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)

In glycogen storage disease type III (glycogen debranching enzyme (DE) deficiency), the activities of serum alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase may be strikingly elevated during childhood but are low during adult life. To determine the pattern of the elevated serum enzyme activities in relationship to diet, the biochemical subtype and clinical symptoms, 13 patients with DE deficiency were studied. Activities of serum aspartate and alanine transaminases, lactate dehydrogenase, and alkaline phosphatase were markedly elevated during infancy. Continued elevation of enzyme activities during childhood appeared to be related to DE deficiency in liver, but unrelated to DE deficiency in muscle. Activity elevations correlated inconsistently with diet and poorly with childhood growth rate or the presence of hypoglycaemia. The serum enzyme activities declined around puberty concomitantly with a decrease in liver size. Although periportal fibrosis and micronodular cirrhosis indicated the presence of hepatocellular damage during childhood, the decline in serum enzyme activities with age and the absence of overt hepatic dysfunction suggest that the fibrotic process may not always progress.
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PMID:Glycogen debranching enzyme deficiency: long-term study of serum enzyme activities and clinical features. 129 83

In the United States, approximately one million patients each year develop a pleural effusion. Pleural effusions have classically been divided into transudative and exudative pleural effusions. A transudative pleural effusion occurs when the systemic factors influencing pleural fluid formation and reabsorption are altered so that pleural fluid accumulates; an exudative pleural effusion occurs when the local factors influencing pleural fluid formation and reabsorption are altered, allowing accumulation of pleural fluid. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis with ascites. The leading causes of exudative pleural effusions are pneumonia, malignancy, and pulmonary embolization. Transudative pleural effusions can be differentiated from exudative pleural effusions by measurement of the pleural fluid protein and lactic dehydrogenase (LDH) levels. The ratio of the pleural fluid protein to the serum protein is less than 0.5, the ratio of the pleural fluid LDH to the serum LDH is less than 0.6, and the absolute value of the pleural fluid LDH level is less than two thirds of the upper normal limit for serum with transudative pleural effusions while at least one of these criteria is not met with exudative effusions. Most patients who have a pleural effusion with congestive heart failure have left ventricular failure. It is believed that the transudation of the pulmonary interstitial fluid across the visceral pleura overwhelms the capacity of the lymphatics to remove the fluid. Most patients with cirrhosis who have a pleural effusion also have ascites. It is also believed that the pleural effusions form when fluid moves directly from the peritoneal cavity into the pleural cavity through pores in the diaphragm. Approximately 40% of patients with pneumonia will have a pleural effusion. If these patients have a significant amount of pleural fluid, a diagnostic thoracentesis should be performed. Chest tubes should be inserted if the pleural fluid is gross pus, if the Gram stain of the pleural fluid is positive, if the pleural fluid glucose level is below 40 mg/dl, or if the pleural fluid pH level is less than 7.00. If drainage with the chest tubes is unsatisfactory, either streptokinase or urokinase should be injected intrapleurally. If drainage is still unsatisfactory, a decortication should be considered. The three leading malignancies that have an associated pleural effusion are breast carcinoma, lung carcinoma, lymphomas and leukemias. The diagnosis of pleural malignancy is made most commonly with pleural fluid cytology; in recent years immunohistochemical tests have proved invaluable in differentiating benign from malignant pleural effusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pleural diseases. 157 32

Total lactate dehydrogenase (LD; EC 1.1.1.27) and its five isoenzymes were determined in sera from (a) 98 cases of cirrhosis at various stages classified according to Child and Turcotte; (b) 37 cases of hepatocarcinoma (HC) at different stages of the Okuda classification; (c) 17 patients with secondary liver neoplasia (SLN), mainly from an abdominal primary site; and (d) 19 cases of abdominal neoplasia without liver metastasis, in an attempt to contribute to the differential diagnosis between these conditions. LD-4 was enhanced in SLN and LD-5 in HC, thus indicating the LD-4/LD-5 ratio as a potential index with which to differentiate between HC and SLN patients. At a cutoff value of 1.05, 91% of these patients were correctly classified (82% for SLN and 95% for HC). Consequently, this biochemical index appears to be an efficient and rapid indicator to distinguish HC from SLN. On the other hand, the LD isoenzymes are unable to discriminate between HC and cirrhosis or between abdominal neoplasia with and without liver metastases.
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PMID:Serum lactate dehydrogenase isoenzyme 4/5 ratio discriminates between hepatocarcinoma and secondary liver neoplasia. 165 Nov 82

