Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amongst 17 patients with hepatic focal nodular hyperplasia (FNH) encountered at Westmead Hospital between 1981 and 1990, FNH was found in association with hepatocellular carcinoma (HCC) in three (3/17), one male and two females, one of whom also had peliosis and an hepatic adenoma. FNH was also found in association with other conditions which may affect hepatic function, structure or circulation, including chronic obstructive airways disease (2), congestive cardiomyopathy (1), chronic active hepatitis (1), granulomatous hepatitis (1), coeliac artery stenosis (1) and metastatic malignant melanoma (1). This report, derived from our experience with FNH over 10 years draws attention to a possible link between FNH, hepatic malignancy and conditions which may disturb the hepatic circulation. We suggest that patients with FNH should be investigated thoroughly and an aggressive management policy should be adopted.
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PMID:Hepatic focal nodular hyperplasia: a benign incidentaloma or a marker of serious hepatic disease? 132 5

Heart transplantation was performed in a 24-year-old man suffering from dilated cardiomyopathy who was also infected with hepatitis B virus and had not yet seroconverted. Most likely due to the immunosuppression, the hepatitis exacerbated and soon led to hepatic dystrophy and precoma. In this phase of congruent rejection of the heart transplant, liver transplantation was performed. During the procedure the patient had stable circulatory parameters and a reduced cardiac output. The heart rate and cardiac output stabilized after release of the anastomosis of the hepatic vessels. The patient survived for 6 months and died at home with signs of a myocardial infarction.
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PMID:[Orthotopic liver transplantation following heart transplantation]. 175 36

A distinct clinical syndrome of cholestasis and hepatitis occurred during early infancy in seven infants with perinatally acquired human immunodeficiency virus 1 infection. In five infants hepatitis was the first manifestation of human immunodeficiency virus 1 infection. The median age of onset of hepatitis was 7 months (range, 5 to 10 months). The mean total bilirubin concentration at presentation was 7.4 mg/dl (range, 3.9 to 11 mg/dl), the mean aspartate aminotransferase was 1512 IU/liter (range, 782 to 2960 IU/liter) and the mean alanine amino-transferase 512 IU/liter (range, 92 to 1247 IU/liter). The absolute CD4 count at the time of onset of hepatitis ranged from 191 to 2298 cells/mm3 (mean, 766 cells/mm3). Six of the seven children died within 12 weeks of onset of hepatitis, three as a result of complications of Pneumocystis carinii pneumonia, and two died of complications secondary to cytomegalovirus. In only one infant was the cause of death the direct consequence of liver failure. The seventh infant died 17 months after the onset of hepatitis of dilated cardiomyopathy. No specific etiologic agent has been identified as the cause of cholestatic hepatitis in these infants. In situ hybridization studies to detect human immunodeficiency virus 1 messenger RNA was negative in the liver tissue obtained at biopsy and autopsy in five of the samples tested.
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PMID:Cholestatic hepatitis in children infected with the human immunodeficiency virus. 810 98

The antiphospholipid syndrome is characterized by clinical evidence of arterial or venous thrombosis, thrombocytopaenia, recurrent fetal loss and repeated positivity of antiphospholipid autoantibodies. The association of antiphospholipid syndrome with the development of adrenal failure has been reported in more than 40 patients in the last 20 years, mostly due to bilateral cortical haemorrhage or thrombosis of adrenal vessels. The presence of antibodies against adrenal cortex was never documented in these patients. Here we report a case of recurrent thrombophlebitis, acute adrenal failure, and chronic hepatitis occurring in a young man found to have antiphospholipid antibodies and lupus anticoagulant. Autoantibodies against adrenal cortex were detected and abdominal ultrasonography showed morphologically normal adrenals. Mild thrombocytopaenia, Coomb's positive anaemia, increase in alanine- and aspartate-aminotransferases and increase in urinary protein excretion were found. Autoantibodies against liver/kidney microsomes were positive and liver biopsy was compatible with autoimmune hepatitis. The patient was treated with cortisone acetate, fludrocortisone and warfarin. Dilated cardiomyopathy was revealed one year later and coronarography did not document any occlusive coronary disease. Three years later, titres of autoantibodies, including those directed towards the adrenal cortex, were increased and others, previously absent, were detected. Nevertheless, the patient's clinical conditions seemed unchanged. At this time, an abdominal CT scan showed adrenal dysmorphisms with bilateral annular calcifications and central hypodensities suggesting previous bilateral adrenal haematomas. The hypercoagulable state that occurs in antiphospholipid syndrome can induce a localized inflammatory response generated by tissue injury, with a consequent release of intracellular antigens and antibodies production. Consequently, tissue-specific autoantibodies positivity may persist until the cells involved in antigen production are completely destroyed.
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PMID:Antiphospholipid syndrome, adrenal failure, dilated cardiomyopathy and chronic hepatitis: an unusual manifestation of multiorgan autoimmune injury? 991 71

