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Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The immunohistochemical detection of the c-erbB-2 oncopeptide (p185erbB2) has been shown to be a valid marker for over-expression of this oncogene. To evaluate the possible relevance of gene expression to the proliferation of hepatocytes and bile ducts in human disease, the authors applied a monoclonal anti-p185 antibody to formalin-fixed, paraffin-embedded tissues from 67 examples of benign proliferative and neoplastic hepatic lesions and fetal liver. Focal membrane-based reactivity for the oncopeptide was detected on tumor cells in two of eight hepatocellular carcinomas and on tumor cells and adjacent bile ducts and hepatocytes in four of six cholangiocarcinomas. Each of the latter four lesions were in patients with primary sclerosing cholangitis. No reactivity was obtained in examples of hepatoblastoma, mixed cholangiocarcinoma-hepatocellular carcinoma, bile duct adenoma, or hepatocellular adenoma. Weak staining for p185erbB2 also was seen in two of seven cases of (sub)massive hepatic necrosis and two examples of postnecrotic
cirrhosis
, all of which were secondary to either hepatitis B or C
virus infection
. No other benign proliferative lesions were labeled by the anti-p185 antibody, including cases of chronic allograft rejection, necrosis secondary to hepatic artery thrombosis, metabolic-associated and nonmetabolic-associated
cirrhosis
, focal nodular hyperplasia, and nodular regenerative hyperplasia. The authors' results indicate that c-erbB-2 may be amplified in specific neoplastic and hepatitis B virus and hepatitis C virus infectious lesions of liver. The authors postulate that: (1) c-erbB-2 immunoreactivity may be a marker for malignant transformation in primary sclerosing cholangitis; and 2) overproduction of p185erbB2 may be an epiphenomenon of hepatitis B virus or hepatitis C
virus infection
.
...
PMID:Immunoreactivity for c-erbB-2 oncopeptide in benign and malignant diseases of the liver. 137 19
A cDNA fragment encompassing the 5'-terminal half of the NS1 region of the hepatitis C virus (HCV) genome was cloned. The cDNA was expressed in insect cells using a recombinant baculovirus, and a protein band of approximately 21K was identified by immunoblotting with a serum sample from a patient with chronic hepatitis C. Antibody to the protein was detected in sera from 13.4% of patients with chronic non-A, non-B hepatitis (NANBH), 20.8% of patients with
liver cirrhosis
and 16.8% of patients with hepatocellular carcinoma with no serum markers for hepatitis B
virus infection
. However, the antibody was not detected in sera from patients with acute NANBH. The prevalence of antibody to the protein encoded by the NS1 region was lower than that of antibody to the HCV core protein, but much higher than that of antibody to the envelope protein. Thus, the NS1 region of the HCV genome is suggested to encode a protein produced during the course of HCV replication.
...
PMID:Expression of the amino-terminal half of the NS1 region of the hepatitis C virus genome and detection of an antibody to the expressed protein in patients with liver diseases. 137 27
269 orthotopic liver transplantations (OLT) were performed in 253 patients at our institution from September 1988 to May 1992. 121 patients had end-stage
cirrhosis
secondary to viral hepatitis type B, delta, or type non-A non-B and C respectively. Reinfection of the graft by persistent viruses is a potential complication in these cases. Passive immunization with anti-HBs hyperimmunoglobulin (HIg) can prevent clinically relevant reinfection of the graft in patients with hepatitis B virus (HBV) infection and low replication rates. Patients with high replication rates will rarely benefit from OLT. Patients with hepatitis delta virus (HDV) infection usually experience HDV reinfection of the graft with subsequent chronic hepatitis although prophylaxis with anti-HBs-HIg was performed. Treatment with interferon alpha had no apparent effect on the incidence of graft reinfection with HBV in this series, but the replication rate of HDV was reduced. Persistent hepatitis C viruses (HCV) usually infect the graft; this was demonstrated in 17 patients by means of the polymerase chain reaction. HCV infection usually causes a mild form of acute hepatitis with transition to a chronic course. Therefore the significance of persistent
viral infection
lies in the potential for chronic hepatitis in the transplanted organ rather than in the danger of acute injury of the allograft.
...
