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)

A competitive enzyme immunoassay for the determination of human insulin-like growth factor I in microtiter plates was established. Using a polyclonal antiserum raised in rabbits against hIGF-I ovalbumin conjugate the assay system was able to detect IGF-I at a range of 12-800 pg/well with a sensitivity of 10 pg/well. It showed a low (< 0.5%) cross reactivity with hIGF-II. The serum concentrations of IGF-I found by EIA agreed well with those found in a conventional RIA (r = 0.965, p < 0.001). Effects of age and sex on IGF-I levels were studied in 260 normal adults. There was no evidence for sex differences but a steep decline of values from the third to the fourth and from the eight to the ninth decade, respectively. To asses the diagnostic capability of the IGF-I determination in liver cirrhosis, 71 sera of patients classified according to Child classes (A-C) were measured. Although significantly diminished concentrations were found in class B vs A and in class C vs B, the diagnostic sensitivity in cross-sectional examinations proved to be low (class A: 0.33, class B: 0.67). Only in the case of extensively destroyed liver parenchyma (Child C: 0.94) IGF-I was a good indicator of impaired hepatocellular capacity. In 29 patients with acromegaly serum IGF-I levels were investigated. All patients with active acromegaly showed increased IGF-I levels. In contrast, in inactive or weakly active acromegaly values were considerably lower.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Measurement of insulin-like growth factor I (IGF-I) in normal adults, patients with liver cirrhosis and acromegaly: experience with a new competitive enzyme immunoassay. 822 82

Current EIA for PIVKA-II is not sensitive enough to detect small Hepatocellular Carcinoma (HCC). In an attempt to increase the diagnostic threshold, the current EIA was modified in two different ways: 1) immunoreaction of PIVKA-II in the sample with its monoclonal antibody was carried out overnight at 5 degrees C instead of for two hours at room temperature (the overnight method), 2) Avidin-Biotin technique was used for the second reaction(the ABC method);and their diagnostic values were determined as compared with the current EIA(2hr method) in a total of 138 patients including 36 patients with HCC. In 27 patients with HCC(< 3 cm in diameter), the rates of abnormal values obtained by the 2hr-, the overnight- and the ABC method were 14.8, 25.9 and 29.6% respectively. False positive rates of these three methods in 69 patients with liver cirrhosis were 1.4, 8.6 and 22.9% respectively. Thus, these two modifications improved the sensitivity of the current EIA and the overnight method appears to be superior to the ABC method in terms of specificity and simplicity. This conclusion was confirmed by ROC analysis.
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PMID:[Determination of PIVKA-II levels in patients with small hepatocellular carcinoma--comparison of new sensitive methods]. 874 93

Plasma iPGE2 and i6-keto PGF1 alpha were measured with an EIA assay in twenty patients with alcohol-related liver cirrhosis (ALC group) and 13 patients with hepatitis B virus as an etiologic factor of liver cirrhosis (HLC group). Significant increase of both prostanoids was observed irrespectively of the etiology of liver cirrhosis. Their levels increased depending on the degree of liver insufficiency with the highest values in patients classified as Child-Pugh C class. A significant, positive correlation with Child-Pugh score was found regarding PGE2 (r = 0.657; p < 0.001) as well as 6-keto PGF1 alpha (r = 0.736; p < 0.001). Correlation (r = 0.789; p < 0.001) was also observed between levels of both prostaglandins. In conclusion we have shown that plasma iPGE2 and i6-keto PGF1 alpha arise simultaneously with the degree of liver insufficiency, that can be a result of activation of non-parenchymal liver cells accompanying hepatic fibrosis.
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PMID:Plasma iPGE2 and i6-keto PGF1 alpha in the course of liver cirrhosis. 906 63

To investigate the prevalence and profile of chronic liver disease due to hepatitis B (HBV) and C (HCV) infection in patients with non-alcoholic chronic liver disease in North India, 148 biopsy proven patients (73 with a history of transfusion and 75 non-transfused) were studied. Detection of hepatitis B included HBsAg, AntiHBc, and HBV DNA testing. Presence of HCV infection was investigated by EIA using second generation tests and confirmed by RIBA III and HCV RNA testing. Eighty three (56.1%) patients had cirrhosis related to hepatitis B, 13 (15.7%) of them had precore (HBeAg -ve, HBVDNA +ve) and 11 (13%) had surface (HBsAg-ve, IgM antiHBc-ve, HBVDNA +ve) mutation. Antibodies to HCV were found in 16 (10.8%) patients. Dual infection with HBV and HCV was seen in 20 (13.5%) patients. Twenty nine (19.5%) patients, had cryptogenic cirrhosis as none of the markers for HBV or HCV infection was positive. In conclusion, our results demonstrate that HBV was the most prevalent viral infection associated with chronic liver disease patients in North India. Prevalence of HCV infection was low. Studies to detect HBV mutants and other viruses should be done in patients with suspected cryptogenic cirrhosis of the liver.
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PMID:Low prevalence of hepatitis C viral infection in patients with non-alcoholic chronic liver disease in India. 925 93

