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)

Clinical observations over the past two decades have pointed to the relationship between heart disease and alcohol abuse, usually without evident malnutrition or cirrhosis. While the prevalence of heart failure in the alcoholic population is now known, subclinical abnormalities of left ventricular function in noncardiac alcoholics who were normotensive have a high prevalence with or without some degree of ventricular hypertrophy by echocardiogram. This is frequently a diastolic rather than systolic abnormality. Congestive cardiomyopathy is not infrequently associated with high diastolic arterial blood pressures. Intoxication itself may contribute to blood pressure elevation. Angina pectoris in the absence of significant coronary disease is another presentation. Although the history may not be readily obtained, the major diagnostic feature in this entity is the history of ethanol ingestion in intoxicating amounts for at least 10 years, often marked by periods of spree drinking. While the course of congestive cardiomyopathy may be progressively downhill in individuals who continue to be actively alcoholic after the onset of heart failure, in one series one third of the patients became abstinent. These patients had a 4 year mortality that was persistently one-sixth of the alcoholic group. Management of heart failure is traditional in these patients. Atrial arrhythmias have been shown to occur during the early ethanol withdrawal phase in patients without other clinical evidence of heart disease. Sudden death in a segment of the alcoholic population is considered arrhythmia related and is commonly associated with cigarette use. Identification of the addicted individual is the essential element to management.
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PMID:Alcoholic cardiomyopathy. 808 32

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

To determine the relationship between nutritional status and ethanol consumption, 250 chronically alcoholic men (mean age 41 +/- 11 years) entering an alcoholism treatment program were studied. A control group of 100 male volunteers (mean age 40 +/- 10 years) was also evaluated. Detailed clinical history, laboratory analysis and nutritional status assessment were carried out in each case and control. In addition, ethanol-related diseases such as liver disease, chronic pancreatitis, cardiomyopathy, myopathy and peripheral neuropathy were ruled out in all patients. The mean daily ethanol consumption of the alcoholics was 235 +/- 62 g over an average of 19 years. All of them belong to a very stable, middle-class working group of men. Only 25 (10%) alcoholics showed evidence of energy malnutrition, 15 (6%), of protein malnutrition, and 6 (2%) of both. In the multivariate analysis, the only independent factors for the development of malnutrition were the total lifetime dose of ethanol and calorie intake (ethanol excluded) (P < 0.01; both), as well as cirrhosis (P < 0.01) when protein malnutrition was considered. Alcoholic cirrhosis was diagnosed in 20 cases, skeletal myopathy in 117, dilated cardiomyopathy in 20 and peripheral neuropathy in 41. When patients with ethanol-related diseases were excluded, no significant differences in nutritional parameters were observed between chronic alcoholics and controls. We conclude that malnutrition is not as frequent as previously thought in middle socioeconomic class male alcoholics and its existence may be considered as another consequence of ethanol intake or secondary to the alcohol-related diseases.
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PMID:Nutritional status in chronically alcoholic men from the middle socioeconomic class and its relation to ethanol intake. 827 79

Dilated cardiomyopathy is a frequent and serious complication of idiopathic hemochromatosis. The mechanism by which disordered iron metabolism induces heart failure is not entirely understood, but myocardial dysfunction appears to be intimately related to the deposition of iron in myocytes. Cardiac function characteristically worsens or improves in proportion to the degree of iron accumulation in cardiac myocytes. The authors report the case of a 47-year-old man with idiopathic hemochromatosis and cirrhosis who developed symptoms of congestive heart failure and was found to have dilated cardiomyopathy 7 months after receiving a liver transplant. An initial endomyocardial heart biopsy demonstrated severe iron deposition in myocytes. The patient's heart failure worsened in the next 3 years and he eventually required a heart transplant. Examination of the explanted heart revealed dilated cardiomyopathy, but the previously demonstrated iron deposits in the cardiac myocytes were depleted. This "uncoupling" of cardiac function and cardiac iron load suggests that a threshold may be reached at which point the metabolic and ultrastructural derangements of iron deposition are no longer reversible, even with the removal of the inciting agent. Furthermore, displacement of myocyte iron stores after liver transplantation implicates altered hepatic iron metabolism as a primary or contributing mechanism in the pathophysiology of idiopathic hemochromatosis.
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PMID:Progressive hemochromatotic cardiomyopathy despite reversal of iron deposition after liver transplantation. 842 14