PMID:[Orthotopic liver transplantation in hepatic cirrhosis: on the problem of infection of the transplant with persistent hepatitis viruses]. 144 5
Hemodialyzed patients and kidney recipients are frequently multiply-transfused and infected by hepatitis B virus (HBV). Hepatitis delta virus (HDV) has a symbiotic association with HBV. The prevalence of HDV infection has, surprisingly, not been assessed in patients in hemodialysis or renal transplantation setting. We retrospectively studied the prevalence of serum delta antigen and antidelta antibodies by a microenzyme-linked immunosorbent assay in 77 of the 80 HBsAg-positive patients who underwent a kidney transplantation over a 10-year period. Of these patients, 73% had active HBV replication as assessed by the presence of serum HBV DNA and 65% had a biopsy-proved chronic active hepatitis, including
cirrhosis
. None of our patients had any marker of HDV infection at the end of the hemodialysis period or at the end of follow-up in transplantation. These results establish that HDV superinfection has indeed been extremely rare during end-stage renal failure and kidney transplantation in France, in contrast to HBV reactivation or hepatitis C
virus infection
.
...
PMID:Absence of hepatitis delta virus infection in chronic hemodialysis and kidney transplant patients in france. 146 75
We evaluated the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in 78 Italian patients with hereditary hemochromatosis as well as the relation between HCV antibody (anti-HCV) status, hepatitis B surface antigen (HBsAg) and liver histology. None of the patients had been transfused or ever consumed more than 60 g of alcohol per day. Eighteen showed histological signs of chronic hepatitis, active
cirrhosis
was present in 12, chronic active hepatitis in 4 and chronic persistent hepatitis in 2. Liver fibrosis or
cirrhosis
without inflammatory activity was observed in 31 subjects, whereas liver histology was normal except for iron overload in 18. The prevalence of HBsAg in the whole series was 5% and of anti-HCV was 20.5%. The prevalence of HBsAg and anti-HCV was significantly higher in the chronic hepatitis group than in the fibrosis/
cirrhosis
(p = 0.01) and the normal groups (p < 0.01). Fourteen of 18 hereditary hemochromatosis patients with chronic hepatitis were HBsAg (4) or anti-HCV (10) positive and all the latter subgroup had HCV-RNA in their serum as shown by the polymerase chain reaction. Although most of the patients with associated chronic hepatitis had
cirrhosis
, their serum ferritin levels and amount of mobilizable iron were significantly lower than those of the fibrosis/
cirrhosis
group (p < 0.01). This indicates that hepatitis
viral infection
acts synergistically with iron in accelerating the development of liver damage.
...
PMID:Liver damage in Italian patients with hereditary hemochromatosis is highly influenced by hepatitis B and C virus infection. 148 15
Parenterally shared blood and sexual transmission are the main routes of spread of hepatitis B in the United States. Most cases resolve spontaneously without specific treatment. Passive immunization provides temporary protection in certain postexposure settings. Active immunization achieves high protection rates. Duration of protection and the need for booster doses are not well defined. Many cases of fulminant B hepatitis, severe chronic active hepatitis, and end-stage
cirrhosis
secondary to hepatitis B are due to hepatitis delta
virus infection
. The delta virus requires the presence of hepatitis B for expression of disease. Hepatitis B prophylaxis should help eliminate delta hepatitis.
...
PMID:Viral hepatitis in the 1990s, Part II: Hepatitis B and delta virus. 152 72
In carriers of HBsAg (Hepatitis B virus surface antigen) the incidence of Hepatitis D
virus infection
was studied in 72 (61.3%) males and 45 (38.5%) females, totally in 117 cases with a mean age of 34.8 years. There were 26 (22.2%) asymptomatic carriers of HBsAg where in other chronic carriers the diagnosis were as follows; 29 (24.7%) chronic persistent hepatitis, 20 (17.0%) chronic lobular hepatitis, 23 (19.6%) chronic active hepatitis and 19 (16.2%) posthepatic
cirrhosis
. The incidence of HDV serologic markers were found to be positive in 19 (16.2%) out of 117 cases.
...
