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 a survey of the prevalence of chronic hepatitis B in a male homosexual population, liver biopsies were done in 28 asymptomatic patients who had persistently raised aminotransferases. Four patients had active cirrhosis (AC), 13 had chronic active hepatitis (CAH) of various degrees of severity and 11 had either chronic persistent hepatitis (CPH) or minor changes of the type seen in hepatitis B virus carriers. Core associated antigens and surface antigen, were demonstrated by the PAP immunoperoxidase method in 20 cases. Core and surface antigens tended to be present in the same areas of the biopsy and quantitation showed higher core to surface antigen ratios in CAH than in CPH, the difference being statistically significant. In seven cases no core-associated antigens were demonstrated in the presence of surface antigen: most of these patients had either inactive disease or active cirrhosis. In one carrier neither antigen was demonstrated. Ten patients had two or more biopsies. Four of these had no treatment and the amounts of core and surface positive cells in the liver did not increase. Six were treated with immunosuppressants. This did not alter the degree of either inflammation or fibrosis. but the number of surface and core antigen positive cells in the liver was higher after treatment in almost every case.
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PMID:Histopathology and localization of viral antigens in the liver of HBsAg positive homosexuals. 731 81

Hepatitis B virus (HBV) DNA and its 5 antigens were studied in 225 cases of paraffin-embedded sections of human liver cirrhosis obtained by biopsy. HBxAg, pre-S1 and pre-S2 antigens were detected by immunohistochemical ABC method, HBsAg and HBcAg by PAP method. HBV DNA by in situ hybridization, and both HBV DNA and HBsAg, HBxAg or HBcAg by double labelling technique of immunohistochemistry and in situ hybridization respectively. The results showed that the positive rates were 70.0% (128/183) for HBsAg, 64.4% (85/132) for pre-S1 antigen, 61.4% (81/132) for pre-S2 antigen, 75.3% (113/150) for HBxAg, 22.4% (39/174) for HBcAg and 62.4% (58/93) for HBV DNA respectively. The double labelling positive rates were 37.3% (19/51) for both HBV DNA and HBsAg, 86.3% (44/51) for both HBV DNA and HBxAg and 39.2% (20/51) for both HBV DNA and HBcAg respectively. More than 80% of the cases with positive sections for HBV DNA and its 5 antigens were associated with liver cell dysplasia (LCD). The results of this study suggest that the occurrence and development of liver cirrhosis were closely related to chronic infection of HBV in China.
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PMID:[Expression and significance of HBV DNA and its 5 antigens in liver cirrhosis]. 778 Nov 8

Glomerulonephritis demonstrable by immunohistochemistry may be present at post mortem in many patients without overt renal diseases. Systematic renal biopsies in severely hypertensive patients have shown a high prevalence of clinically undiagnosed glomerulonephritis. We have examined the kidneys of 423 consecutive subjects who came to post mortem and full-filled criteria for the diagnosis of hypertension. Patients were considered to be hypertensive if this had been clinically documented during life or if the heart weight/body weight ratio was > 0.005 in the absence of known other causes of cardiac hypertrophy. Normotensive controls were selected on the basis of clinically documented normal BP or a heart weight/body weight ratio of < 0.001. Kidneys were examined by immunohistology (PAP technique using human IgA, IgG, IgM antibodies). Excluding cases with liver cirrhosis, only two of the 337 patients with hypertension (= 0.6%) and none of the 49 normotensive patients had mesangial IgA deposits (P = 0.77). This finding argues against the frequent occurrence of latent glomerulonephritis in elderly patients with manifest hypertension.
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PMID:Prevalence of immunecomplex-associated glomerulonephritis in hypertensive subjects. 800 18

Surgical specimens of 20 cases of human intrahepatic cholangiocarcinoma (n = 12) and cholangiohepatocarcinoma (n = 8) were studied immunohistochemically by ABC technique for HBxAg, pre-S1 and pre-S2 and by PAP method for HBsAg and HBcAg. The neighboring liver tissues with chronic hepatitis or cirrhosis surrounding the tumor were also examined in 19 cases. Of the cancerous tissues, 15 were positive for HBxAg (75%), 8 positive for pre-S1 and pre-S2 (40%), respectively and 2 for HBsAg (10%). Sixteen of 19 liver tissues surrounding the tumor were also positive for HBxAg (84.2%), 9 for pre-S1 and pre-S2 each (47.4%), 6 for HBsAg and HBcAg each (31.6%). The results suggest that a close relationship exists between cholangiocarcinoma and cholangiohepatocarcinoma and hepatitis B virus infection. The HBxAg might play an important role in the pathogenesis of cholangiocarcinoma.
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PMID:[Expression of five different antigens of HBV in human intrahepatic cholangiocarcinoma and cholangiohepatocarcinoma]. 817 60

