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)

Among 262 inpatients with hematologic diseases who were referred for chemotherapy or immunosuppressive therapy between January, 1985, and December, 1989, nine (3.4%) patients, including two with Hodgkin's disease (HD), three with acute myeloblastic leukemia, one with chronic myelogenous leukemia, two with multiple myeloma and one with aplastic anemia, were found to be hepatitis B virus (HBV) carriers before their chemotherapy began. All six HBV carriers who received chemotherapy containing glucocorticoid showed mild-to-moderate elevations in serum transaminase levels after the chemotherapy. Five showed a rise in titer of the hepatitis B surface antigen, HBsAg. In contrast, three HBV carriers not receiving glucocorticoid showed no change in serum transaminase after chemotherapy. One HBV carrier with HD suffered from severe icteric hepatitis after the withdrawal of multiagent chemotherapy containing glucocorticoid. The HBV-DNA polymerase rose markedly and was accompanied by a marked rise in titer of HBsAg. The results warn us to keep in mind the possibility of glucocorticoid inducing an activation of HBV infection, which may result in severe hepatitis in some HBV carriers. Although further investigation is required, it is recommended that HBsAg-positive patients with hematologic malignancies should, if possible, be treated without glucocorticoid.
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PMID:Activation of hepatitis B virus infection by chemotherapy containing glucocorticoid in hepatitis B virus carriers with hematologic malignancies. 175 16

A multicenter prospective randomized trial of four versus six weeks of amphotericin B, 0.3 mg/kg per day, plus flucytosine, 150 mg/kg per day, was performed with 194 patients with cryptococcal meningitis. One or more toxic drug reactions developed in 103 patients: azotemia (51), renal tubular acidosis (two), leukopenia (30), thrombocytopenia (22), diarrhea (26), nausea/vomiting (10), and hepatitis (13). The four- and six-week regimens were complicated by toxicity in 44 percent and 43 percent of cases, respectively. Toxicity appeared during the first two weeks of therapy in 56 percent and during the first four weeks in 87 percent. Azotemia did not occur more frequently in renal transplant recipients or diabetic patients. Cytopenias did not appear more often in patients with hematologic malignancies or those receiving immunosuppressive therapies. Toxic reactions that contributed to death developed in five patients (two with azotemia, one with pancytopenia, one with hepatitis, one with ileus). Amphotericin B-induced azotemia was not a significant risk factor for the subsequent development of bone marrow, gastrointestinal, or hepatic toxicity attributable to flucytosine. Flucytosine toxicity was associated with peak serum flucytosine levels of 100 micrograms/ml or more during two or more weeks of therapy (p = 0.005). Peak 5-fluorouracil levels were not predictive of toxicity. An initial dose of flucytosine is recommended based on the creatinine clearance: 150 mg/kg per day at a creatinine clearance above 50 ml/minute, 75 mg/kg per day at a creatinine clearance of 26 to 50 ml/minute, and 37 mg/kg per day at a creatinine clearance of 13 to 25 ml/minute. The serum creatinine level should be monitored twice weekly and the creatinine clearance weekly during therapy in order to anticipate changes in serum flucytosine concentration. In addition, it is recommended that the serum flucytosine level be determined two hours after an oral dose once a week, and that the dose be adjusted to maintain a level of 50 to 100 micrograms/ml.
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PMID:Toxicity of amphotericin B plus flucytosine in 194 patients with cryptococcal meningitis. 330 26

The widespread use of alpha-interferon (IFN-alpha) therapy in different diseases draws attention to its side effects, such as autoimmune-related diseases, especially thyroid autoimmune dysfunctions. Data about hepatitis and nonhematologic neoplasia are available, while data about hematologic malignancies are fragmentary. We studied the incidence of autoimmune-related disturbances and thyroid dysfunctions in 54 consecutive patients suffering from hematologic malignancies, treated with recombinant human IFN-alpha for a mean time of 15.9 +/- 8.9 months. Our results minimize the incidence of autoimmune dysfunctions in hematologic malignancies as side effects of IFN-alpha therapy. We registered the appearance of autoantibodies in only 3 females (5% of total): 2 patients (1 affected with essential thrombocythemia and one with multiple myeloma) presented antithyroglobulin antibodies with no clinical symptoms; 1 patient, affected with essential thrombocythemia, developed antinuclear antibodies with arthralgia and myalgia. ARA criteria for systemic lupus erythematosus were not fulfilled but the therapy had to be interrupted. No patient developed thyroid dysfunction. In patients with hematologic malignancies, the dosage and the duration of IFN-alpha treatment do not seem to influence the appearance of autoantibodies, while female sex appears to be a risk factor.
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PMID:Autoimmune thyroid dysfunctions in hematologic malignancies treated with alpha-interferon. 772 47

