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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The management of blunt splenic trauma in children has remained controversial, with different physicians advocating observation, splenorrhaphy, and splenectomy. Proponents for each position have debated the relative importance of rebleeding (delayed splenic rupture), posttransfusion hepatitis with its sequelae, and overwhelming postsplenectomy sepsis. In an attempt to guide the clinician, a decision analysis was performed. Variables evaluated included the incidence of transfusion, postsplenectomy sepsis, posttransfusion hepatitis, chronic active hepatitis, cirrhosis, and rebleeding. The quality-adjusted life expectancies (QALEs) when the average incidence of the variables were used in the decision analysis were 62.69 years for observation, 62.32 years for splenorrhaphy, and 61.14 years for splenectomy. Sensitivity analysis showed that there was very little difference between observation and splenorrhaphy when the transfusion rate and hepatitis rate were varied. But these treatment options produced longer QALEs than splenectomy. Therefore, in appropriately selected patients, observation is a safe and effective therapeutic option. If an operation is necessary, every effort should be made to preserve the spleen. Splenectomy may still be required in those cases of complete devascularization, persistent hemorrhage, or other associated significant injuries.
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PMID:Decision analysis in children with blunt splenic trauma: the effects of observation, splenorrhaphy, or splenectomy on quality-adjusted life expectancy. 843 76

Since the discovery of the hepatitis C virus (HCV), it has become evident that this infectious agent is a primary cause of posttransfusion and sporadic non-A, non-B hepatitis. Identification and introduction of surrogate markers for posttransfusion hepatitis and later introduction of anti-HCV screening has decreased the incidence of posttransfusion hepatitis. Community-acquired HCV infection is less common than posttransfusion HCV hepatitis. HCV infection may lead to liver cirrhosis without prior evidence of laboratory or histologic infection. Populations at risk for HCV infection include patients receiving organ transplants, health care workers, infants born to HCV-infected mothers, and hemodialysis patients. Intravenous drug abusers and their sexual partners also demonstrate a high rate of HCV infection. Nosocomial HCV transmission may occur despite the observance of universal precautions. Dental or surgical intervention, salivary inoculation, family members infected with HCV, cocaine abuse, HIV infection, and lower socioeconomic status also each correlate with an increased risk of infection. HCV infection is associated with many immune-mediated diseases. There may also be some relationship between human leukocyte antigens and HCV infection. Since there currently is no HCV vaccine, prevention of exposure remains the only possibility for reducing HCV transmission and prevalence.
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PMID:Mode of hepatitis C virus infection, epidemiology, and chronicity rate in the general population and risk groups. 901 73

Hepatitis G virus (HGV) and GB virus C (GBV-C) are two newly discovered viral agents, different isolates of a positive-sense RNA virus that represents a new genus of Flaviviridae. The purpose of this review is to analyze new data that have recently been published on the epidemiology and associations between HGV and liver diseases such as posttransfusion hepatitis, acute and chronic non-A-E hepatitis, fulminant hepatitis, cryptogenic cirrhosis, and hepatocellular carcinoma. The role of HGV in coinfection with other hepatitis viruses, the response to antiviral therapy, and the impact of HGV on liver transplantation are also discussed. HGV is a transmissible blood-borne viral agent that frequently occurs as a coinfection with other hepatitis viruses due to common modes of transmission. The prevalence of HGV ranges from 0.9 to 10% among blood donors throughout the world and is found in 1.7% of volunteer blood donors in the United States. The majority of patients infected with HGV by blood transfusion do not develop chronic hepatitis, but hepatitis G viremia frequently persists without biochemical evidence of hepatitis. Serum HGV RNA has been found in 0 to 50% of patients with fulminant hepatitis of unknown etiology and 14 to 36% of patients with cryptogenic cirrhosis. The association between HGV and chronic non-A-E hepatitis remains unclear. Although HGV appears to be a hepatotrophic virus, its role in independently causing acute and chronic liver diseases remains uncertain.
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PMID:Hepatitis G virus: is it a hepatitis virus? 926 69