One-hundred and thirty-three consecutive ascitic patients hospitalized in our Liver Unit were prospectively investigated, to define the accuracy of ascitic fluid analysis in identifying malignancy. Patients with extrahepatic cancer and peritoneal carcinomatosis were characterized by positive cytology and higher ascitic levels of fibronectin, lactic dehydrogenase, carcinoembryonic antigen, and total protein than both patients with uncomplicated cirrhosis and patients with cirrhosis and liver cancer. Ascitic cytology, fibronectin, and lactic dehydrogenase (LDH) were the most sensitive and specific markers of extrahepatic malignancy. In contrast, none of these markers was useful in identifying patients with primary liver cancer complicating cirrhosis. For them, the only alteration of the ascitic fluid was an elevated alpha-fetoprotein concentration. The sensitivity, specificity, and accuracy of ascitic alpha-fetoprotein for detecting liver cancer were 87%, 95%, and 94%, respectively. Combining cytology with the determinations of fibronectin (or LDH) and alpha-fetoprotein in ascitic fluid satisfactorily differentiated 28 of 32 cases of malignancy-related ascites, with very low incidence of false-positives (4-6%). Therefore, in view of the frequent difficulties in detecting liver cancer as a complication of cirrhosis in patients with ascites, it is advisable to determine all these three markers in the same ascitic sample.
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PMID:Utility of ascitic fluid analysis in patients with malignancy-related ascites. 169 Sep 13

The liver is an estrogen responsive organ. Clinically, estrogens may play a role in the induction of liver tumors and, experimentally, estrogens are involved in the control of hepatocyte proliferation. The results of a prospective controlled clinical trial using an anti-estrogen, tamoxifen, in patients with unresectable hepatocellular carcinoma (HCC) are presented below. Thirty-eight consecutive cirrhotics with HCC were allocated to either 30 mg/day tamoxifen or no treatment. The two groups of patients were matched for mean age, male/female ratio, Child-Pugh risk group, approximate tumor volume (US and/or CT scan) and etiology of the underlying cirrhosis. The drug appeared to have no side effects. Survival was significantly prolonged in tamoxifen-treated patients with 22% (vs. 5%) survival at 12 months. No differences were observed between males and females or alcoholic and non-alcoholic cirrhosis. In 53% of tamoxifen-treated patients the levels of alpha-fetoprotein dropped and, in this subgroup, survival was further prolonged. Tumor volume, lactate dehydrogenase (LDH) and alkaline phosphatase slowly increased, suggesting a slower, but continuous, progression of the disease. In conclusion, anti-estrogen treatment appears effective in the palliation of unresectable or otherwise untreatable HCC. A reduction in alpha-fetoprotein levels appears to be a favorable prognostic index.
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PMID:Unresectable hepatocellular carcinoma: a prospective controlled trial with tamoxifen. 170 74

An attempt was made to estimate noninvasively portal pressure (PP) in patients with chronic liver disease, using the theory of quantification, a kind of multivariate analysis. Forty-one patients with liver cirrhosis and 22 patients with chronic hepatitis in whom hepatic venous catheterization had been performed were studied. Seventeen parameters (age, sex, mean blood pressure, red blood cell count, platelet count, prothrombin time, lactate dehydrogenase, alkaline phosphatase, total bilirubin, albumin, gamma-globulin, indocyanine green retention at 15 min, blood urea nitrogen, hepatomegaly, splenomegaly, ascites and edema) were selected for the estimation of PP. The estimated PP correlated significantly with the data obtained by hepatic venous catheterization with a high correlation coefficient of 0.835 (p less than 0.01). An investigation using the theory of quantification was also undertaken to determine which of the 17 parameters selected above was most useful in estimating PP. Among the 17 parameters indocyanine green retention at 15 min, red blood cell count, prothrombin time, hepatomegaly and splenomegaly seemed to contribute significantly to the estimation of PP. When the formula was applied to 31 successive patients with chronic liver disease (external samples), the correlation between the estimated and measured PP was 0.455 (p less than 0.01). These results indicate that the formula is clinically useful in estimating PP in patients with chronic liver disease.
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PMID:[Estimation of portal pressure using the theory of quantification]. 201 41

We report the diagnostic, prognostic and therapeutic features of non-Hodgkin's lymphoma in eight patients in whom the disease was seen as a primary tumor of the liver. This series illustrates the variety of situations in which lymphoma might be diagnosed: (a) abdominal pain and hepatomegaly (three cases), (b) incidental finding at evaluation of a patient with cirrhosis (two cases), (c) secondary neoplasm after treatment for Hodgkin's disease (one case) and (d) complication of AIDS (two cases). In most cases, clinical and/or radiological features were nonspecific. However, the combination of the following features must be considered as suggestive: occurrence of an apparently primary hepatic tumor in an immunocompromised patient, absence of the usual serum tumor markers and increased serum lactic dehydrogenase activity. The final diagnosis was based on histological examination of specimens obtained by ultrasonically guided liver biopsies or at surgery. All cases belonged to unfavorable histological subtypes. Immunohistochemical findings on paraffin-embedded sections demonstrated the B-lymphocyte lineage of the seven tumors available for study. In the three patients without coexisting disease, complete remission was obtained by surgery alone or combined with chemotherapy. In the two patients with coexisting cirrhosis, outcome was rapidly unfavorable, with death occurring less than 3 mo after diagnosis. Among the three immunocompromised patients, two experienced a rapid unfavorable outcome, and the remaining one was in complete remission after surgery and chemotherapy. In conclusion, primary non-Hodgkin's lymphoma of the liver arising in patients without coexisting disease has a slow progression and might be successfully treated by surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-Hodgkin's lymphoma presenting as a primary tumor of the liver: presentation, diagnosis and outcome in eight patients. 202 91

