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 patients required surgical drainage of infections in the pleural space or lung during a four-year period (1984-1987). Thirty-nine patients had a history of heavy intravenous drug use and 28 of those not addicted to drugs were addicted to alcohol. Impaired immunity was believed to be present in 72 (90%) due to malnutrition (45 patients), acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (13), hepatic cirrhosis (1), diabetes (1), or multiple causes (12). Sixty-four patients had acute purulent empyema; 9, tuberculous empyema (often a mixed infection); 2, tuberculous pleural effusion with complications; 2, lung abscesses requiring open drainage; 2, chronic bronchopleural fistulae; and 1, empyema secondary to an esophageal perforation. Fifty-three (66%) were treated with tube thoracostomy only and 27 required additional procedures, including open drainage (19 patients), decortication (5), lung resection (2), chest wall resection (1), and parietal pericardiectomy (1). Overall mortality was high (30%); mortality had a strong correlation with malnutrition or immune deficiency. Very low serum albumin levels were common and were the most important single determinant of a fatal outcome: (table; see text) Other important determinants of mortality were: total lymphocytes less than 1000 (50% mortality); anergy to tests for delayed hypersensitivity (39% mortality); AIDS or AIDS-related complex (54% mortality). Analysis of the records of the 24 patients who died has led to the conclusion that despite the advanced disease present and the poor condition of most patients at least one third of the deaths could have been avoided if important errors in diagnosis and medical or surgical management could have been prevented.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malnutrition: an important determinant of fatal outcome in surgically treated pulmonary suppurative disease. 274 75

There is no clear explanation for the known fact that peripheral levels of T lymphocytes are decreased in alcoholic hepatic cirrhosis. Cellular immune deficiency in cirrhosis has been attributed to this phenomenon. In order to confirm this observation and clarify its cause, the different lymphocyte populations of the peripheral blood of 52 patients with alcoholic hepatic cirrhosis and of 30 control subjects were studied. Absolute lymphocyte counts were decreased in cirrhotic patients (p less than 0.05) due to a marked reduction of T lymphocytes (p less than 0.001). Furthermore, T lymphocytes and, to a lesser degree, B lymphocytes, but not the remaining lymphocyte populations (referred to as "other lymphocytes" in this study), were decreased in relation to the existence of portal hypertension. Thus, a significant reduction of T and B lymphocytes (p less than 0.001) exists in cirrhotics with portal hypertension with respect to those without portal hypertension. The sequestering action of the hypertrophic spleen in patients with portal hypertension could be responsible for this phenomenon.
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PMID:[Alcoholic liver cirrhosis, portal hypertension, and behavior of different lymphocyte populations]. 697 Aug 68

We have studied morbidity and mortality related to hepatitis C virus infection in haemophilic patients treated at our centre. 11/255 HCV seropositive patients have developed hepatic decompensation. 20 years after first exposure to lyophilized clotting factor concentrate the risk of hepatic decompensation is estimated to be 10.8% (95% CI 3.8-17.8%). There is a significantly increased risk associated with HIV infection, and also with increased age. For HIV seropositive patients the rates of decline in CD4 lymphocyte count and the development of p24 antigenaemia are significant risk factors for hepatic decompensation. Cirrhosis was seen in 9/19 HIV seropositive patients at post mortem. There was an association of cirrhosis with increased age but not with CD4 count, p24 antigenaemia, or AIDS. In conclusion, HCV infection is associated with serious liver disease in haemophilic patients, but so far this has been restricted to a minority of those at risk. HIV co-infection accelerates progression to hepatic decompensation, and we speculate that this is probably due to enhanced HCV replication in the presence of immune deficiency.
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PMID:The progression of HCV-associated liver disease in a cohort of haemophilic patients. 799 96