Several reports suggest that posttransfusion hepatitis C causes more aggressive histological activity than disease that is acquired via other routes. We sought to determine whether mode of transmission affects disease outcome. We studied the demographics, presenting laboratory data, and clinical course of 627 consecutively evaluated nonalcoholic patients with chronic hepatitis C. Two hundred eighty-two patients (45%) were transfusion recipients, 262 (42%) acquired the disease via other routes of percutaneous exposure, and 83 (13%) were without risks. Liver histology was available in 463 patients (215 transfusion recipients, 195 non-transfusion recipients, and 53 who were were without risks) and showed noncirrhosis in 274 (59%), cirrhosis in 173 (37%), and hepatocellular carcinoma in 16 patients (4%) who also had underlying cirrhosis. Duration of follow-up was 1 to 25 years (mean, 48 months; median, 21 years). One hundred eighteen of 173 (68%) cirrhotic patients were transfusion recipients; 40 of 173 (23%) cirrhotic patients acquired infection via other percutaneous exposure, and the remainder were without known risk factors (P < .001). Among the 215 patients with blood transfusions for whom histology was available, 118 of 215 (55%) had cirrhosis and 89 of 215 (41%) were noncirrhotic (P < .001); 8 transfused patients (4%) had hepatocellular carcinoma. In the percutaneous group, 40 of 195 (21%) of the patients were cirrhotic versus 153 of 195 (78%) who were noncirrhotic (P < .001); 2 patients (1%) had hepatocellular carcinoma. During the follow-up period, 59 of 189 (31%) of the cirrhotic patients (including those 16 individuals with hepatocellular carcinoma) developed hepatic decompensation. By univariate analysis, the risk of liver failure was related to age at viral acquisition, but by logistic regression analysis, only mode of transmission, and not age or estimated disease duration, predicted risk of liver failure. Patients with posttransfusion hepatitis C were more likely to develop decompensation than individuals who were not transfusion recipients (relative risk, 3.921; CI = 2.205 to 7.015). Serum albumin, prothrombin time, and platelet count at presentation were independent laboratory predictors of subsequent hepatic decompensation. The rate of hepatocellular carcinoma development among all cirrhotic patients during the follow-up period was 1.2% per year. Patients with posttransfusion hepatitis C are at greater risk of cirrhotic decompensation than those individuals with non-transfusion-acquired disease. The risk of liver failure is more closely related to the mode of transmission than to age at viral acquisition or to the duration of infection.
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PMID:Clinical outcome of hepatitis C as a function of mode of transmission. 993 40

A novel DNA virus, TT-virus (TTV), has been reported in patients with non-A-G posttransfusion hepatitis in Japan. We sought to determine whether TTV infection occurs in North American blood donors and to further determine the prevalence of TTV infection in several groups of patients with liver disease, including patients with cryptogenic cirrhosis and idiopathic fulminant hepatic failure. TTV infection was sought by detection of TTV DNA in serum by polymerase chain reaction (PCR) using primers generated from a conserved region of the TTV genome. Blood donors, patients with cryptogenic cirrhosis, idiopathic fulminant hepatic failure, and patients with other forms of advanced liver disease with and without a history of parenteral exposures were studied. TTV infection was present in 1% (1 of 100) of blood donors, 15% (5 of 33) of patients with cryptogenic cirrhosis, 27% (3 of 11) of patients with idiopathic fulminant hepatic failure, 18% (2 of 11) of patients with a history of exposure to blood products, and 4% (1 of 25) of patients without parenteral risk factors. For all patients tested, a history of prior exposure to blood products was associated with an increased risk of TTV infection (relative risk, 4.5; 90% confidence intervals, 0.6-43.9). We conclude that TTV infection is present among North American blood donors and is common in patients with liver disease, including cryptogenic cirrhosis and fulminant hepatic failure. Further studies are required to determine the role of TTV in the pathogenicity of acute and/or chronic liver disease.
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PMID:TT-virus infection in North American blood donors, patients with fulminant hepatic failure, and cryptogenic cirrhosis. 973 81

A novel human DNA virus, TTvirus (TTV), was identified from a patient with posttransfusion hepatitis of unknown etiology. It is thought to be a new hepatitis virus, but the clinical significance of this virus is uncertain. We investigated the frequency of TTV viremia by PCR in 39 non-B, non-C hepatitis (NBNC) patients with hepatocellular carcinoma (HCC), and clinical features of these patients. TTV viremia was detected in 20 (51.3%) of 39 NBNC hepatitis patients with HCC. Liver cirrhosis (LC) were found in 11 (55%) of 20 TTV-positive patients and 16 (84%) of 19 TTV-negative patients (p < 0.05). The levels of AST, LDH, LAP, gamma GTP in TTV-positive patients were significantly higher than those in TTV-negative patients (p < 0.05). (AST: 58 +/- 26 vs 42 +/- 23 IU/l, LDH: 468 +/- 127 vs 366 +/- 123 IU/l, LAP: 339 +/- 242 vs 206 +/- 80 IU/l, gamma GTP: 207 +/- 207 vs 105 +/- 107 IU/l) These results suggest clinical differences between TTV-positive and TTV-negative patients in NBNC hepatitis patients with HCC.
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PMID:[Detection of TT virus (TTV) in non-B, non-C hepatitis patients with hepatocellular carcinoma, and clinical features of these patients]. 1039 Oct

