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)

Pre S2 was investigated using a monoclonal ELISA in 100 samples from 52 patients with different forms of infection with Hepatitis B virus. Pre S2 was present in 18 of 19 patients with acute hepatitis. Its persistence for more than 150 days after beginning of symptoms was associated to a chronic hepatitis state. It was also present in 11 patients with chronic hepatitis or cirrhosis, 15 asymptomatic Hepatitis B carriers and 3 of 4 patients with hepatic carcinoma. Pre S2 became negative in only 1 of 3 patients treated with interferon who had a positive response according to HBe and HBs antigens. Thus, Pre S2 is present in patients with evidence of viral replication. It is more a marker of persistent Hepatitis B infection than of chronic liver damage.
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PMID:[Pre S2: a marker for chronicity and/or liver damage in hepatitis B infection?]. 134 Sep 59

The results of 8936 abdominal ultrasonographies were analysed. Primary hepatic cancer was detected in 27 (0.3%) patients of whom 8 (28.6%) showed concomitant chronic hepatitis or cirrhosis. Ultrasonographic signs of primary carcinoma as well as their clinical features were evaluated. The reliability of ultrasonography proved 85.7% which assures better treatment and ability assessment.
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PMID:[Echography in primary malignant liver tumor in clinical and practical medical disability expertise]. 134 65

Phenotypic expression of sialylated Lewis(x) antigen by means of the monoclonal antiserum SNH3 was studied in 87 livers, which included normal and steatotic livers and livers with chronic persistent and chronic active hepatitis, alcoholic hepatitis, allograft rejection, focal nodular hyperplasia, hepatocellular carcinoma, cholangiocarcinoma, metastatic carcinoma, cirrhosis of various causes (autoimmune, alcoholic, viral, drug induced, Wilson's disease, and primary biliary cirrhosis). The biotin-streptavidin-peroxidase method was used on formaldehyde-fixed, paraffin-embedded sections. Sialylated Lewis(x) antigen was not demonstrated in normal livers. Hepatocellular expression in a diffuse or perinodular honeycomb pattern was seen in cirrhosis, irrespective of cause. Sialylated Lewis(x) antigen was also observed in hepatocytes around metastatic carcinoma in the absence of inflammation, cirrhosis, or regeneration. Some bile ductules, most likely ductular hepatocytes, but not bile ducts, expressed sialylated Lewis(x) antigen. Sialylated Lewis(x) antigen was seen diffusely in fibrolamellar hepatocellular carcinoma, focally in other hepatocellular carcinomas, and either focally or diffusely in cholangiocarcinomas.
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PMID:Expression of sialylated Lewis(x) antigen in chronic and neoplastic liver diseases. 135 99

In every patient, in particular males of all ages presenting with chronically progressive diseases or cirrhosis of the liver, ultrasonography and an AFP test should be performed at intervals of six months. If hepatocellular carcinoma of the liver (HCC) is suspected (i.e. by increase of AFP or a positive result in ultrasonography), diagnosis should be confirmed by further investigations such as fine-needle biopsy guided by sonography, angiography and CT-scan. Adequate therapeutical measures such as resection of the tumor, chemotherapy, injection of alcohol or liver transplantation can thus be initiated in time. Besides efforts for early diagnosis of carcinoma of the liver, preventive measures (vaccination for hepatitis B, restrictive use of blood transfusion, reduction of alcoholism, thorough therapy of hemochromatosis, etc.) may contribute to the reduction of chronic diseases of the liver and of associated HCC.
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PMID:[Early diagnosis of hepatocellular carcinoma]. 137 85

We measured blood platelet count and plasma beta-thromboglobulin concentration in 67 patients with acute or chronic liver diseases. Plasma TXB2 and 6-keto-PGF1a concentration were also measured in these patients. The results showed that blood platelet count of less than 100 x 10(9)/L was found in 14% of the patients with acute hepatitis, 23% with chronic hepatitis, 67% with hepatic cirrhosis but without splenectomy and 40% with primary liver carcinoma. Platelet count is lowest in patients with hepatic cirrhosis without splenectomy but normal in patients with hepatic cirrhosis after splenectomy. Plasma beta-TG concentration increased in patients with acute or chronic liver diseases. A negative correlation was found between beta-TG concentration and platelet count in chronic liver diseases. It is suggested that platelet is in activated state in vivo and this may be one of the important reasons for both decrease of platelet count and impairment of platelet function. Plasma TXB2 concentration increased in chronic liver diseases, while plasma 6-keto-PGF1a concentration decreased. The balance between TXA2 and PGI2 is upset; this may be an important mechanism for activation of platelets in vivo.
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PMID:[Studies on plasma beta-thromboglobulin, thromboxane A2, prostaglandin I2 concentration and platelet count in liver diseases]. 139 19