In a National Audit of 1500 liver biopsies, 38% were for suspected malignancy. To measure their contribution to clinical decisions, the initial diagnoses, biopsy diagnoses, final diagnoses, and outcomes were coded by computer and compared. Most patients (92%) were investigated for advanced malignancy. The accuracy of clinical diagnosis was 78% against final diagnosis. Liver biopsy was seen as 'confirming' clinical diagnosis overall. This was achieved in 67% (75% with ultrasound guidance), and specificity was almost 100%. However, hepatocellular cancer was confirmed by biopsy in only 32% and haematological malignancy in 13% of suspected cases. Within 3 months, 44% of patients with histological malignancy had died. Histological tumour type was not used in 36% of final diagnoses. Of patients with a malignancy-negative liver biopsy--showing reactive hepatitis, normality, or cholangitis/cholestasis--25%, 47% and 60%, respectively, had final malignant diagnoses. In 6% of patients, biopsy showed chronic liver disease. Only 12% of deaths were autopsied. Liver biopsy contributes very high specificity to the diagnosis of malignancy, and detects non-malignant disease. Failure to use tumour type may result in sub-optimal therapy. Improving diagnostic practice requires more information on outcomes, including autopsies.
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PMID:Liver biopsy in the diagnosis of malignancy. 854 67

Hepatitis G virus (HGV) is a newly described virus that has been implicated in transfusion-associated hepatitis. The prevalence of HGV in a group of multitransfused patients with hematological malignancy was studied using a reverse transcription polymerase chain reaction technique. Transfusion histories and serum aspartate aminotransferase (AST) levels were recorded. HGV was detected in 29 of 60 (48%) patients. There was no difference in HGV positivity rates between those with normal AST levels and those with raised AST levels. Analysis of patients by treatment type showed that 20 of 33 (61%) patients who received a bone marrow transplantation procedure were HGV positive compared with 9 of 27 (33%) treated with conventional combination chemotherapy (P = .036) despite similar transfusion histories. There was no significant difference in HGV positivity between patients treated before the introduction of United Kingdom blood donor screening for hepatitis C virus antibody:18 of 39 (46%) and those treated after the introduction of screening 11 of 21 (52%). HGV infection appears to be extremely common in these patients; however, the clinical significance of these findings with respect to liver dysfunction is not yet clear.
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PMID:High prevalence of hepatitis G virus in bone marrow transplant recipients and patients treated for acute leukemia. 916 Jun 93

We report a case of a 41-year-old man with acute myelogenous leukemia who developed fulminant hepatitis from reactivation of trace hepatitis B virus (HBV) 2 months after complete remission. Although he became positive for HB surface antigen at the onset of fulminant hepatitis, he had been negative for HBV serum markers, and only HBV DNA was detected by polymerase chain reaction (PCR) amplification on admission. The original stocks of serum samples from all blood donors were tested again for HBV DNA by PCR, and all samples were negative. This case demonstrates that testing for HBV DNA by PCR is necessary before chemotherapy, because silent HBV carriers are rare and fulminant hepatitis may be induced by chemotherapy in patients with hematologic malignancies.
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PMID:Fulminant hepatitis type B after chemotherapy in a serologically negative hepatitis B virus carrier with acute myelogenous leukemia. 1137 46

Lamivudine was administrated to six patients with acute exacerbation of hepatitis B who were undergoing immunosuppressive therapy. All patients had chronic hepatitis B and were receiving immunosuppressive therapy for other primary diseases (hematologic malignancies, collagen diseases, renal transplantation) when the hepatitis flared up. Only one patient tested positive for the hepatitis B virus e (HBe) antigen. All patients had normal ALT levels and were anti-HBe-positive before immunosuppressive therapy. The patients were treated with 150 mg of lamivudine daily. Lamivudine was well tolerated and showed no effect on the primary disease. In all patients, hepatitis B virus (HBV) DNA levels decreased in response to lamivudine administration. Four patients recovered from exacerbation, but two patients died from complications. Molecular analysis revealed that, regardless of whether patients had the wild HBV genotype or mutations within the core promoter or precore HBV regions, the effectiveness of lamivudine therapy was the same. These results demonstrated that lamivudine is very effective for treating acute exacerbation of chronic hepatitis B that occurs while a patient is undergoing immunosuppressive therapy, regardless of the phenotype of the virus.
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PMID:Lamivudine treatment for acute exacerbation of hepatitis B in patients undergoing immunosuppressive therapy. 1188 19

