Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with primary biliary cirrhosis who were increasingly incapacitated by xanthomatous neuropathy are described. Treatment with a low fat diet and cholestyramine was unhelpful but repeated plasmaphoresis by simple venesection in one and plasma exchange using an IBM blood cell separator in the other over a period of several months completely relieved the symptoms of the neuropathy, caused skin xanthomata to recede, and lowered plasma lipid levels in both patients. There was no evidence that this procedure was associated with any deleterious effects on the liver. The size of the cholesterol pool in xanthomata in one patient was estimated to be approximately 35 g, and from the plasma cholesterol response to plasmaphoresis at varying frequency it was suggested that the excess of cholesterol synthesis over degradation was less than 0.3 g/day in one patient and less than 0.4 g/day in the other. On the basis of the response in these patients it is suggested that the turnover rates of lipid pools are relatively slow in biliary cirrhosis and that cholesterol accumulation is more likely to be due to a reduced catabolic rate than to an increased synthetic rate of cholesterol. Plasmaphoresis or plasma exchange are useful methods of treatment for the rare patient afflicted by this resistant and distressing complication of biliary cirrhosis.
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PMID:Plasmaphoresis and plasma exchange in the treatment of hyperlipaemia and xanthomatous neuropathy in patients with primary biliary cirrhosis. 434 39

Muscle weakness, neuropathy, and transient rises in hepatic enzyme activity have been reported with the use of the antiarrhythmic agent amiodarone. A 68 year old teetotaller with normal liver function was given amiodarone for resistant supraventricular arrhythmias. He presented 19 months later with vomiting, muscle weakness and wasting, sensory neuropathy, and hepatomegaly. Liver biopsy showed fibrosis and the presence of hyaline. The amiodarone was withdrawn. Three months later he developed ascites. Oesophageal varices were found and he later died. The liver showed micronodular cirrhosis. The large volume of distribution and long half life of amiodarone may explain the persistence of toxicity, which may have been aggravated by simultaneously administered doxepin in this case. Amiodarone should be withdrawn if abnormal liver function or neuropathy develops.
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PMID:Neuropathy and fatal hepatitis in a patient receiving amiodarone. 632 31

The toxic effects of chronic ethanol abuse on cerebral and hepatic function have long been recognized. The role of ethanol abuse as an etiologic factor in heart disease is less clear and is often attributed to coexistent malnutrition. However, malnutrition has been dissociated from ethanol use in many patients with congestive cardiomyopathy. Studies in various animals provide major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period. Abnormalities that result from ethanol in test animals include depression of left ventricular performance and metabolic and morphologic changes that parallel the changes in human alcoholics with subclinical mechanical dysfunction of the heart, such as symptomatic cardiac arrhythmias, particularly during intensive alcohol ingestion. What causes the progression to heart failure or arrhythmias is not known, but several factors may be involved. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, excessive exposure to trace metals or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the apparent infrequency of heart failure in patients with cirrhosis or neuropathy supports the view that the cardiac abnormality is often not dependent on malnutrition. Clinical data indicate that the cessation of alcohol intake may reverse the disease or interrupt its progression in many patients. However, the pathogenetic process may continued unabated in some who become abstinent.
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PMID:Ethanol abuse and heart disease. 702 Sep 81

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

It was the aim of our study to prove a potential correlation (a) between laboratory findings of cholestasis and autonomic neuropathy (AN) and (b) between the severity of AN and the prolongation of the corrected QT-time (QTc). The five standard tests of autonomic cardiac neuropathy were investigated. QTc was calculated according to Bazett's formula. 12 out of 14 patients with primary biliary cirrhosis, 18 out of 21 patients with HBsAg positive liver diseases and 11 out of 14 patients with cirrhosis of other origin had AN. No significant correlation between the laboratory parameters of cholestasis and AN was found. Abnormal QTc values (> 440 m/sec) were observed significantly more often (p < 0.002) in patients with AN than in patients without AN. Significant linear regression (p < 0.01) could be confirmed between the prolongation of the QTc-time and the severity of AN. Besides the non-invasive investigation of the cardiovascular reflexes the evaluation of the QT-time might be an additional diagnostic means to identify patients with an increased cardiovascular risk in chronic non-alcoholic liver diseases.
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PMID:Prolongation of the QTc-interval reflects the severity of autonomic neuropathy in primary biliary cirrhosis and in other non-alcoholic liver diseases. 748 30

