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)

Eighty-six patients were followed for 6.5 years to study the epidemiological, virological, and histological course of chronic delta hepatitis and the relationship of this disease with HIV and HCV infection. Patients were classified into four groups according to simultaneous HCV and/or HIV infection: group 1, HDV infection (20 cases); group 2, HDV and HCV infection (11 cases); group 3, HDV and HIV infection (12 cases), and group 4, HDV, HCV, and HIV infection (43 cases). All but 14 patients were asymptomatic at presentation. Liver histology showed chronic active hepatitis in 53 cases and cirrhosis in 19 cases. During followup, 52 patients remained asymptomatic, 34 developed hepatic dysfunction, 28 died, and 1 received a liver transplant. Among the 28 patients who died, 4 had HDV infection; 3 HDV and HCV infection; 3 HDV and HIV infection; and 18 HDV, HCV, and HIV infection. Death was due to liver failure in 16 (57%), AIDS in 10 (36%), and was unrelated to liver disease in 2 (8%) cases. There results demonstrate that chronic delta hepatitis is a severe disease, especially among drug users with HIV and HCV infection. The high morbidity and mortality of chronic delta hepatitis justifies the use of antiviral therapy to modify the natural course of the disease.
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PMID:Chronic delta hepatitis: is the prognosis worse when associated with hepatitis C virus and human immunodeficiency virus infections? 873 62

Hepatitis C virus (HCV) infection is the major cause of chronic liver disease in individuals with haemophilia. A wide spectrum of disease severity is found in this group, ranging from mild hepatitis to cirrhosis. We have studied a cohort of 87 anti-HCV positive haemophiliacs who have been infected with HCV for 10-25 years and assessed the relative value of invasive and non-invasive methods of evaluating liver disease. The severity of liver disease was assessed using ultrasound scan (n = 77), upper GI endoscopy (n = 50), laparoscopic liver inspection (n = 33) and liver biopsy (n = 22). Invasive investigations were performed without any significant bleeding complications. Evidence of severe liver disease was found in approximately 25% of patients. There was agreement between the severity of liver histology and the information derived from the laparoscopic liver inspection, endoscopy and ultrasound in 86%. Co-infection with HIV was significantly associated with more severe liver disease (P = 0.006). This study provides further evidence that liver disease is emerging as a major complication in haemophiliacs and severe liver disease is more common in those co-infected with HIV. We have shown the potential value of laparoscopic liver inspection, in combination with endoscopy and ultrasound, in staging the extent of liver disease, and suggest that most patients may be managed without resorting to liver biopsy.
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PMID:Investigation of chronic hepatitis C infection in individuals with haemophilia: assessment of invasive and non-invasive methods. 875 28

We report an Hepatitis B Virus reactivation, in a patient with an end-stage Human Immunodeficiency Virus infection who developed a rapidly progressive liver failure in four months. The main histological features include ballooning of hepatocytes and ground glass transformation, without significant inflammation. Immunohistochemical staining showed a high expression of viral antigens. This case can be related to "Fibrosing Cholestatic Hepatitis", first described after liver transplantation for cirrhosis B. The mechanism of hepatocellular damage is likely to be a direct cytotoxicity of hepatitis B virus.
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PMID:[Fibrosing cholestatic hepatitis by B virus reactivation in AIDS]. 876 76

Most haemophiliacs treated with non-virally-inactivated clotting factor concentrates have been infected with hepatitis C virus (HCV). We have studied the natural history of chronic HCV infection by following all 138 HCV-positive patients from our centre for periods of up to 28 years. As well as the clinical and biochemical characteristics, we studied 116 liver samples from 63 patients obtained at elective biopsy (n = 103) or autopsy (n = 13). 36 (26%) of the patients were HIV positive, and three were chronic carriers of hepatitis B. Evidence of previous exposure to hepatitis A and B was found in 37.2% and 48.1% respectively. Raised transaminase levels were found in 82.6% of patients. 11 of 15 patients with normal transaminases tested by PCR for HCV RNA were positive, indicating that most patients, even in this group, have chronic hepatitis C infection. Cirrhosis was diagnosed by liver histology in 19 patients, and nine patients developed liver failure. The incidence of cirrhosis rose rapidly 15 years after HCV infection to 15.6 per 1000 person-years. Multivariate analysis showed that HIV status, length of time since HCV infection and age at HCV infection were independently associated with both the development of cirrhosis and liver failure. Two patients developed hepatocellular carcinoma: one of these was exposed only to a single batch of FVIII concentrate 11 years earlier. Chronic hepatitis C is increasingly recognized as a major cause for morbidity and mortality in haemophiliacs, especially those who are HIV positive and who were infected at an older age.
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PMID:The natural history of chronic hepatitis C in haemophiliacs. 907 37