We describe a 73-year-old woman who presented with purpura, recurrent ulcerations of both lower limbs as well as worsening of her condition. Laboratory tests revealed a mixed cryoglobulinemia (type-II). Two years after diagnosis, an amputation of the right femur had been performed due to extensive necrotizing ulcerations. Further complications such as membranoproliferative glomerulonephritis, cirrhosis of the liver with portal hypertension and ultimately, hepatocellular carcinoma developed. A chronic hepatitis C infection was diagnosed rather late, mainly because of the false negative results of the first generation EIA. This case report illustrates the various complications-hepatic and extrahepatic-of chronic hepatitis C infection. The pathogenesis of mixed cryoglobulinemia remains unclear. However, a current literature review suggests a strong association with chronic hepatitic C. Diagnosis, clinical features and course of hepatitis C infection are discussed.
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PMID:[A patient with cryoglobulinemia and hepatitis C]. 943 96

Risk factors for hepatitis C infection include I.V. drug use (42%); history of blood transfusion (6%); exposure to multiple heterosexual partners (6%); exposure to a household contact (3%); health care employment (2%); or hemodialysis (1%). Forty percent of patients have no identifiable risk factors. The HCV is a single-stranded, positive-sense RNA virus. Six major genotypes have been identified; each contains a series of subtypes. In the U.S., prevalences are type 1 (74%); type 2 (15%); type 3 (6%); and type 4 (1%). Within an infected individual, HCV also exists as a spectrum of closely related genotypes referred to as a quasispecies, and more complex quasispecies correlate with longer duration of disease, higher levels of viremia, genotype 1 infection, and poorer response to interferon therapy. Diagnosis is made by measuring anti-HCV by EIA, with confirmation by RIBA or HCV RNA. Patients with chronic HCV infection, with or without aminotransferase elevation, have detectable serum RNA by PCR. Standard therapy is interferon alfa 2b (Intron A) at a dosage of 3 million units 3 times a week for 6 months. This results in a 40%-50% complete response at the end of treatment (normal aminotransferases and undetectable HCV RNA), but relapse occurs in 60%-80% of cases over the next six months. Longer (12 month to 18 month) courses are now widely advocated. Better patient selection, e.g., those with low serum HCV RNA levels and absence of cirrhosis, and increased duration of therapy may lead to better response rates. Combination therapy with other antiviral agents, such as ribavirin, has dramatically reduced relapse rates.
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PMID:Hepatitis C: controversies, strategies and challenges. 1002 68

To evaluate the clinical feasibility of the antibody titer against a chimeric polypeptide (named Core 518), in which a domain of Core and NS3 of hepatitis C virus (HCV) was fused, ELISA was performed in a total of 76 serum samples. Each serum was serially diluted using two-fold dilution method with distilled water into 10 concentrations. They were all positive for second generation anti-HCV assay (HCV EIA II; Abbott Laboratories). Genotyping RT-PCR, quantitative competitive RT-PCR, and RIBA (Lucky Confirm; LG Biotech) were also assayed. Anti-Core 518 antibody was detected in x 12800 or higher dilutions of sera from 35 of 43 chronic hepatitis C (81.4%) and nine of 16 hepatocellular carcinoma sera (56.3%), one of four cirrhosis (25%), 0 of four acute hepatitis C, and one of nine healthy isolated anti-HCV-positive subjects (p=0.0000). The anti-Core 518 antibody titers were well correlated with the presence of HCV RNA in serum (p=0.002). The anti-Core 518 antibody titers decreased significantly in nine of ten responders to IFN-alpha treatment. Monitoring anti-Core 518 titers may be helpful not only for differentiating the status of HCV infection among patients with various type C viral liver diseases, but also for predicting responses to IFN-alpha treatment.
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PMID:Monitoring antibody titers to recombinant Core-NS3 fusion polypeptide is useful for evaluating hepatitis C virus infection and responses to interferon-alpha therapy. 1033 62