Two-hundred and fifty chronically alcoholic men (mean age, 41 +/- 11 years) entering an alcoholism treatment program were studied. Detailed clinical history, nutritional assessment and measurement of muscle strength by electronic myometer were performed in each case. In addition, hepatic ultrasonography and liver biopsy, echocardiography and radionuclide cardiac scanning, and electrophysiologica testing of peripheral nerves were performed when there was clinical evidence of liver disease, cardiomyopathy or neuropathy, respectively. Alcoholic cirrhosis was diagnosed in 20 cases, skeletal myopathy in 117, dilated cardiomyopathy in 20 and peripheral neuropathy in 41 cases. No patients with chronic myopathy or cardiomyopathy showed either clinical or laboratory evidence of malnutrition. Patients with cirrhosis showed a significantly lower lean body mass than controls (P = 0.03) and significantly lower nutritional protein levels than those alcoholics without cirrhosis. Alcoholics with peripheral neuropathy had significantly lower anthropometric parameters and nutrition protein levels than their counterparts (P < 0.001). However, in the multivariate analysis, the only independent factor for developing these complications of alcoholism was the total lifetime dose of ethanol (P < 0.001). We conclude that alcohol-related diseases are common in asymptomatic alcoholic men and these diseases appear to be due to an accumulative toxic effect of ethanol. Age and nutritional status do not seem to play a part in the development of such diseases.
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PMID:Relationship between ethanol-related diseases and nutritional status in chronically alcoholic men. 827 78

Clinical symptoms and/or signs of peripheral neuropathy were found in 17 of the 19 patients we studied with liver cirrhosis. In 16 of the 19 patients electrophysiological abnormalities were also observed. Mild-moderate alterations involved both motor and sensory fibres, with a higher incidence in the lower rather than upper limbs, and indicated a fibre loss rather than a fibre demyelination. These changes were observed in both alcoholic and non-alcoholic cirrhotics, suggesting a primary role of liver cirrhosis per se. In fact, both the clinical and electrophysiological abnormalities were related to the severity of the liver disease. A careful clinical examination could reveal the presence and extent of neuropathy in most cirrhotic patients.
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PMID:Peripheral neuropathy in liver cirrhosis. A clinical and electrophysiological study. 856 4

The aim of this study was to identify the risk factors of alcohol-related peripheral neuropathies. A case-control study was performed to compare two groups of alcoholic patients, one with peripheral neuropathy and the other without, but with alcohol-related cirrhosis, pancreatitis or cardiomyopathy. Ninety patients were recruited in four in-patient units of a French hospital: 32 patients had a peripheral neuropathy and 58 patients did not. Univariate analysis showed no differences between the two groups for sex, age, body mass index and duration of the alcoholic disease. Peripheral neuropathies were associated with a higher frequency of parental history of alcoholism, severity of alcohol dependence, heavier alcohol consumption and more alcohol-related somatic diseases. Multivariate analysis showed a strong relationship between a parental history of alcoholism and the presence of a neuropathy, when the severity of the alcoholic disease was taken into account (adjusted OR = 6.8, IC95% [2.2-21.6], P < 0.001). The hypothesis that neuropathy may be a marker of an inherited susceptibility to alcoholism is discussed.
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PMID:Parental history of alcoholism: a risk factor for alcohol-related peripheral neuropathies. 867 15

Historically, alcohol use by the diabetic patient has been controversial. Recent studies in the general population have shown an improvement in mortality with moderate alcohol intake (one to three drinks per day). This improved mortality is greatest in those individuals who have a higher risk of ischemic heart disease. The mechanisms of the beneficial effects of alcohol include positive effects on insulin resistance, HDL cholesterol, platelet aggregation, and fibrinolysis. Since the diabetic patient has an especially high risk of ischemic heart disease because of these factors, the use of a moderate amount of alcohol should not be discouraged. The short-term risks of heavy or continuous alcohol intake include hypoglycemia, glucose intolerance, and ketone and lactate accumulation. In the long term, heavy alcohol intake is associated with an increased prevalence of cancer, hypertension, cirrhosis of the liver, and symptomatic neuropathy. Moderate alcohol intake taken with a meal has been shown to have little or no effect on postprandial glycemic excursions.
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PMID:Alcohol and the NIDDM patient. 873 20

Type III glycogen storage disease (GSD) is a disorder of carbohydrate metabolism caused by a deficiency of debranching enzyme. Different subtypes with different clinical pictures have been recognized. During childhood and early adulthood, the symptoms generally regress, and normal adulthood appears possible in most patients without symptoms or signs of cirrhosis. We report on an adult patient with GSD who developed endstage cirrhosis and a small hepatocellular carcinoma. She had GSD subtype IIIb, i.e., there were no signs of cardiomyopathy, myopathy, or neuropathy. She underwent a successful transplantation, representing the first case treated this way for this indication to our knowledge, and she is doing well after 1 year. Debranching enzyme activity was absent both in the liver and in the leukocytes before transplantation. The debranching enzyme activity remained absent in the leukocytes after transplantation. We conclude that patients with GSD type III may develop end-stage cirrhosis and hepatocellular carcinoma and therefore need hepatological follow-up during adulthood.
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PMID:Type IIIb glycogen storage disease associated with end-stage cirrhosis and hepatocellular carcinoma. The Liver Transplant Group. 904 94


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