Postinfantile giant cell hepatitis has been associated with various aetiologies, including drug taking, autoimmune diseases and viral infections. We present a fatal case of giant cell hepatitis in a patient with chronic lymphocytic leukaemia. No liver biopsy was available ante-mortem. The patient was treated with corticosteroids and aciclovir for suspected autoimmune hepatitis and reactivation of Epstein-Barr virus in the context of his haematological malignancy. Post-mortem liver biopsy showed severe giant cell hepatitis while the study of liver tissue by electron microscopy revealed paramyxo-like viral particles in the cytoplasm of the affected hepatocytes similar to those observed in previous reports of giant cell hepatitis. This case illustrates that the diagnosis of the underlying cause of giant cell hepatitis may be complicated because a heterogeneous group of different aetiologies needs to be investigated. The identification of the causative agent is essential before commencing any kind of therapy. A few sporadic case reports of paramyxo-like virus related, postinfantile giant cell hepatitis have shown that ribavirin was quite effective treatment but further clinical evaluation is needed.
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PMID:A fatal case of postinfantile giant cell hepatitis in a patient with chronic lymphocytic leukaemia. 1270 15

Hepatitis B virus (HBV) reactivation is well documented in infected patients who have hematologic malignancies, precluding appropriate chemotherapy courses and, therefore, increasing the possibility of relapse of malignancies. The objective of this study was to evaluate lamivudine treatment to prevent hepatitis B reactivation in children with cancer who acquired infection with HBV and so allow completion of optimal chemotherapy. Ten children (7:3 M:F; median age: 9.8 years), undergoing chemotherapy for hematological malignancies and suffering from immunosuppressive-induced hepatitis B virus reactivation, were treated concurrently with lamivudine (3 mg/kg bw, od) for up to 18 months. All were HBsAg+ve, HBsAb-ve, HBV-DNA+ve. Serology markers (HBsAg/Ab, HBeAg/Ab, HBV-DNA) and ALT were tested 3 monthly. Histological assessments were performed pre- and 18 months post-lamivudine therapy. During lamivudine therapy chemotherapy courses were completed for all children, and none of the patients suffered reactivation of hepatitis. After a median follow-up of 10 months, remission of malignancy was maintained in 7/10 patients while 3 patients relapsed. HBeAg+ve seroconversion occurred in 4/9 HBeAg+ve children within 3 months. After 9 months of therapy, 8/10 were HBV-DNA-ve. Six out of 7 children with histological evidence of chronic hepatitis showed marked improvement post-therapy. Lamivudine therapy for up to 18 months in children receiving chemotherapy helped prevent recurrence of hepatitis B exacerbations and improved the underlying chronic hepatitis, while facilitating completion of appropriate chemotherapy regimens without compromise.
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PMID:Lamivudine facilitates optimal chemotherapy in hepatitis B virus-infected children with hematological malignancies: a preliminary report. 1516 May 13

Lymphoma is a common hematological malignancy. Hepatitis viruses, especially hepatitis B and hepatitis C, are known risk factors for development of non-Hodgkin lymphomas. However, there are a number of patients with hepatitis in whom no virus can be identified and it was therefore postulated that there may be other agents which may be causing hepatitis. Many new hepatitis viruses have indeed been identified and proposed to have possible roles in pathogenesis of many disorders. Hepatitis G virus (HGV) is an example of a newly detected hepatitis virus. Whethere there is a correlation between infection and development of non-Hodgkin's lymphoma is of interest. Therefore an appraisal of the prevalence of HGV RNA among patients with B cell non-Hodgkin's lymphoma comparing with healthy control subjects was performed. According to the literature review, three reports covering 247 cases of non Hodgkin's lymphoma were recruited. The overall prevalence of HGV RNA positivity was found to be 7.2 % (18/247). Of the three reports, only two had complete data on the prevalence in both patients with B cell non-Hodgkin's lymphoma and healthy control subjects andwere used for further metanalysis study, covering 178 cases and 355 healthy subjects. The overall antibody positive rate in the patients and healthy subjects were 8.4 % (15/178) and 0.8 % (3/355), respectively, with an odds ratio is 10.8. According to this study, it can be seen that individuals who are HGV RNA positive may be at very high risk of B cell non-Hodgkin's lymphoma development.
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PMID:Individuals with HGV-RNA are at high risk of B cell non-Hodgkin's lymphoma development. 1610 37


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