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)

This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two. Bone x-ray films showed generalized osteoporosis in all patients. Renal function and arterial blood pH were within normal limits in every patient. The diagnosis of primary hyperparathyroidism in each patient was based on repeated demonstrations of hypercalcemia, hypophosphatemia, and markedly elevated serum immunoreactive parathyroid hormone concentrations. In all six patients, removal of the parathyroid adenoma resulted in disappearance of symptoms; normalization of serum calcium, phosphorus, and immunoreactive parathyroid hormone levels; and in four of the six, improvement in radiographic evidence of osteoporosis during follow-up of from 1 to 6 years. The association of cirrhosis, portacaval shunt, and primary hyperparathyroidism has not been documented previously. Our six patients with primary hyperparathyroidism constitute 3.4 percent of 174 survivors of emergency portacaval shunt in a series of 264 unselected, consecutive patients with cirrhosis and bleeding esophageal varices. Hepatic osteodystrophy is known to have occurred in only 11 of these 174 survivors. Primary hyperparathyroidism may be a more common cause of hepatic osteodystrophy than has been previously recognized, and should be considered in patients with cirrhosis in whom weakness, bone pain, and bone demineralization develop, particularly if they have a portacaval anastomosis.
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PMID:Hyperparathyroidism, cirrhosis, and portacaval shunt. A new clinical syndrome. 325 57

Alcoholic liver disease (ALD) in Japan was compared clinicopathologically with the occurrence in the U.S.A. ALD found in Japan was more frequently complicated by other hepatic diseases including non-A, non-B chronic hepatitis than ALD found in the U.S.A. (9.9% versus 21.9%). Patients with such complications were excluded from this study. The chief complaints of the total of 51 alcoholics studied in the U.S.A. were abdominal distension or jaundice and those of 98 alcoholics studied in Japan were non-specific: general fatigue, weakness or appetite loss. The U.S. patients exhibited more elevated levels of serum bilirubin (8.1 +/- 7.5 versus 1.9 +/- 2.4 mg/dl, mean +/- SD) and a higher incidence of leukocytosis (49.0% versus 5.1%). While the serum glutamic-oxalacetic transaminase (GOT) levels were not significantly different between the two groups (146.5 +/- 116.8 versus 140.8 +/- 147.7 IU/L), the serum glutamic-pyruvic transaminase (GPT) levels among Japanese alcoholics were higher (38.6 +/- 31.4 versus 87.4 +/- 99.1 IU/L) and in about one quarter of these patients, serum GPT was higher than serum GOT, a feature not seen in the patients in the U.S.A. Comparative histopathologic study of 337 U.S. patients and 210 Japanese patients disclosed a higher frequency of cirrhosis (46.9% versus 33.8%), the presence of Mallory bodies (58.5% versus 13.8%) and marked neutrophilic exudation (45.1% versus 6.2%). Thus, the majority of Japanese alcoholics exhibited progression of liver disease, eventually leading to cirrhosis, due to hepatocellular drop-out and fibrosis caused by a mechanism different from alcoholic hepatitis. In addition, ALD in the U.S.A. revealed more striking extension of fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The characteristics of alcoholic liver disease in Japan. Clinicopathologic comparison with alcoholic liver disease in the United States. 369 16

A 33-year-old Japanese male, who had a three year history of biopsy-proved liver cirrhosis, was admitted to the hospital on June, 24, 1983 with a sudden onset of fever (38.6 degrees C), chills, generalized pain, nausea, anorexia, weakness, and eruption over the entire body. The patient went into shock and died about 7 hours after admission. Blood cultures before death were positive for V. vulnificus. Postmortem microscopic examination revealed "necrotizing vasculitis" in the small and large intestines, stomach, and skin, and also showed marked toxic epidermal necrolysis. This case matches the primary septicemia caused by V. vulnificus described by Blake et al. In addition, this case suggests that the septicemia was acquired through the gastrointestinal tract, especially the small intestine, because the V. vulnificus was isolated from blood and numerous Gram-negative bacilli around the submucosal vessels were observed in the area with acute necrotizing vasculitis.
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PMID:Vibrio vulnificus septicemia. 403 4

