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)

We describe a hepatitis B virus carrier who satisfied the criteria of autoimmune hepatitis proposed by the International Autoimmune Hepatitis Group. A 43-year-old Japanese female showed human leukocyte antigen typing including DR4 in addition to hypergammaglobulinemia, presence of autoantibodies, and liver histology suggestive of autoimmune hepatitis. Moreover, the predominant presence of hepatitis B core antigen in nuclei rather than in cytoplasm of hepatocytes suggested less of a possibility of liver cell damage related to hepatitis B virus infection. She completely responded to immunosuppressive therapy and no clinical or biochemical relapse has been recognized to date.
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PMID:Hepatitis B virus carrier status linked to autoimmune hepatitis. 883 98

Idiopathic granulomatous hepatitis is a rare disease of unknown cause that is characterized by recurrent fevers and granuloma in the liver. Attempts to define an exact etiology of the fever of granulomatous hepatitis frequently do not yield a precise diagnosis. Idiopathic granulomatous hepatitis was confirmed after a thorough work up and negative cultures and serologies were obtained, and in the absence of another condition that could lead to granulomas in the liver. We have experienced a 67-year-old female patient who presented with prolonged fever for 2 months and revealed granuloma in liver biopsy. She was treated with glucocorticosteroid and defervescence resulted.
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PMID:Idiopathic granulomatous hepatitis manifested with fever of unknown origin. 885 54

Bone marrow transplantation (BMT) has been previously reported as a successful mode of treatment for hepatitis B and associated severe aplastic anemia (SAA). Non-A, non-B, non-C hepatitis is one of the causes of SAA. The etiology of SAA caused by non-A, non-B, non-C hepatitis is unknown. There is evidence that the immune response and, specifically, T cells and monocytes have a major role in both HCV- and HBV-induced liver damage. The liver damage caused by non-A, non-B, non-C hepatitis may be associated with similar mechanisms. We describe an 8-year-old girl who developed SAA post-non-A, non-B, non-C hepatitis infection. She was treated by in vivo CAMPATH-1G antibodies followed by T cell depleted HLA-matched BMT and cyclosporin A, resulting in gradual improvement and almost normalization of liver function. We suggest that treatment with CAMPATH-1G followed by T cell-depleted BMT and cyclosporin A could be a novel mode of therapy for viral non-A, non-B, non-C hepatitis-induced liver damage and associated SAA.
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PMID:In vivo CAMPATH-1 followed by T cell-depleted bone marrow transplantation: a potential new mode of therapy for hepatitis-associated severe aplastic anemia (SAA). 886 69

Liver transplantation is the treatment of choice for many patients with acute and chronic hepatic failure. Although uncommon, hepatic failure may occur during pregnancy or after delivery, and liver transplantation may be life-saving. We report a case of a liver transplant performed during pregnancy in a patient with decompensated cirrhosis from chronic autoimmune hepatitis. A patient with chronic autoimmune hepatitis developed decompensated cirrhosis at approximately 18 weeks' gestation. Despite attempts at medical stabilization, her condition worsened, and an orthotopic liver transplant was performed at 23 weeks. The procedure was complicated by transient hypotension, and fetal death was diagnosed postoperatively. Her postoperative course was complicated by hypotension, infection, oliguric renal failure, anemia, thrombocytopenia, and rejection. She spontaneously labored on the 6th postoperative day and delivered without difficulty a 560-g stillborn male. The patient recovered and was discharged 31 days after surgery on prednisone, tacrolimus, mycostatin, erythropoietin, and iron. Liver transplantation may be a valuable therapeutic option for treatment of pregnant or puerperal women with hepatic failure.
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PMID:Hepatic transplantation during pregnancy and the puerperium. 902 84

Pericarditis is a frequent and serious complication of chronic uremia. The uremic pericarditis can get much improvement by aggressive heparin-free hemodialysis therapy. However, the presenting symptoms and signs are too nonspecific to identify at early stage. Cardiac tamponade is the late and fatal complication, and need the immediate & adequate management. A 35-year-old female patient suffered from nausea, vomiting and right upper quadrant dull pain in November 1993, and was admitted to a local hospital. Uremia (BUN: 210 mg/dl, serum Cr.: 13.2 mg/dl) and abnormal liver function (SGOT: 330 IU/L, SGPT: 449 IU/L) were found, then she received regular hemodialysis therapy. About 10 days later, acute exacerbation of liver function (SGOT: 2,488 IU/L, SGPT: 1,048 IU/L), consciousness disturbance and hypotension occurred during hemodialysis. She was referred to our ER immediately. At ER, she had been on comatous, shock state with pulseless electric activity. After resuscitation and serial evaluation, cardiac tamponade was diagnosed. Emergent pericardiocentesis and then bilateral partial pericardiectomy were done about 2 hours later. The pericardial effusion was bloody without evidence of malignancy, bacterial or TB infection. The pathology of pericardium revealed chronic inflammation only. HBsAg, Anti-HCV Ab, and anti-HAV IgM were undetectable. So the etiology of acute hepatitis was diagnosed as ischemic hepatitis. Her general condition and vital sign became stable thereafter. The liver function also improved rapidly. She was discharged one month later and received maintainance hemodialysis therapy and no evidence of recurrence till now.
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PMID:[Acute uremic pericarditis presented as cardiac tamponade with acute ischemic hepatitis: a case report]. 904 74