Type IV glycogenosis (polyglucosan body disease) is a rare congenital autosomal recessive inherited disorder, caused by lack of the branching enzyme (amylo-1,4-1,6 transglucosidase). This deficiency leads to storage of abnormal glycogen (polyglucosan bodies) in the liver and other tissues. The clinical onset of the disease is insidious with non-specific gastrointestinal symptoms followed by progressive hepatic failure. Usually patients die due to hepatic cirrhosis within 4 years. Sometimes myopathy of the heart and skeletal muscle is also present. In these cases, the clinical onset is often later than in typical cases. We report on two brothers with primarily cardiac manifestation and late onset of the disease. The older one started to suffer from progressive dilated cardiomyopathy at the age of 18 years, presenting with severe heart failure, hepatosplenomegaly, ascites and peripheral oedema. He also demonstrated myopathy and muscular atrophy especially of the shoulder and lower limbs. Initially he improved on medical therapy, but one year later severe heart failure recurred followed shortly afterwards by sudden cardiac death. Right heart and skeletal muscle biopsies were performed while he was alive. These, as well as the autopsy, revealed massive accumulation of polyglucosan bodies. In both heart and skeletal muscle, complete branching enzyme deficiency could be proven. His 14-year-old brother showed similar clinical findings of mild dilated cardiomyopathy. His muscle biopsy also revealed polyglucosan body myopathy. Thus, in young patients presenting with congestive cardiomyopathy, type IV glycogenosis has to be considered in the differential diagnosis.
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PMID:A new variant of type IV glycogenosis with primary cardiac manifestation and complete branching enzyme deficiency. In vivo detection by heart muscle biopsy. 888 67

Amiodarone is one of the most effective antiarrhythmic drugs available and is widely prescribed despite several potentially life-threatening side-effects. Hepatotoxicity is the most frequent one during long-term oral therapy: occasionally acute hepatitis necessitates the suspension of treatment but monitoring of a transient increase in serum aminotransferases is usually sufficient; the clinical-morphological pictures of liver cirrhosis have also been reported. Fulminant hepatitis soon after a parenteral load of the drug is far less well described in the literature. Most published cases were reversible after the suspension of treatment. A negative challenge after oral amiodarone exposure suggested that polysorbate 80, a solvent added to the intravenous infusion and already implied in the pathogenesis of a similar syndrome observed in infants, is a more likely cause of this complication. The occurrence of acute hepatitis complicating parenteral amiodarone treatment does not preclude subsequent oral use of the drug: an evidence-based therapeutic behavior now definitively consolidated. Because of the rarity of this diagnosis, we report 3 cases of short-term hepatotoxicity secondary to amiodarone treatment for supraventricular tachyarrhythmias: in 2 male patients with dilated cardiomyopathy and in a female with liver disease. The diagnosis was presumptive and based on a thorough drug history, the temporal relationship, the time-course of liver dysfunction, the exclusion of other causes and on the rapid improvement observed after parenteral amiodarone withdrawal in 2 cases; in no case could we find any other explanation for the liver damage. Since amiodarone is sometimes still an irreplaceable antiarrhythmic drug, we raise the question of whether careful and continuous vigilance should be mandatory in patients receiving the drug or whether it is possible to introduce a pharmaceutical preparation not containing the vehicle that induces acute liver toxicity.
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PMID:Three cases of severe acute hepatitis after parenteral administration of amiodarone: the active ingredient is not the only agent responsible for hepatotoxicity. 1240 66

In an adult beta-thalassaemic patient admitted on account of the sudden onset of nausea, vomiting and biliary pain, the concomitant jaundice was considered "obstructive" on the basis of ultrasonographic evidence of cholecysto-choledocal stones. However, when the patient was re-evaluated it was found that concomitant Gilbert's disease, hepatitis C virus related cirrhosis and dilated cardiomyopathy had a detrimental effect on clinical and laboratory findings.
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PMID:A puzzling jaundice. 1274 30