Infections are thought to be important in the pathogenesis of many heart diseases. Coxsackievirus B3 (CVB3) has been linked to chronic dilated cardiomyopathy, a common cause of progressive heart disease, heart failure and sudden death. We show here that the sarcoma (Src) family kinase Lck (p56lck) is required for efficient CVB3 replication in T-cell lines and for viral replication and persistence in vivo. Whereas infection of wild-type mice with human pathogenic CVB3 caused acute and very severe myocarditis, meningitis, hepatitis, pancreatitis and dilated cardiomyopathy, mice lacking the p56lck gene were completely protected from CVB3-induced acute pathogenicity and chronic heart disease. These data identify a previously unknown function of Src family kinases and indicate that p56lck is the essential host factor that controls the replication and pathogenicity of CVB3.
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PMID:The tyrosine kinase p56lck is essential in coxsackievirus B3-mediated heart disease. 1074 50

Coxsackievirus B3 (CVB3) infection can result in myocarditis, which in turn may lead to a protracted immune response and subsequent dilated cardiomyopathy. Human decay-accelerating factor (DAF), a binding receptor for CVB3, was synthesized as a soluble IgG1-Fc fusion protein (DAF-Fc). In vitro, DAF-Fc was able to inhibit complement activity and block infection by CVB3, although blockade of infection varied widely among strains of CVB3. To determine the effects of DAF-Fc in vivo, 40 adolescent A/J mice were infected with a myopathic strain of CVB3 and given DAF-Fc treatment 3 days before infection, during infection, or 3 days after infection; the mice were compared with virus alone and sham-infected animals. Sections of heart, spleen, kidney, pancreas, and liver were stained with hematoxylin and eosin and submitted to in situ hybridization for both positive-strand and negative-strand viral RNA to determine the extent of myocarditis and viral infection, respectively. Salient histopathologic features, including myocardial lesion area, cell death, calcification and inflammatory cell infiltration, pancreatitis, and hepatitis were scored without knowledge of the experimental groups. DAF-Fc treatment of mice either preceding or concurrent with CVB3 infection resulted in a significant decrease in myocardial lesion area and cell death and a reduction in the presence of viral RNA. All DAF-Fc treatment groups had reduced infectious CVB3 recoverable from the heart after infection. DAF-Fc may be a novel therapeutic agent for active myocarditis and acute dilated cardiomyopathy if given early in the infectious period, although more studies are needed to determine its mechanism and efficacy.
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PMID:Coxsackievirus B3-associated myocardial pathology and viral load reduced by recombinant soluble human decay-accelerating factor in mice. 1253 88

Heart transplantation (HTx) in Taiwan, which started in 1987, now includes more than 500 cases. From July 1988 to September 2003, we performed 215 cases of orthotopic HTx in 164 male and 51 female recipients of mean age of 47.3 +/- 14.3 years, (range 2.7 to 74.9 years). The leading etiologies were dilated cardiomyopathy (CMP), 68.5%; ischemic CMP, 20.2%; and valvular CMP, 4.2%. The actuarial survival rates at 1, 5, and 10 years are 88.3%, 77.1%, and 57.2%, respectively. We performed the first case of HTx in Asia after bridging for 14 days with an indigenous total artificial heart (TAH; the Phoenix-7 model); we performed the first case of infant HTx without blood transfusion and also the first case of autotransplantation of heart for repair of a left ventricular rupture after a mitral valve replacement. These cases were all successful with the longest surviving HTx recipient in Asia. We have used the biatrial anastomosis technique in all cases. We discovered familial CMP due to mitochondrial defects in two pediatric cases. Because of the scarcity of donor hearts, we have used size-mismatched hearts as well as suboptimal and hepatitis-positive donor hearts, all with satisfactory outcomes. Our experience has shown comparable results to Western programs, with efficacy and cost-effectiveness. We find the technique of biatrial anastomosis for orthotopic HTx to result in a low incidence of tricuspid regurgitation and conduction anomalies. The use of suboptimal and size-mismatched donor hearts is also promising.
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PMID:Heart transplantation at Cheng Hsin General Hospital in Taiwan: 15-year experience. 1556 Dec 53