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

Problems raised by major hepatobiliary surgery affect the total economy of the human body. The liver is implicated in all body metabolism processes and possible problems during partial or total hepatectomy can only be solved by a knowledge of liver physiology. The liver plays a major role in the metabolism of products of digestion, whether these are carbohydrates or amino acids arriving in the portal blood. The most important activity of the liver is the preservation of a constant level of glucose by ensuring a fixed and predictable concentration to extrahepatic tissues. It ensures a very precise control of plasma and tissue flow of amino acids and thus protein synthesis and neoglycogenesis. Synthesis and degradation of non-esterified fatty acids, ketogenesis, cholesterol synthesis and triglyceride production result from the action of the liver on lipid metabolism. Free cholesterol is the precursor of bile acids and steroid hormones, but esterified cholesterol is not synthetized in the liver. Apart from its role in bilirubin metabolism, it has a key role to play in correct functioning of most endocrine systems: many are catabolized in the liver. But one of the most interesting properties of the hepatic tissue, as far as the surgeon is concerned, is liver regeneration, which combines hypertrophy with hyperplasia. This is dependent on age, hepatotrophic factors of portal blood, and extraportal factors. A study of hepatic metabolic processes allows assessment of the consequences of partial hepatectomy. Postoperative hypoglycemia, in the absence of a continuous infusion of glucose, is easily explained by the weakness of hepatic reserves in glycogen. Albumin levels fall during the first 7-10 days after liver resection, but this hypo-albuminemia is often marked by the need to infuse large quantities of frozen fresh plasma to try to avoid lesions of the other specific proteins, which are coagulation factors. Lipid metabolism disorders are of little clinical consequence. Hepatic resection is being alarming when it involves 80 to 90% of the hepatic mass and menaces the life of the patient. The existence of a previous liver alteration worsens the consequences of major hepatobiliary surgery. Indications for hepatic resection must be weighed carefully in patients with cirrhosis, liver regeneration being totally absent after resection. Metabolic consequences of total hepatectomy followed by transplantation are identical in kind to those of partial hepatectomy but are increased in frequency and start during operation. Postoperative surveillance must be strict to avoid marked variations in glycemia with the risk of hypoglycemia, and variations in kaliemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Hepatic insufficiency and nutritional problems after major hepatobiliary surgery]. 643 25

The prognostic significance of a battery of clinical, laboratory, and histological indicators was assessed in relation to mortality risk in a 1-year study of 253 patients with alcoholic liver disease, of whom 51 died within such time. The relative risk associated with each abnormality was calculated. A number of abnormalities was found to be statistically associated with a higher risk of death. Among the clinical abnormalities, these were: collateral circulation, edema, ascites, encephalopathy, spider nevi, anorexia, and weakness. Among the laboratory tests, these were: albumin, bilirubin, hemoglobin, abnormal prothrombin time, and alkaline phosphatase. Two hundred and sixteen of these patients had liver biopsies in which the quantifiable abnormalities were scored. Among the histological findings, the alterations significantly related to mortality were necrosis, Mallory, and inflammation, while the presence of cirrhosis per se did not influence the mortality risk. The relative risk factors for mortality associated with the histological alterations were lower than those derived from clinical or laboratory measurements. The advantage of using only clinical and laboratory items to derive a global, quantitative expression of severity is discussed. The relative mortality risks provided a means of calculating a "unit of severity" for each clinical and laboratory abnormality. A combined clinical and laboratory index (CCLI) results when these mortality-risk units are added. Such a combined index had a quasi-linear relationship with the risk of mortality for the complete population. This method compared well with severity scores derived from computerized, linear step-wise discriminant function (SDF) analysis and from a logistic regression (LR) analysis. The factors chosen to have independent prognostic significance by the SDF analysis were: encephalopathy, albumin, prothrombin time, and hemoglobin, while only encephalopathy, albumin, and hemoglobin were chosen by the LR analysis. Within a range of values, LR can provide a good discrimination in relation to mortality, similar to that observed for the CCLI in its complete range. However, there are some advantages to the CCLI method vs. the LR or SDF analyses. The CCLI is less susceptible to being unduly influenced by a nonspecific effect of treatment on the items chosen than the SDF and LR analyses, as the CCLI contains a large number of factors. Obtaining a single-severity score such as the CCLI is of value in: (a) assessing the effectiveness of treatment modalities; (b) analyzing the success of randomization; (c) separating cohorts of different severity, and (d) comparing new liver tests, histological abnormalities, or specific biological events with the severity of alcoholic liver disease.
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PMID:Assessment of prognostic factors in alcoholic liver disease: toward a global quantitative expression of severity. 662 18