To determine the course of hepatic recovery from subchronic oral administration of carbon tetrachloride (CCl4), male F-344 rats were gavaged with 0, 20, or 40 mg CCl4/kg, 5 days/week, for 12 weeks. Exposure to CCl4 caused dosage-dependent increases in relative liver weight and the serum levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, and cholesterol as well as a dosage-dependent decrease in hepatic cytochrome P450. Centrilobular hepatocellular vacuolar degeneration, necrosis, and cirrhosis occurred at both 20 and 40 mg/kg, with dosage-dependent severity. Reversibility of these reported effects varied with parameter. By Day 8 postexposure, necrosis had disappeared and all serum indicators and cytochrome P450 had returned to control levels. By Day 15 postexposure, the severity of the vacuolar degeneration had decreased. Reversibility of cirrhosis was dosage dependent; complete recovery occurred in the low- but not the high-dose group by Day 15. The disappearance of the increase in relative liver weight was also dependent on dosage; the low- but not the high-dose group had returned to the control level by Day 22. In an attempt to measure persistent hepatic damage, liver uptake relative to the spleen was determined for a sulfur colloid labeled with technetium-99m and for tritiated 2-deoxyglucose. Neither method consistently measured hepatic damage in cirrhotic livers due, in part, to the high degree of variability in the tracer uptake data.
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PMID:Assessment of hepatic indicators of subchronic carbon tetrachloride injury and recovery in rats. 225 19

Values for total lactate dehydrogenase (LD, EC 1.1.1.27) and LD isoenzyme-5 were determined in serum of 106 patients with benign hepatic disorders, 54 of whom had acute liver disorders, either acute hepatitis (39 patients) or acute circulatory disturbances (15 patients). Fifty-two had chronic hepatic disorders, either cirrhosis (25 patients) or chronic right heart failure (27 patients). Overall, values for LD were above normal for 86 percent of the 106 patients with benign hepatic disorders. In 83 percent of 30 patients with non-fulminant viral hepatitis, LD values were below 350 U per L, while in all nine patients with either fulminant viral or toxic hepatitis, and in all 15 patients with acute circulatory disturbances, LD values were above 500 U per L. In all 52 patients with chronic hepatic disorders, LD values were below 350 U per L. In patients with acute liver disorders, both the total LD and LD-5 proportions were sensitive for liver injury (87 percent and 91 percent, respectively). On the other hand, LD-5 proportion was much less sensitive than total LD in patients with chronic liver disorders (40 percent versus 85 percent). In conclusion, a difference was found in LD values and LD-5 ratios between patients with non-fulminant viral hepatitis and patients with other causes for acute liver injury. The LD-5 proportions are more sensitive for hepatic injury in patients with acute liver disorders than in those with chronic liver disorders.
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PMID:Alterations in total lactate dehydrogenase and its isoenzyme-5 in hepatic disorders. 240 42

The activity of dipeptidyl aminopeptidase IV was studied in the sera of 378 hospitalized patients. The mean activity of dipeptidyl aminopeptidase IV was elevated significantly in patients with neoplasmata and hepatitis, but not in patients with liver cirrhosis. Significant correlations (p less than 0.001) existed with gamma-glutamyl transferase, glutamate dehydrogenase, alkaline phosphatase and leucine aminopeptidase. A significant correlation with lactate dehydrogenase existed only in patients with neoplasmata. Principal component analysis, performed with aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, leucine aminopeptidase, lactate dehydrogenase and dipeptidyl aminopeptidase IV, revealed correlations between the activities of aspartate aminotransferase and alanine aminotransferase, and between alkaline phosphatase and leucine aminopeptidase, but neither dipeptidyl aminopeptidase IV nor lactate dehydrogenase showed any correlation with either of these two groups. In lectin affinity chromatography with concanavalin A and wheat germ lectin sepharose, serum dipeptidyl aminopeptidase IV from liver cirrhosis patients showed the same binding pattern as that from healthy subjects. The activity and glycosylation of dipeptidyl aminopeptidase IV in serum and hepatic plasma membranes was investigated in rats, following the induction of hepatitis with galactosamine. In the serum, dipeptidyl aminopeptidase IV activity was elevated as early as 6 h after galactosamine injection, and the elevated activity persisted until the 7th day. At the same time dipeptidyl aminopeptidase IV activity was also elevated in the hepatic plasma membrane. Ninety eight percent of hepatic dipeptidyl aminopeptidase IV bound to concanavalin A as well as to wheat germ lectin and this value was unchanged during hepatitis. In the serum of control rats, 90% of dipeptidyl aminopeptidase IV bound to concanavalin A but only 39% to wheat germ lectin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dipeptidyl aminopeptidase IV in hospitalized patients and in galactosamine hepatitis of the rat: Activity and lectin affinity chromatography in serum and hepatic plasma membranes]. 257 17


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