Evaluation of liver biopsies in hepatitis C is aimed at confirming the clinical and serologic diagnosis, grading of necroinflammatory activity, staging of consecutive fibrosis, ruling out or confirming liver diseases of different etiology, and assessment of therapeutic effects. Usually, the course of chronic hepatitis C virus (HCV) infection is slow, with mild inflammatory changes. Nevertheless, even in mild asymptomatic chronic hepatitis C episodes of higher inflammatory activity associated with extensive piecemeal necrosis and porto-central bridging, necrosis can accelerate the course of the disease. For this reason, the traditional, morphologically based classification of chronic hepatitis and the term "chronic persistent hepatitis" have lost their predictive usefulness, especially in hepatitis C. Chronic hepatitis should be characterized by etiologic designation as well as grade and stage of the disease. Portal lymphoid aggregates, some inflammatory bile duct damage and mild steatosis are the most characteristic features by which hepatitis C can be differentiated from other progressive inflammatory liver diseases. Antibodies directed against HCV antigens allow identification of viral proteins by immunohistochemistry. Immunostaining for hepatitis B antigens, for alpha-1-antitrypsin and copper staining are helpful in detecting hepatitis B and congenital liver diseases (Wilson's disease, alpha-1-antitrypsin deficiency) as possible causes of chronic progressive inflammatory liver disease. Centrilobular Mallory's hyalin, identified by immunostaining for ubiquitin in combination with perivenular fibrosis, is helpful in diagnosing concomitant alcoholic liver disease. In our own biopsy material (n = 100) and autopsy material (n = 58), HIV/HCV-coinfected patients have a significantly higher rate of fibrosis and cirrhosis than HIV patients without HCV infection. Hepatitis C can apparently aggravate the course of HIV infection. Our morphologic findings support the clinical observation that chronic HCV infection seems to be the main cause of liver failure, especially in the risk group of HCV/HIV-coinfected hemophiliacs.
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PMID:Histopathologic findings in chronic hepatitis C. 883 87

We investigated the frequency of HBsAg clearance and the possible role of viral superinfection in a long-term follow-up of 184 patients with chronic hepatitis B (CHB). Our subjects were 184 patients with chronic hepatitis B and the follow-up was 12-216 months (mean 66.2 +/- 53.7 months). The investigative methods used were: immunoenzymatic assays for HBV, HCV, HDV, and HIV markers; polymerase chain reaction (PCR) for HBV DNA; and liver biopsy and immunoperoxidase. During the follow-up, 20 of the 184 patients cleared serum HBsAg. A comparison of patients with persistent HBsAg(group I) and of those who cleared this marker (group II) showed a significant difference in mortality (P = 0.002) between the two groups and a tendency to a more severe exacerbation (flare) in group II (P = 0.07). Antibodies to hepatitis C and D virus as well as antibodies to HIV were equally distributed in both groups. Thirteen patients (7.9%) from group I, but none from group II, subsequently developed hepatocellular carcinoma. These results suggest that the frequency of spontaneous clearance of HBsAg during chronic HBV infection is low. No determinant factor for the clearance was found, including the presence of liver cirrhosis. Serum HBV DNA was undetectable by PCR after clearance in 16 out of 17 patients.
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PMID:Spontaneous hepatitis B surface antigen clearance in a long-term follow-up study of patients with chronic type B hepatitis. Lack of correlation with hepatitis C and D virus superinfection. 888 37

We report a case of tuberculous peritonitis in a patient with concomitant HIV infection and liver cirrhosis. A 50-year-old man with viral B and delta liver cirrhosis and AIDS was diagnosed with spontaneous Escherichia coli peritonitis and successfully treated with beta-lactamins. Three months later, ascites reappeared and Mycobacterium tuberculosis was identified in peritoneal fluid cultures. The triple antituberculosis regimen was adjusted to his level of liver failure but the patient died of hepatic encephalopathy. Concomitant HIV infection and liver cirrhosis favour tuberculous peritonitis but they also make its diagnosis extremely difficult. Considering the poor prognosis of this infection when untreated, tuberculous peritonitis should be systematically suspected in such patients.
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PMID:Unusual presentation of a tuberculous peritonitis in a patient with concomitant AIDS and liver cirrhosis. 893 May 71