The patient was a 59-year-old man who had been in hospital suffering from aplastic anemia with transfusion hemosiderosis. Sudden onset of weakness, shaking chills and headache was observed after his staying out overnight on July 25, 1981. His temperature was 39.3 degrees C and he complained of abdominal pain and abdominal distension. His blood pressure dropped to a dangerous level and tonic convulsions that had begun in the upper body gradually extended to the whole body and he died 23 hours after his return. V. vulnificus was isolated by the blood culture performed before death. During his stay away from the hospital, he had eaten raw cuttlefish, which was considered to be the source of infection. V. vulnificus is one of the halophilic marine vibrios and is isolated frequently in summertime from the sea foods and sea water near Japan. It has been disclosed that the presence of underlying diseases such as liver cirrhosis, hemochromatosis can predispose a person to fatal sepsis by V. vulnificus. In this case, besides leukocytopenia, the presence of hemosiderosis induced by many transfusions was considered to be a major cause leading to the fulminating course of the disease.
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PMID:[Fatal Vibrio vulnificus infection in a patient with aplastic anemia]. 667 24

Hepatic function tests were performed on 48 dogs that had been given primidone, phenytoin, or a combination of anticonvulsant drugs for 6 months or longer. Except for histories of seizures, 44 of the dogs were healthy at the time the tests were performed. Abnormal test results were observed most frequently in dogs given only primidone and in dogs given combinations of anticonvulsant drugs. The test results that were abnormal most often were those for alanine transaminase and alkaline phosphatase activities, and sulfobromophthalein excretion. The dosage of anticonvulsant drug was found to modify certain test results. Statistically significant positive correlations were found between the dosage of primidone and serum alanine transaminase activity and between the dosage of phenytoin and serum alkaline phosphatase activity. Four of the dogs were examined because of signs of weakness and anorexia and 2 also had ascites. Three of the 4 dogs were euthanatized 2 to 49 days after admission with clinical signs compatible with hepatic failure, and cirrhosis of the liver was confirmed at necropsy. The fourth dog died at home and was not necropsied. Four of the remaining 44 dogs that apparently were healthy at the time of examination had abnormalities in hepatic biochemical test results that were comparable with those in the 4 dogs with clinical illness. We concluded that, although results of hepatic biochemical tests frequently may be abnormal in dogs given anticonvulsant drugs long-term, severe hepatic injury is observed less often.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Compromised hepatic function in dogs treated with anticonvulsant drugs. 669 76

A patient with cystic fibrosis and cirrhosis developed a progressive neurological syndrome associated with ataxia, proximal weakness, and ophthalmoplegia. Profound deficiencies of vitamins A, D, and E were present. Visual acuity and results of retinal funduscopy were normal. The pattern reversal visual evoked potential was initially abnormal (P100 latency, 136 and 130 ms from left and right eyes, respectively) but became normal (less than 3 standard deviations from mean control P100 latency) over a two-month period when vitamin E was administered. This case documents a potentially reversible visual evoked potential abnormality in a visually asymptomatic patient with vitamin E deficiency.
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PMID:Reversible visual evoked potential abnormalities in vitamin E deficiency. 673 99

Advanced chronic hepatic disease was observed in 5 dogs that had received anticonvulsant drug therapy for 2 to 3 years. Clinical signs included anorexia, weakness, and restlessness, and 2 dogs also had ascites. There were remarkable increases in the serum activities of alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase. The total serum bile acid concentration was high in 3 of 4 dogs that were tested. Sulfobromophthalein excretion was delayed in all dogs. Histologic examination of liver specimens from 4 of the dogs demonstrated macronodular or micronodular cirrhosis.
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PMID:Hepatic cirrhosis associated with long-term anticonvulsant drug therapy in dogs. 711 8


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