A 46-year-old woman with common variable immune deficiency acquired acute non-A, non-B hepatitis from contaminated intravenous gamma globulin in 1983. For 6 years she had fluctuating elevations of her serum aminotransferase levels. In 1990 her serum was documented to be hepatitis C virusribonucleic acid positive by polymerase chain reaction, and her liver biopsy revealed chronic hepatitis with early cirrhosis (Knodell score, 15 points). Hepatitis C virus genotyping indicated that she had been infected with the type 3 genotype. She subsequently underwent treatment with interferon alpha (IFN-alpha) for 1 year and experienced biochemical, virologic, and histologic (Knodell score, 9) suppression. She was continued on maintenance therapy for an additional 7 years, with sustained biochemical and virologic suppression. During the sixth year of therapy, complications of portal hypertension were noted with mild ascites and eventually bleeding esophageal varices. This case report documents a favorable biochemical, virologic, and histologic response to IFN-alpha therapy in this setting; supports the notion that the natural progression of hepatitis C virus infection may be more aggressive in patients with common variable immune deficiency; and, although complications of portal hypertension eventually occurred, the suppressive maintenance IFN therapy may have delayed their onset. The future establishment of the long-term effects of IFN therapy on important clinical outcomes is necessary to understand better its therapeutic benefit in chronic hepatitis C infection.
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PMID:Long-term interferon alpha maintenance therapy for chronic hepatitis C infection in a patient with common variable immune deficiency. 1047 89

Little is known about treatment of hepatitis C virus (HCV) infection in "other groups" than the general population, namely patients with hematologic or renal disorders and patients with human immune deficiency (HIV) co-infection. The aim was to better define HCV therapies in these groups. We analyzed the medical literature focusing on treatment of HCV infection in other populations to suggest conclusions about indications based on tolerance and efficacy. As in the general population, the decision to treat should be based mainly on liver pathology, and to a lesser extent on virologic profiles (genotype, quantitative viremia). Hemophilia does not modify therapeutic strategies which combine interferon-alpha and ribavirin. Similar combinations should be discussed in patients with inherited hemoglobin disorders but iron overload (secondary hemochromatosis) associated with multiple transfusions may decrease the potential efficacy of interferon-alpha and chronic anemia may limit the use of ribavirin. In hemodialyzed patients, therapy by interferon-alpha is feasible with 3 MU subcutaneously after each hemodialysis three times weekly for 6-12 months. Virologic results are at least similar to those obtained in the general population with frequent pathological improvement. Combinations are not possible because ribavirin is contraindicated for pharmacokinetic reasons. In kidney recipients, interferon-alpha is deleterious and inefficient; ribavirin monotherapy has a potential interest which remains to be evaluated. In HIV co-infected patients, treatment is mandatory given the high rate of cirrhosis and the improved survival related to multiple anti-HIV therapies (which have no clear efficacy for quantitative HCV viremia). Due to the limited efficacy of interferon-alpha monotherapy, the combination of interferon-alpha and ribavirin appears to be the logical treatment. An important point is the in vitro inhibition of phosphorylation by ribavirin of HIV reverse transcriptase inhibitors which has to be analyzed in vivo before the combination can be recommended. On the basis of the results of liver biopsy, antiviral treatments may be proposed for HCV-infected patients with hematologic or renal disorders as well as for HIV co-infected patients. The choice of therapy (monotherapy or combined therapies) should be based on the clinical situation (contraindicated with chronic anemia or renal failure, for example) and its duration on the virologic factors of response as in the general population.
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PMID:Treatment of chronic hepatitis C in special groups. 1062 89

Hepatitis C virus infects around 600,000 French people, mainly after parenteral exposure (in association with transfusion before 1990 and with intravenous drug use). Spontaneous resolution at the acute stage of the infection occurs in around 30% of cases while chronic infection is observed in around 70% of cases and its main risk is evolution to cirrhosis. Three predictive factors of cirrhosis have been identified: the duration of infection (greater than 20 years), the age at contamination (greater than 40 years) and a chronic alcohol consumption (> 80 g/day). Immunosuppressive situations (drug-related immune suppression for the prevention of graft rejection in allograft recipients or human immune deficiency virus-coinfection) as well as hepatitis B virus coinfection enhance the risk of cirrhosis and reduce the time of occurrence of cirrhosis. These predictors have to be considered in the information to the patients and in therapeutic decisions. They explain that any hepatitis C virus-infected patient has to undergo a liver biopsy to evaluate the necro-inflammatory activity and the fibrosis of the liver disease to delineate the place of a follow-up with a control of aggravation factors (alcohol discontinuation) and of an antiviral therapy.
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PMID:[Clinical forms and prognosis of hepatitis C]. 1090 93