Chylous ascites and chylothorax are rare clinical entities and usually caused by neoplasms, particularly lymphomas, liver cirrhosis, superior vena cava thrombosis, nephrotic syndrome, and some cardiac events such as dilated cardiomyopathy or right heart failure. Constrictive pericarditis is an extremely rare cause of this clinical state. We report a 41-year-old male patient undergoing haemodialysis who presented with chylous ascites and chylothorax. Echocardiography and heart catheterisation revealed constrictive pericarditis. He underwent pericardiectomy and after the operation the ascites and pleural effusion resolved rapidly. We suggest that constrictive pericarditis should be considered in the differential diagnosis of chylous ascites and chylothorax.
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PMID:Chylous ascites and chylothorax due to constrictive pericarditis in a patient undergoing haemodialysis. 1512 33

We studied accelerated death benefit (ADB) claims at the Dai-ichi Mutual Life Insurance Company (Dai-ichi Life). The ADB provision is designed to pay all or a portion of the death benefit if the insured is expected to die within 6 months. Dai-ichi Life paid 243 ADB claims and did not pay 17 ADB claims between December 1994 and March 1998. Of the 260 ADB claims, 253 (97.3%) were caused by malignant neoplasm, 2 by intracranial hemorrhage, 2 by angina pectoris, 1 by dilated cardiomyopathy, 1 by hepatic cirrhosis, and 1 by bleeding gastric ulcer. The age range of the 243 paid claims at the time when the attendant physician predicted a life expectancy below 6 months was 21.6-72.6 years (48.7 +/- 8.7 years [Mean +/- SD]). By the end of March 2000, 236 cases were followed up among the above 243 paid ADB claims. Of the 236 followed-up cases, 149 (63.1%) died within 6 months and 203 (86.0%) died within 1 year. The range of survival periods of these 236 cases was 6-1516 days (210 +/- 237 days). Of the 217 dead cases due to malignant neoplasm, 45 (20.7%) died of gastric cancer, 44 (20.3%) of lung cancer, 24 (11.1%) of liver cancer, 16 (7.4%) of colon cancer, 13 (6.0%) of rectum cancer, and 12 (5.5%) of pancreatic cancer.
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PMID:Analysis of accelerated death benefit claims at a Japanese life insurance company. 1530 85

The patient was a 62-year-old woman with a personal history of chronic alcoholism and a medical history of duodenal ulcer, congestive heart failure, atrial fibrillation, dilated cardiomyopathy, and recurring urinary tract infections. She had osteoporosis, cirrhosis of the liver and portal hypertension. She had undergone surgery for multiple arm fractures after an accidental fall in the previous year and had received NSAIDs without concomitant gastric protection. On the fourth day of hospitalization she had an episode of haematemesis. The patient continued to take NSAIDs as required, as well as habitual medication of propranolol 40 mg/day, spironolactone 25 mg/day, furosemide 40 mg/day, pantoprazole 40 mg/day and strontium 2 g/day. Upper digestive endoscopy (UDE) revealed level I/II (Baveno) oesophageal varicose veins with no signs of haemorrhage and portal hypertensive gastropathy. The duodenal bulbous was deformed by an extensive ulcer with blood clots and one vessel was visible along the antero-superior portion (Forrest IIa classification). Numerous superficial ulcers with haemosiderin pigment at D2 were observed. Endoscopic haemostasis was achieved with epinephrine and bipolar probe. Food was suspended and the patient received continuous intravenous treatment with pantoprazole 8 mg/h. UDE repeated after 48 hours showed no signs of haemorrhaging from the ulcer. After 72 hours, the pantoprazole dose was changed to 40 mg every 12 hours and food was allowed. After 12 days with no recurrence of the haemorrhagic incident, the patient was prescribed oral pantoprazole 40 mg once daily and released from hospital.
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PMID:Recurrent duodenal ulcer due to nonsteroidal anti-inflammatories following the suspension of antiulcer medication. 1993 84


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