Eighty-three patients with chronic end-stage renal failure, including 65 on haemodialysis and 18 on intermittent peritoneal dialysis, were evaluated for hepatitis B virus profile and antibodies to hepatitis C virus (HCV). All those positive for HBsAg were excluded from the study. Nineteen patients were found to be positive for antibodies to HCV by the ELISA II test. Eight cases were already positive for HCV antibody when they started dialysis in our unit, the other 11 became positive during dialysis in our unit. Only one of the patients on peritoneal dialysis was positive for HCV. A liver biopsy was obtained from 17 patients, who consented to the procedure. All the cases were evaluated for the number of blood transfusions received, HIV infection and the approximate time of contracting the HCV infection. Liver enzymes were determined every month. Only three patients had abnormally raised serum aminotransferase at the time of biopsy. The various histopathological lesions detected were chronic active hepatitis (n = 3, including one with changes consistent with cirrhosis), chronic persistent hepatitis (n = 4), non-specific hepatitis (n = 3) and haemosiderosis (n = 3); four biopsy samples were normal. There was no correlation between the biochemical and histopathological changes. Moreover, patients with normal serum aminotransferase levels had abnormal histopathological changes. All were negative for HIV and none of the patients had received a renal graft. Twelve patients had received blood transfusions varying from 2 to 12 units, four had not received any blood, and in one the history of blood transfusion could not be confirmed. The four patients with anti-HCV antibodies who had not received blood transfusion had relatively mild disease--non-specific hepatitis (n = 2) or normal biopsy (n = 2). One patient with cirrhosis died 30 months after liver biopsy from hepatic insufficiency and three received renal transplants. Others are continuing on dialysis and their biochemical tests are within normal limits 12-45 (30 +/- 14) months after biopsy. In conclusion, biochemical tests are poor indicators of liver disease, and liver biopsy is a definitive way of evaluating the patients of dialysis with positive HCV antibodies for prognosis.
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PMID:Liver disease in dialysis patients with antibodies to hepatitis C virus. 894 88

Porphyria cutanea tarda (PCT) is believed to be associated with reduced hepatic uroporphyrinogen decarboxylase activity and risk factors such as alcohol abuse and medication with oral contraceptives and certain other drugs. Recently it has been suggested that hepatitis C virus (HCV) infection may also be associated with PCT. We have therefore reviewed the prevalence of HCV infection in a series of patients with PCT in the Lothian region of Scotland. We identified 12 patients with PCT, all of whom had abnormal liver function tests. Liver histology revealed chronic active hepatitis in six patients, micronodular cirrhosis in four patients, hepatocellular carcinoma in one patient and normal findings in one HIV positive patient. Out of 12 patients tested, 11 were positive for anti-HCV antibodies by second generation enzyme linked immunosorbent assay (ELISA 2), and by recombinant immunoblot assay (RIBA 2); positive serology was confirmed by polymerase chain reaction (PCR). In a second group of 14 patients with chronic HCV infection matched for age and sex with the PCT patients, all had normal urinary uroporphyrin excretion. We have thus confirmed in Scotland early reports from Spain and Italy that PCT is strongly associated with HCV infection. This could explain the development of inflammatory changes in the liver and progression of liver disease in patients with PCT. Porphyrin metabolism, however, appears normal in patients with chronic HCV infection without PCT.
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PMID:The association of hepatitis C viral infection with porphyria cutanea tarda in the Lothian region of Scotland. 895

Interferon is the only treatment shown to be effective on hepatitis C in controlled trials. The response to treatment is generally assessed in terms of a return to normal transaminase activity, but also negative PCR testing for viral RNA and histopathological examination of the liver. At a dose of 3 MU three times a week for 6 months, 25% of patients have a persistent return to normal transaminase activity, 25% relapse when interferon is withdrawn, and the remaining 50% have persistently high levels at the end of treatment and are considered resistant. The rate of persistent responses increases to 40% when treatment is extended to one year. Viral RNA becomes undetectable in the serum of 80% of these responders. Most also have a histological improvement, but so do a number of patients who relapse or who are resistant. In the longer term, interferon could prevent the onset of liver cancer in patients with viral C cirrhosis. Interferon is generally well tolerated at the doses currently used, most side effects (hematologic, neuropsychiatric and thyroid disorders) resolving when treatment is stopped. The following factors are clearly predictive of the response to interferon : young age, short time since onset, absence of cirrhosis, lower-level viremia, and infection by HCV genotypes other than 1b. Interferon is markedly less effective in immunodeficient patients (transplant, HIV infection, etc.). Several add-on treatments have been tried, but ribavirin appears to be the most promising, both during initial interferon therapy and for patients who relapse or are resistant to a first course. Interferon therapy of the acute phase of hepatitis C significantly reduces the risk of chronic liver disease. There is no vaccine against HCV infection.
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PMID:[Prevention and treatment of hepatitis C]. 899 9


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