The discovery of hepatitis C was the direct result of the landmark discoveries of hepatitis B virus (HBV) and hepatitis A virus (HAV) and their serologies. Screening tests for HAV and HBV made it possible in the mid-1970s to examine cases of transfusion-associated hepatitis (TAH) and to demonstrate that only approximately 25% resulted from HBV and that none were related to HAV. Consequently, approximately 75% of TAH became classified as non-A, non-B hepatitis (NANBH). Subsequently, chimpanzee studies demonstrated that NANBH was a result of a transmissible agent Although it has been difficult to convince clinicians that NANBH was a serious disease because the overt manifestations are generally mild, it gradually became apparent that the NANBH agent often resulted in chronic hepatitis and sometimes evolved into cirrhosis. The NANBH agent remained a virologic enigma for the next decade until researchers at the Chiron Corporation used an ambitious molecular approach on large volumes of high-titer infectious chimpanzee plasma from the Centers for Disease Control and Prevention (CDC). They extracted RNA, cloned it into an expression vector, and screened the expressed product with presumed immune sera. A single positive clone was found in the millions screened, and, within a year, the entire genome was sequenced and the agent was identified as a novel flavivirus--the hepatitis C virus (HCV). Retrospective analysis of pedigreed samples at the National Institute of Health (NIH) showed that 70% to 90% of NANBH cases were HCV related. The impact of HCV blood donor screening has been enormous. The single-antigen first-generation enzyme immunoassay (EIA-1) prevented 40,000 HCV infections within the first year, and the second-generation assay (EIA-2) has actually reduced new transfusion-related HCV infections to almost zero.
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PMID:Discovery of non-A, non-B hepatitis and identification of its etiology. 1065 50

The aim of the study was to evaluate epidemiology and clinical course of HCV infection in children and adolescents with end-stage renal disease. The study involved 70 patients, aged 1-25 years, 31 M, 39 F: group of 40 dialysed (27 HD, 13 CAPD) and 30 patients suffering from different chronic renal disease as a control group. Anti-HCV antibodies were assayed by EIA 3rd gene (Abbott Diagnostic) and were sought by LIATEK HCV 3rd gene. HCv RNA was detected and measured by a standardised HCV RNA PCR assay (Amplicor Roche). HCV genotypes were identified by InnoLIPA (Innogenetics). HCV infection was diagnosed in 20 (50%) dialysed and in 3 (10%) non-dialysed patients. None of the HCV infected patients presented the clinical symptoms of hepatitis; the mild activity of ALT was observed in 8 cases only. HCV viremia was relatively low: 365 x 103 copies/mL in PD and 110,9 x 103 copies/mL in HD patients. 3 genotypes of HCV were identified: 1a, 1b and 4c/4d. In 3 cases liver biopsy was performed, no cirrhosis was diagnosed.
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PMID:[Epidemiology and clinical course of HCV infection in children and adolescents with chronic renal failure]. 1089 36

Carcinoembryonic antigen (CEA) is an oncofoetal protein first identified by Gold and Freedman (1965) in colorectal cancer. It is a cell surface tumor marker which has been characterised as a heterogenous group of glycoproteins. It is also present in a variety of benign and non-neoplastic diseases like ulcerative colitis, Adenomatous polyp, Liver cirrhosis and other cancers like GI tract tumors, Cancer of the breast, lung, ovary, pancreas, prostate, hepatoma etc. Elevated CEA levels serve as clinical tool in the diagnosis, monitoring, detecting early any recurrence or metastasis and in prognostication for confirmed colorectal cancers. In order to develop an Enzyme Immuno Assay and immunocytochemical assay for CEA, an MAb designated as CIBCHTB1 has been generated using CEA isolated from a cell line HT115, human adenocarcinoma of the colon, as immunogen by the conventional Hybridoma technology. This MAb of IgG1 isotope was selected by screening of culture supernatents by ELISA and then by its high binding affinity with HT115 cells as revealed by flowcytometric analysis. By ABC method of immunocytochemical assay, this Ab exhibited strong staining of cells in frozen tissue sections of normal colon and malignant colorectal lesions and various other types of human cancers. This MAb has useful application to study the expression of CEA in human cancers. Serum CEA levels of patients with colorectal cancers and other CEA producing cancers and controls determined by EIA using this MAb were in good correlation with the results obtained using commercial kit. The diagnostic potential of this Mab in the management of colorectal cancers is discussed.
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PMID:Monoclonal antibody CIBCHTB1 defining an epitope on carcinoembryonic antigen (CEA). 1134 Nov 76


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