A novel DNA virus (TTV) was identified recently in Japanese patients with posttransfusion hepatitis non-A-E and has been implicated as a cause of acute and chronic liver diseases of unknown etiology in some patients. The frequency of TTV infections was investigated in 284 blood donors, 105 patients with different liver disorders before and after liver transplantation (OLT), as well as in 64 patients with chronic hepatitis C who received antiviral therapy. TTV infections were found more frequently by nested-PCR in patients with liver disorders (15%) as compared to blood donors (7%). TTV occurred independently of the aetiology of the liver disease (e.g., cryptogenic cirrhosis [12.5%], alcoholic cirrhosis [16%], fulminant hepatic failure non-A-E [35%], and chronic hepatitis C [12.5%]; p=n.s.). After OLT, a high rate of TTV de novo infections (44%) was observed. However, TTV viremia after OLT (in 56 out of the 105 patients) was not associated with graft hepatitis. Analysis of patients with chronic hepatitis C coinfected with TTV who have been treated with interferon alpha alone or in combination with ribavirin revealed that TTV is an interferon-sensitive virus. Phylogenetic analysis of TTV sequences suggest that at least four different genotypes and several subtypes exist in Germany. In conclusion, the high prevalence of TTV infections observed in patients with parenteral risk factors is an argument in favour of transmission of the virus via blood and blood products. A relevant hepatitis-inducing capacity of TTV, however, seems unlikely, considering the observation that in the majority of patients, TTV infection after OLT was not accompanied by graft hepatitis.
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PMID:Occurrence of a novel DNA virus (TTV) infection in patients with liver diseases and its frequency in blood donors. 1044 Aug 18

Hepatitis C Virus (HCV) causes most cases of posttransfusion hepatitis. Chronic HCV infection is highly related to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Current therapies are only minimally effective and no vaccine has been developed. DNA-based immunization could be of prophylactic and therapeutic value for HCV infection. By intramuscular inoculation in BALB/c mice with an HCV recombinant plasmid pCI-HCV-C, we found significant levels of IgM antibody, but no significant IgG rise. After boost the immunized mice with recombinant HCV-core protein (cp1-10; 1-164aa), the anticore IgG, verified by Western-blotting, rose rapidly, which was two weeks earlier than that with control plasmid. Spleen cells from pCI-HCV-C immunized mice gave higher proliferation index (PI) than control (P < 0.05). The PI of cp1-10 boosted mice was even higher. Proliferation blocking assay with mAb proved the responding cell to be of CD4+ CD8- phenotype, supporting specific priming of T helper cells. A 51Cr-releasing CTL assay specific for HCV-core was developed, and a specific CTL response against HCV-core was demonstrated in both pCI-HCV-C immunized mice and mice boosted with cp1-10. Strong cytotoxic activity against peptide-pulsed p815 cells (H-2d), but not EL-4 cells (H-2b), suggested MHC class I restriction of the CTL activity. Blocking of CTL with mAb proved the effector cells to be of CD4- CD8+. Three CTL epitopes in HCV-core protein were demonstrated. We failed to detect CTL when immunized only with core protein. The results suggested that vaccination with HCV-core derived DNA sequences could be an effective method to induce humoral and cellular immune responses to HCV.
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PMID:Characterization of the humoral and cellular immune responses against hepatitis C virus core induced by DNA-based immunization. 1046 52

Hepatitis C was responsible for the majority of cases of posttransfusion hepatitis before the introduction of a specific screening test for blood donors. Infected recipients may remain asymptomatic for many years, but cirrhosis and hepatocellular carcinoma may develop decades after infection. Lookback, or the identification of recipients of potentially contaminated blood, is now being conducted in many countries, including Holland, Denmark, the United Kingdom, Canada, New Zealand, and the United States. In targeted lookback, recipients of blood from donors subsequently found to be positive for hepatitis C are notified and advised to undergo testing. In general lookback, all patients who received blood before being tested for hepatitis C are advised to undergo testing. Difficulties with both forms of lookback illustrate the importance of vein-to-vein tracking of blood products, including the potential utility of a centralized registry of blood product recipients.
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PMID:Hepatitis C lookback. 1105 13

The paper describes aspects in the natural evolution of hepatitis C virus (HCV) infection with severe outcomes induced by the typical or atypical clinical manifestations or chronic carrier state. In the interval 1995-1999 in the Iasi district morbidity from all types of viral hepatitis ranged from 153.4 cases per 100,000 inhabitants in 1995 to 66.6 in 1999. The features of A viral hepatitis epidemiological process was the multiannual cyclic pattern. From estimating the circulation of HCV in the population of Iasi district, several population categories have been screened for the presence of HCV antibodies (anti-HCV). Testing 87,894 blood samples assessed the prevalence of anti-HCV in blood donors. Different annual values resulted: 1.5% in 1997 and as a result of routine screening, only 0.3% in 1999. The cases of posttransfusion hepatitis (PTH) admitted to the Clinic of Infectious Diseases of Iasi, the diagnosis of which was supported by epidemiological history and confirmed serologically by the presence of anti-HCV were of 12 in 1995 (36.4% of all PTH), 20 in the interval 1996-1999, with an average for the 4 study years of 7.5%. Anti-HCV was found in 24.4% of series of 4,594 patients with viral hepatitis, in 32.1% of 582 individuals with various disorders or at risk, of which those with liver cirrhosis accounted for 37%, and in 9.6% of 94 patients with neurological disorders. Of the 1083 tested physicians and nurses working in health care settings at risk 6.6% were anti-HCV-positive.
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PMID:The prevalence of the owner of serologic markers for the hepatitis C virus, in a north-eastern territory of Romania. 1209 39


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