscopy numerous lysosomes with electron-dense, whorled, lamellar inclusions characteristic of a secondary phospholipidosis were observed. Initially, withdrawal of AD led to a slight improvement of serum aminotransferase levels, but unfortunately his general condition deteriorated and he died from complications of pneumonia and renal failure. Long-term administration of daily low doses of AD carries the risk of progression to irreversible liver injury. Therefore, periodic examination of liver function and/or liver biopsy is required for the management of patients receiving long-term treatment with AD.
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PMID:Liver cirrhosis induced by long-term administration of a daily low dose of amiodarone: a case report. 1614 55

1. Fenofibrate and xuezhikang are two types of drugs widely used in the treatment of dyslipidaemia in China. The main purpose of present study was to test the efficacies and explore the potential mechanisms of action of the two lipid-lowering agents on high-fat diet-induced non-alcoholic fatty liver disease (NAFLD). 2. Rats were randomly divided into four groups, with eight rats per group. One group was given normal diet, whereas the other three groups were fed a high-fat diet. Forty-two days later, two of the high-fat diet-fed groups were administered fenofibrate (100 mg/kg, p.o.) and xuezhikang (300 mg/kg, p.o.) for another 42 consecutive days. The other two groups were administered placebo (saline) by gavage. 3. Typical pathological symptoms of NAFLD occurred in the high-fat diet groups. Fenofibrate and xuezhikang treatment markedly improved NAFLD, ameliorating dyslipidaemia and fat accumulation in the liver, improving insulin resistance and ameliorating oxidative stress. Hepatic steatosis, necro-inflammation and collagen deposition were lessened in the drug-treated groups. However, both xuezhikang and fenofibrate failed to reverse hepatomegaly and fenofibrate even aggravated it. Xuezhikang reversed aminotransferase abnormalities, but fenofibrate had less of an effect. 4. The common therapeutic mechanism of action of fenofibate and xuezhikang likely involves inhibition of the hepatic expression of tumour necrosis factor-alpha. Fenofibrate upregulated mRNA levels of peroxisome proliferator-activated receptor (PPAR) alpha in the liver, whereas xuezhikang had no effect on the hepatic expression of PPARalpha and this may explain, in part, their different effects on the NAFLD rats. 5. The results suggest that fenofibrate and xuezhikang may have potential clinical application in the treatment of NAFLD. However, the side-effects of fenofibrate and the underlying constituents of xuezhikang need to be determined and investigated further.
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PMID:Effects of fenofibrate and xuezhikang on high-fat diet-induced non-alcoholic fatty liver disease. 1720 32

The correlation between biochemistry, imaging-studies and histology is a matter of controversy in non-alcoholic fatty liver disease (NAFLD) and the major pathophysiology of non-alcoholic steatohepatitis (NASH) is still unknown. We aimed to perform a comparative analysis between clinical, biochemical and histological variables of NAFLD. One-hundred and five NAFLD patients (F/M: 51/54), were studied, all with no-alcohol intake. The groups were followed-up for six months. Necroinflammation and fibrosis were more severe in patients with diabetes (p = 0.002, and p = 0.0001, respectively). In comparing NAFL to NASH, plasma nitric-oxide and malondialdehyde levels were significantly higher (p = 0.05, for-both), and vitamin-E and-C levels were significantly lower in NASH (p = 0.002, and 0.001, respectively). The serum ferritin levels were higher in NASH patients (p = 0.016). While the ultrasonographic grade was significantly higher, the liver-spleen density gradient was significantly lower in NASH group (p = 0.017, and 0.005, respectively). Within a six month period, serum ALT levels dropped into the normal range in 23/76 (30.3%) patients and serum ALT in the 6th month correlated significantly with the severity of steatosis, inflammation and fibrosis in initial biopsy (p = 0.023, 0.035, 0.011, respectively). In conclusion, the probability of severe liver disease is higher in patients with elevated-ALT in NAFLD. Serum ferritin levels have some prognostic significance in liver damage and fibrosis. Overt diabetes is predictive of advanced fibrosis and inflammation. However impaired glucose-tolerance is not. The advice on diet and exercise for six months after diagnosis may be a good strategy in NAFLD. The patients with normal-ALT without hepatomegaly, morbid-obesity and diabetes seem to have a good prognosis, however some of these patients may still require liver biopsy.
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PMID:Clinical, biochemical and histological correlations in a group of non-drinker subjects with non-alcoholic fatty liver disease. 1807 37

Ezetimibe is a novel cholesterol and plant sterol absorption inhibitor that reduces plasma low-density lipoprotein-cholesterol by selectively binding to the intestinal cholesterol transporter, Niemann-Pick C1-Like 1. Mice deficient in Niemann-Pick C1-Like 1 are protected from high fat/cholesterol diet-induced fatty liver as well as hypercholesterolemia. The object of the present study was to determine whether ezetimibe treatment could reduce hepatic steatosis in diet-induced obese mice. C57BL/6J mice were fed a high fat/cholesterol containing semi-purified diet (45% Kcal fat and 0.12% cholesterol) for 7 months after weaning. These mice were not only obese, but also developed hepatomegaly and hepatic steatosis, with varying degrees of liver fibrosis and steatohepatitis. About 87% of the mice on the high fat/cholesterol diet for 7 months had elevated plasma alanine aminotransferase activity, a biomarker for non-alcoholic fatty liver disease. Chronic administration of ezetimibe for 4 weeks significantly reduced hepatomegaly by decreasing hepatic triglyceride, cholesteryl ester and free cholesterol in diet-induced obese mice fed high fat/cholesterol diet for 7 months. Chronic ezetimibe treatment also significantly decreased plasma alanine aminotransferase activity. These results suggest that ezetimibe may be a novel treatment for high fat/cholesterol-induced non-alcoholic fatty liver disease.
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PMID:Ezetimibe improves high fat and cholesterol diet-induced non-alcoholic fatty liver disease in mice. 1832 14

Glycogenic hepatopathy (GH) has been reported as a very rare and under recognized complication in long-standing poorly controlled type 1 diabetes (T1D) patients. GH is characterized by transient elevation of liver transaminase and hepatomegaly caused by reversible and excessive glycogen accumulation in hepatocytes. It has been reported that GH is indistinguishable from non-alcoholic fatty liver disease, which is more commonly seen in diabetic patients, even after a history is taken and a physical examination or imaging studies have been performed. GH can only be diagnosed by liver biopsy. We here demonstrate a 21-year-old male patient with new-onset fulminant T1D complicated with diabetic ketoacidosis who subsequently developed GH just after the initiation of insulin treatment. The marked liver dysfunction (serum levels of aspartate aminotransferase 769 IU/L and alanine aminotransferase 1348 IU/L) and hepatomegaly improved spontaneously via glycemic control without any specific treatments thereafter. Moreover, the insulin requirement dramatically decreased from 168 to 80 units per day as GH improved, suggesting a potential role of GH in insulin resistance. GH was diagnosed based on the histological findings of the liver in our case, but we were able to predict GH before the biopsy based on the findings in the gradient-dual-echo magnetic resonance imaging sequence combined with ultrasound and/or computed tomography examinations of the liver.
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PMID:A case of glycogenic hepatopathy developed in a patient with new-onset fulminant type 1 diabetes: the role of image modalities in diagnosing hepatic glycogen deposition including gradient-dual-echo MRI. 2267 96


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