We describe a 43-year-old woman with clinical features compatible with autoimmune cholangiopathy recently reported by Ben Ari et al. She was negative for anti-mitochondrial antibody, positive for high titer anti-nuclear antibody with homogeneous pattern, high levels of serum immunoglobulin G and nearly normal levels of serum immunoglobulin M for more than five years. In the early stages of the disease, the elevations of serum transaminase, alkaline phosphatase and gamma-glutamyl transpeptidase were well controlled by the administration of ursodeoxycholic acid. After five years of follow-up, she showed the second exacerbation of liver function tests, which then rapidly improved by prednisone administration. To analyze the antigen diversity recognized by T-cells in the liver, T-cell receptor repertoire was examined by immuno-histochemistry. The liver biopsy obtained in the early stage showed clonal accumulation of V beta 5.1-positive cells in portal areas, which was found in patients neither with primary biliary cirrhosis nor autoimmune hepatitis. In conclusion, these data suggest that T-cell response in autoimmune cholangiopathy is different from those two autoimmune liver diseases, which may imply a distinct entity of the disease.
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PMID:Clonal accumulation of V beta 5.1-positive cells in the liver of a patient with autoimmune cholangiopathy. 906 73

Hepatitis due to herpes simplex virus (HSV) is unusual in healthy individuals. To date, only 56 cases of HSV hepatitis in adult patients have been reported, including 21 pregnant patients. We describe a 25-year-old white woman in her 30th week of gestation who had progressive acute hepatitis. Histologic examination of the liver biopsy specimen showed diffuse microabscesses involving more than 50% of the hepatic parenchyma, with multiple hepatocytes containing Cowdry type A and ground-glass nuclear inclusions. The diagnosis of herpes hepatitis was confirmed by positive immunoreactivity to HSV antibodies in the tissue sections. Intravenous acyclovir therapy was immediately initiated, and the patient's condition improved dramatically. She then had a normal baby at term. Subsequently, the patient had a second pregnancy and an uncomplicated vaginal delivery without recurrence of the disease. Even though alterations of the humoral and cell-mediated immunity occur during pregnancy, herpes hepatitis is rare in pregnant women. Since the prompt administration of antiviral drugs is a lifesaving measure, we recommend including HSV hepatitis in the differential diagnosis of acute hepatitis in pregnancy.
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PMID:Gestational herpes simplex virus hepatitis. 907 13

A case of progressive encephalomyelitis with rigidity (PEWR) associated with hepatitis C virus (HCV) is reported. A 58 year-old woman presented with a clinical picture of progressive quadriparesis, sensory loss, sphincter dysfunction, painful muscle spasms in the upper and lower limbs and continuous muscle unit activity in electromyography. She developed hepatitis, pancreatitis and HCV-RNA was detected in the plasma by reverse transcription-polymerase chain reaction (RT-PCR). Postmortem histopathological examination showed encephalomyelitis with perivascular lymphocyte cuffing, infiltration and neuronal loss mainly affecting the brainstem and cervical spinal cord. The RT-PCR analysis of the postmortem brain, brainstem, liver, pancreas, plasma and CSF samples revealed the presence of HCV genome in all specimens except CSF. Clinical features, postmortem histopathology and PCR results and the possible etiopathogenesis of PEWR are briefly discussed.
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PMID:PCR detected hepatitis C virus genome in the brain of a case with progressive encephalomyelitis with rigidity. 908 76

Adenosine deaminase (ADA) deficiency typically causes severe combined immunodeficiency (SCID) in infants. We report metabolic, immunologic, and genetic findings in two ADA-deficient adults with distinct phenotypes. Patient no. 1 (39 years of age) had combined immunodeficiency. She had frequent infections, lymphopenia, and recurrent hepatitis as a child but did relatively well in her second and third decades. Then she developed chronic sinopulmonary infections, including tuberculosis, and hepatobiliary disease; she died of viral leukoencephalopathy at 40 years of age. Patient no. 2, a healthy 28-year-old man with normal immune function, was identified after his niece died of SCID. Both patients lacked erythrocyte ADA activity but had only modestly elevated deoxyadenosine nucleotides. Both were heteroallelic for missense mutations: patient no. 1, G216R and P126Q (novel); patient no. 2, R101Q and A215T. Three of these mutations eliminated ADA activity, but A215T reduced activity by only 85%. Owing to a single nucleotide change in the middle of exon 7, A215T also appeared to induce exon 7 skipping. ADA deficiency is treatable and should be considered in older patients with unexplained lymphopenia and immune deficiency, who may also manifest autoimmunity or unexplained hepatobiliary disease. Metabolic status and genotype may help in assessing prognosis of more mildly affected patients.
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PMID:Adenosine deaminase deficiency in adults. 910 4

We report the case of a 50-year-old female with malignant lymphoma presenting hemophagocytic syndrome and liver failure. She developed high fever, marked jaundice, and progressive liver failure, followed by evidence of disseminated intravascular coagulation (DIC). The course was complicated by severe hepatitis and the patient died six days after admission. Pathological diagnosis on autopsy specimens of the lung hilar lymph nodes was non-Hodgkin's T cell lymphoma, of the diffuse small cell type. Histopathologic examination of the liver demonstrated diffuse liver cell destruction with prominent T lymphocyte infiltration in the portal and periportal area. In addition to marked lymphoma cell infiltration, hemophagocytosis by prominent infiltrative macrophages was observed in various organs, such as the liver and bone marrow, indicating the hemophagocytic syndrome. The hemophagocytic syndrome characterized in the present case may have been responsible for the extremely rapid and fulminant course.
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PMID:A case of malignant lymphoma with hemophagocytic syndrome presenting as hepatic failure. 915 62


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