Pancreatitis-associated protein I (PAP I) is a secretory protein first described as an acute phase reactant during acute pancreatitis. Recently, induction of the PAP I gene was also described in liver during hepatocarcinogenesis. To investigate the molecular mechanisms of this induction, we used constructs carrying progressive deletions of the PAP I promoter fused to the CAT gene. We showed that the silencer conferring tissue specificity on the PAP I gene was inactive in hepatoma cells. Then, in an vitro transcription system, we compared the transcription capacity of nuclear extracts from normal liver and HepG2 cells on constructs containing the silencer. The results confirmed that a trans-acting factor interacting with the PAP I silencer was present in liver cells and absent from hepatoma cells. On the other hand, immunohistochemistry showed that PAP I was expressed in a limited number of transformed hepatocytes. It was concluded that expression of PAP I in hepatocarcinoma occurred through inactivation of its silencer element and was not concomitant in all malignant cells. On that basis, we assayed PAP I in serum from patients with chronic hepatitis, liver cirrhosis or hepatocarcinoma. PAP I levels were normal in chronic active or persistent hepatitis, significantly higher in cirrhosis and strongly elevated in hepatocarcinoma. Because those clinical entities often develop in that sequence, serum PAP I appeared as a potential marker of hepatocarcinoma development.
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PMID:Mechanism of PAP I gene induction during hepatocarcinogenesis: clinical implications. 895 91

PAP Immunohistochemical technique was used to detect the expression and distribution of EGF-R in gastric mucosa in portal hypertensive pigs with cirrhosis. Our result showed that the EGF-R content in gastric mucosa of portal hypertensive pigs was significantly lower than that in control group. Microscopically, the portal hypertension (PHT) group imparted "feeble positivity" or "negative results" and the control group showed "strong positivity". It was suggested that the decrease of EGF-R content in gastric mucosa weakened defense mechanism of gastric mucosa and increase its vulnerability. It is believed that the decreased EGF-R in gastric mucosa is ascribed to the lesions of gastric mucosa during PHT with cirrhosis.
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PMID:Immunohistochemical analysis of EGF-R in gastric mucosa in portal hypertensive with cirrhosis. 981 87

Hepatocarcinoma-intestine-pancreas/pancreatic associated protein (HIP/PAP) gene was identified because of its increased expression in 25% of human hepatocellular carcinoma. HIP/PAP protein, a C-type lectin, binds laminin, acts as an adhesion molecule for hepatocytes, and has also been described as an acute phase secretory protein during acute pancreatitis in humans and rats. We investigated HIP/PAP protein expression in patients with various liver diseases associated with ductular reaction. At the same time, we analyzed patients with hepatocellular carcinoma and cholangiocarcinoma, and tested HIP/PAP protein levels in sera to establish the pattern of secretion. Our data show that HIP/PAP expression was not restricted to hepatocellular carcinoma, but was also detected in cholangiocarcinoma cells as well as in reactive non-malignant bile ductules. In contrast, HIP/PAP protein expression was undetectable in normal mature hepatocytes, but some ductular cells localized at the interface of portal tracts with parenchyma were HIP/PAP immunoreactive in normal liver. Finally, we present evidence that HIP/PAP serum levels were increased in 21/28 (75%) patients with hepatocellular carcinoma, and in 25/51 (49%) patients with nonmalignant cirrhosis. Altogether, these results suggest that HIP/PAP protein may be implicated in hepatocytic and cholangiolar differentiation and proliferation.
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PMID:Hepatocarcinoma-intestine-pancreas/pancreatic associated protein (HIP/PAP) is expressed and secreted by proliferating ductules as well as by hepatocarcinoma and cholangiocarcinoma cells. 1055 Mar 9

AIM:To investigate the expression of integrins in rats liver during 3'-Me -DAB induced hepatocarcinogenesis and to find out the relationship between integrins and liver cancer metastasis.METHODS:The expressions of integrins alpha(1), alpha(2), alpha(3) and alpha(5) and epidermal keratin (EK) were observed by immunohisto chemical PAP method.RESULTS:In the normal liver tissues, hepatocytes express integrins alpha(1) and alpha(5) and in the bile duct epithlium, EK. In liver cirrhosis, hepatocytes highly express integrins alpha(1), alpha(2), alpha(3) and alpha5and in hyperplastic bile duct epithelium, integrins alpha(1), alpha(5) and EK. Expression of integrins alpha(1), alpha(2), alpha(3) and alpha(5) were obviously decreased in the preneoplastic nodules and primary carcinoma but expressions of integrins alpha(1) and alpha(5) in metastasis in the lung and diaphragma were higher than those in primary carcinoma.CONCLUSION:Integrins alpha(1) and alpha(5) may play a major role in chemically induced hepatocarcinogenesis and metastasis in rats.
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PMID:Changes of integrin expression in rat hepatocarcinogenesis induced by 3'-Me-DAB. 1181 63


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