A 43-year-old man with common variable immune deficiency underwent liver transplantation for cirrhosis caused by hepatitis C virus (HCV). HCV had been acquired from a contaminated batch of immunoglobulin. He developed cirrhosis within 3 years of infection with the virus, then liver failure requiring liver transplantation. The immediate post-transplant course was uncomplicated. Five months after transplantation he developed liver failure, and the histological appearances were those of severe cholestatic hepatitis. Withdrawal of immunosuppression resulted in recovery from liver failure. Clearance of the HCV from serum was also observed and has been sustained during follow-up (despite the subsequent reintroduction of low-dose immunosuppression). The patient is alive and well more than 5 years after transplantation. His post-transplant course has been remarkable for the aggressive recurrence then clearance of the HCV.
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PMID:Successful outcome of liver transplantation in a patient with hepatitis C and common variable immune deficiency. 1212 17

Many inherited metabolic diseases affect the liver in neonates, children, or adults. The histopathologic changes are diverse and may be acute or chronic. They can be considered primary (when the injury is from the cytopathic effect of an accumulated metabolite) or secondary (e.g., an infection caused by an immune deficiency). All forms of liver disease are described: for example, intrahepatic cholestasis, neonatal hepatitis with giant-cell transformation, paucity of bile ducts, steatosis, steatohepatitis, necroinflammatory diseases (acute or chronic), fibrosis, cirrhosis, and neoplasms (benign or malignant). Familiarity with the morphologic changes is important in clinicopathologic correlation, diagnosis, and understanding of pathogenetic mechanisms.
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PMID:Inherited metabolic diseases of the liver. 1212 65

The authors present a report of a seventeen year old girl with common variable immunodeficiency (CVID) and liver cirrhosis. A child of healthy, non-consanguineous parents was diagnosed at the age of 13 years to have immune deficiency and an early stage of liver cirrhosis. Patient revealed the following signs of immune deficiency: decreased level of serum immunoglobulins, considerably decreased number of B cells and CD4 cells and a lack of proliferative response to mitogen stimulation. The USG, scintigraphy and biopsy of liver confirmed the diagnosis of liver cirrhosis. The patient has been receiving intravenous immunoglobulins (IVIG) as substitutional treatment of CVID.
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PMID:[Common variable immunodeficiency concomitant with liver cirrhosis--case report]. 1241 90

Morbidity and mortality from co-morbid hepatitis B (HBV) and hepatitis C (HCV) infection in HIV co-infected patients are increasing; hence, the management of HIV and HBV or HCV co-infected individuals is now one of the most challenging clinical management issues. Less than 10% of all HIV-infected patients show markers of chronic HBV infection. Hepatitis B in HIV co-infected patients is characterized by high levels of HBV replication and a high risk for cirrhosis. Treatment of HBV with lamivudine (3TC) remains the best treatment option at this time. Initial results of studies of adefovir or tenofovir, however, demonstrate good antiretroviral efficacy, even in patients with 3TC-resistant HBV. In Europe, it is estimated that approximately 30% of HIV-infected individuals are co-infected with HCV. HIV accelerates HCV liver disease especially when HIV-associated immune deficiency progresses. Within 10-15 years of initial HCV infection, 15-25% of patients who are co-infected with HIV develop cirrhosis compared with 2-6% of patients without HIV infection. With the introduction of pegylated interferon in combination with ribavirin, promising treatment options have become available for HIV/HCV co-infected patients leading to early virological response rates of approximately 50%. The high number of HIV/HCV and HIV/HBV co-infections, as well as the much more unfavorable course of HBV and HCV in these patients, underlines the need to establish treatment strategies for HBV and HCV in HIV co-infected individuals.
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PMID:Management of hepatitis B and C in HIV co-infected patients. 1456 59


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