Virus infection was conventionally considered to cause myocarditis, which resulted in development of dilated cardiomyopathy. Recent studies suggest that hepatitis C virus (HCV) is involved in the development of dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy in addition to myocarditis. Furthermore, left ventricular aneurysm represents the same morbid state not only after myocardial infarction but also after myocarditis. There were wide variations in the frequency of detection of HCV genomes in cardiomyopathies in different regions or in different populations. Major histocompatibility complex class II genes may play a role in the susceptibility to HCV infection, and may influence the development of different phenotypes of cardiomyopathies. If it is the fact that the myocardial damage is caused by HCV, it might be expected that interferon (IFN) treatment would be useful for its treatment. Patients receiving IFN treatment of hepatitis were screened by thallium myocardial scintigraphy, and an abnormality was discovered in half of patients. Treatment with IFN resulted in disappearance of the image abnormality. It has thus been suggested that mild myocarditis and myocardial damage may be cured with IFN. We have recently found that high concentrations of circulating cardiac troponin T are a specific marker of cardiac involvement in HCV infection. By measuring cardiac troponin T in patients with HCV infection, the prevalence of cardiac involvement in hepatitis C virus infection will be clarified. We are proposing a collaborative work on global network on myocarditis/cardiomyopathies due to HCV infection.
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PMID:Role of hepatitis C virus in cardiomyopathies. 1632 60

Unhealthy alcohol use is among the leading causes of morbidity and mortality in the United States. Among military personnel, service members between the ages 18 and 25 had a 27.3% prevalence of heavy drinking in the previous 30 days, compared to 15.3% among civilians in the same age group. In the civilian world, > 100 million patients are treated in U.S. emergency departments (ED) annually; 7.9% of these visits are alcohol related. Alcohol is associated with a broad range of health consequences that may ultimately present in the ED setting: traumatic injuries (e.g., motor vehicle crashes, intentional violence, falls); environmental injuries (e.g., frostbite); cardiovascular problems (e.g., hypertension, dilated cardiomyopathy); gastrointestinal disorders (e.g., hepatitis, pancreatitis, gastrointestinal bleeding); neurological problems (e.g., encephalopathy, alcohol withdrawal, withdrawal seizures), as well as psychological problems (e.g., depression, suicide). Seminal work has been done to create behavioral interventions for at-risk drinkers. These motivational interventions have been found to be successful in encouraging clients to change their risky behaviors. We present such a technique, called the Brief Negotiated Interview as performed in a civilian ED setting, in hopes of adapting it for use in the military context. Military health care providers could easily adapt this technique to help reduce risky levels of alcohol consumption among service members, retirees, or military dependents.
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PMID:Brief interventions to reduce harmful alcohol use among military personnel: lessons learned from the civilian experience. 1680 38

Chronic hepatitis C can be associated with extrahepatic manifestations; thus, we explored the association of this viral infection with dilated cardiomyopathy in a group of sixty-three patients with a cardiac ejection fraction of less than 40% determined by an echocardiogram in a prospective study. Two of the forty-one patients with non-ischemic cardiomyopathy (4.8%) had serum antibodies to the hepatitis C virus and one of those had hepatitis C virus RNA (2.4%) in serum, consistent with chronic hepatitis C. One of the 22 patients with ischemic cardiomyopathy (4.5%) had serum antibodies to the hepatitis C virus but the hepatitis C virus RNA was not detected in their serum, consistent with prior infection but not chronic hepatitis C. In this study, chronic hepatitis C was not prevalent in the group of patients, although the only patient with chronic hepatitis C had non-ischemic cardiomyopathy. As a genetic predisposition to develop cardiomyopathy secondary to chronic hepatitis C has been suggested to be relevant in this type of complication, studies that include different racial and ethnic groups are warranted, as treatment of the hepatitis may lead to resolution of the cardiomyopathy.
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PMID:Prevalence of hepatitis C virus infection in patients with cardiomyopathy. 1950 52


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