PMID:[Incidence of hepatitis D virus infection in chronic hepatitis B virus carriers]. 152 42
Controversy surrounds the indication of liver transplantation in patients with hepatitis B
virus infection
. The major problem is the very high risk of infection of the graft. Some investigators have suggested that the presence of HBsAg is a contraindication to liver transplantation. Between February 1975 and December 1990, 178 HBs positive patients were transplanted at Paul Brousse Hospital in Professor H. Bismuth's Department, 137 for post hepatitis
cirrhosis
and 41 for fulminant hepatitis. Since April 1984 we have decided long term immunoprophylactic therapy for all patients with HBs infection. But only from August 1987 our supply of purified anti HBs immunoglobulin has been adequate to treat all our patients according to the following protocol: 10.000 IU during the peroperative phase, 10.000 IU immediately after intervention, 10.000 IU every day for the first 6 days, 10.000 IU when the anti HBs levels were under 150 IU/l. One hundred thirty-nine patients were treated by this method. 110 cleared HBs antigen from their sera and their liver were biologically and histologically free of B virus infection. 29 patients showed reappearance of HBs antigen in their sera and nearly all of them developed objective, histologically confirmed, graft lesions. These lesions are those of classical infection: acute hepatitis, active chronic hepatitis and
cirrhosis
. So 79% of patients were successfully treated with a follow up of 45 months to 6 months. We also studied the prognostic factors under treatment. The study shows: in the case of fulminant hepatitis, 93% success versus 77% in post hepatitis
cirrhosis
; in the case of Delta superinfection, 94% success versus 66% with pure B infection; in the absence of HBVDNA in the patient's sera before transplantation, 92% success versus 20% in the presence of HBVDNA. For a better understanding of the overall results, the two following parameters have to be considered: some patients relapsed after stopping their treatment, some other patients, despite repositivation of HBs antigen in their sera showed a paradoxal good evolution. These considerations enable us to obtain HBVDNA positive patients: 10% success, HBVDNA negative patients: Fulminant hepatitis: 100% success B Delta post hepatitis
cirrhosis
: 100% success B post hepatitis
cirrhosis
: 92% success.
...
PMID:[Relapse prevention in liver transplant patients treated for liver involvement due to hepatitis B virus]. 163 19
The aim of this study was to determine the risk of developing primary liver cancer in patients with a diagnosis of alcoholism,
liver cirrhosis
, or both. Three population-based, mutually exclusive cohorts were defined on the basis of hospital discharge diagnosis between 1965 and 1983. Complete follow-up through 1984--excluding the first year of follow-up--showed that among 8,517 patients with a diagnosis of alcoholism, 13 cancers occurred, vs. 4.2 expected (standardized incidence ratio (SIR) = 3.1; 95% confidence interval (CI) = 1.6 to 5.3); among 3,589 patients with
liver cirrhosis
, 59 cancers occurred, vs. 1.7 expected (SIR = 35.1; 95% CI = 26.7 to 45.3), and among 836 patients with both diagnoses, 11 cancers occurred, vs. 0.3 expected (SIR = 34.3; 95% CI = 17.1 to 61.3). Thus, alcoholism alone entailed a moderately increased risk and alcoholism with
liver cirrhosis
did not increase the high relative risk for liver cancer more than
cirrhosis
alone. We conclude that alcohol intake may be a liver carcinogen only by being causally involved in the development of
cirrhosis
; and further, that the risk of developing liver cancer following
cirrhosis
in this population is similar to or higher than that after chronic hepatitis-B-
virus infection
in other Western countries.
...
PMID:Alcoholism and liver cirrhosis in the etiology of primary liver cancer. 163 37
Male sex, age,
cirrhosis
, and HBsAg are the major risk factors for hepatocellular carcinoma (HCC). The geographic distribution of HCC is highly uneven, such that three distinct incidence areas are recognized. To clarify the reason(s) for this geographic variability of HCC, the risk factors in each incidence area were assessed. In parallel with the geographic distribution of HCC, HBsAg prevalence was highest in both HCC patients and in general population in Africa and Asia, where mothers of HCC patients are frequently HBsAg-positive, suggesting that hepatitis B virus hyperendemicity and perinatal infection account for the high HCC incidence in these areas.
Cirrhosis
, which is found on autopsy in 80% of the cases of HCC patients worldwide, is the most prevalent risk factor for HCC in areas where hepatitis B
virus infection
is less common. However, HBsAg carriage adds to the HCC risk carried by
cirrhosis
and explains the higher incidence of HCC in cirrhotics from Africa and Asia as well as elsewhere. Available data suggest that chronic HCV infection is a risk factor for
cirrhosis
and HCC. HBV vaccination should decrease HCC incidence rates worldwide; however, HCC prevention in regions where HBsAg carriage is infrequent may also require prevention of the other causes of
cirrhosis
in order for HCC rates to decline.
...
PMID:Hepatocellular carcinoma. A worldwide problem and the major risk factors. 164 41
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