Intrahepatic impedance was measured using a special electrode in 44 patients, 38 of whom identified abnormalities of the hepatic parenchyma. Impedance values were compared with ultrasound findings and with the histological results of needle biopsy. Impedance was relatively unaffected in the presence of cirrhosis (n = 7) or chronic hepatitis (n = 5). It was markedly decreased in the presence of cysts (n = 4) and of hepatocarcinoma (n = 4). Values were variable in secondary carcinoma of the liver (n = 16). This preliminary study suggests that the measurement of intrahepatic impedance could contribute to the etiological diagnosis of hepatic tumour lesions.
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PMID:[Measurement of impedance of hepatic tissue transformed by pathological process. A preliminary communication]. 144 80

The therapeutic effects of interferon alpha-2b (Intron A; Scherag) in patients with chronic active hepatitis caused by hepatitis B virus (HBV) were assessed in a randomised, case-controlled clinical trial conducted between January 1988 and June 1990. Treatment involved a short course of prednisone followed by interferon alpha-2b, initially 10 million U by subcutaneous injection, 3 times a week for 16 weeks. All patients were symptomatic, were known to have had hepatitis B surface antigen and hepatitis B e antigen (HBeAg) in their blood for at least 6 months, and had elevated serum aminotransferase activities with histological evidence of chronic active hepatitis. Patients with carcinoma, renal or haematological abnormalities or decompensated cirrhosis were excluded. In 6 of 10 patients randomised to receive interferon and 1 of 10 controls, HBeAg and HBV DNA were cleared from the blood during the 12-month study period (P < 0.05). An indeterminate response with clearance of HBV DNA but persistence of HBeAg was noted in 1 patient receiving interferon. Serum aminotransferase levels decreased only in those patients who had responded to treatment, but this did not reach statistical significance for the group as a whole. Histological studies, where available, showed decreased hepatic periportal necrosis in patients who underwent treatment. Two patients relapsed to HBeAg-positive status 2 months after their initial seroconversion; 1 became clear again during a repeat course of interferon. Side-effects of treatment were common and included fever, malaise, myalgias and myelosuppression. One patient developed hypothyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of interferon alpha-2b following prednisone withdrawal in the treatment of chronic viral hepatitis B. A case-controlled, randomised study. 144 11

To base the clinico-pathogenetic nonuniformity of cholestasis in different liver diseases, 135 patients distributed into groups were examined. Group I was made up of 48 patients with chronic persistent hepatitis, group II of 34 patients with chronic active hepatitis, group III of 29 patients with liver cirrhosis, and group IV of 24 patients with primary and metastatic liver carcinoma. The data obtained suggest the existence of different forms of cholestasis: multicomponent cholestasis, partial bilirubin cholestasis, partial choleacid cholestasis. In the group I patients, the incidence of cholestasis was 8.3%, in group II 2.9%, in group III 3.4%. The incidence of partial choleacid cholestasis was 4.2% in group I, 2.9% in group II, and 6.9% in group III. The presence of partial cholestasis may be caused by the impairment of the assumed "personal" carrier for different bile components.
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PMID:[The clinico-pathogenetic variants of cholestasis in different liver diseases]. 150 86

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

In Italy, a dramatic decline of hepatitis B infection occurred in recent years as a result of nonmedical and medical factors. The national type-specific surveillance system shows that the age of maximum incidence changed from early childhood, when the risk of becoming a chronic carrier after infection is very high, to late adolescence. Data of several seroepidemiologic studies are consistent with this picture, but could not be compared with previous data on similar age groups. In 1981, a seroepidemiologic study on a national sample of 5,005 recruits showed a high prevalence of serologic markers of hepatitis B infection among young adults in Italy. In 1990, the authors replicated that original study on a national sample of 4,993 recruits. The adjusted prevalence of hepatitis B core antibodies among Italian male recruits dropped from 16.8% to 5.8% in 9 years. The authors anticipate a substantial reduction in the rate of production of chronic carriers and the rates of liver cirrhosis and primary liver carcinoma in Italy in the next decades. Vaccination campaigns, especially if combined with nonimmunologic preventive measures, will further reduce the rate of hepatitis B infection in Italy.
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PMID:Changing epidemiology of hepatitis B in Italy: public health implications. 159 87


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