Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis virus infection, especially type C (hepatitis C virus [HCV]), has been suggested to be one of the important pathogenetic factors for low- and high-grade B-cell lymphoma, including splenic marginal zone lymphoma (SMZL), in southern Europe. Here, we analyzed the incidences of HCV and hepatitis B virus (HBV) infections, and the clinicopathologic features in 29 cases of splenic diffuse large B-cell lymphoma (DLBCL), 10 SMZL, 3 splenic mantle cell lymphoma, 1 hairy cell leukemia, 13 B-chronic lymphocytic leukemia, and 12 hepatosplenic T-cell and natural killer cell lymphoma. Fifteen (51.7%) splenic DLBCL cases were HCV antibody-positive, and another 6 (20.7%) had the HBsAg. The incidence of each was significantly (P < .01) higher than those of HCV (9.3%) and HBV (1.9%) infections in 54 node-based DLBCL cases. Four examined HCV-positive DLBCL cases showed no type II cryoglobulinemia. HCV RNA was detected in fresh tumor tissues from 6 of 7 examined DLBCL cases, and HBV DNA was present in another 2, as evaluated by real-time polymerase chain reaction. Immunohistologically, tumor cells in 5 of 7 examined DLBCL cases showed intracytoplasmic reactions for HCV NS3 and E2 proteins and the viral receptor CD81. Of 6 cases, 2 showed an intranuclear reaction for the HBV surface protein. By Southern blot analysis, no rearrangement of the Bcl2 gene was detected in the tumor tissue of 7 HCV-positive DLBCL cases. For the other types of malignant lymphoma, 1 case each of SMZL (10%) and hepatosplenic T-cell and natural killer cell lymphoma (8.3%) showed HCV infection. In conclusion, persistent human hepatitis virus infections, especially HCV, may play an important role in the tumorigenesis of splenic DLBCL in Japan.
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PMID:Splenic large B-cell lymphoma in patients with hepatitis C virus infection. 1611 4

Primary hepatic lymphomas are rare tumors. We report a case of a 72 year-old woman with a past history of colonic adenocarcinoma who presented primary hepatic lymphoma of MALT-type. The patient had been operated on 3 years before for colonic adenocarcinoma, pT3N0, revealed by a bowel obstructive syndrome. She had been treated by chemotherapy for 6 months. During the follow-up, the computed tomography-scan (CT-scan) revealed the presence of a not well-demarcated mass in segment III of the liver, measuring 4 cm in diameter. The tumor was hypodense and was not enhanced on dynamic study. The mass was already present on the initial CT-scan. Left lobectomy was performed with the diagnosis of liver metastasis of the colonic adenocarcinoma. Surgical specimen showed a tumor composed of a dense infiltrate of small lymphocytes positive for B-cell markers on immunohistochemistry. The tumor contained reactive lymphoid follicles and there were numerous lympho-epithelial biliary lesions. The patient is alive and free of disease 2 years after the diagnosis. Primary hepatic lymphoma of MALT-type is a low-grade B cell lymphoma. Twenty-five cases had been reported in the literature so far. The patients were 16 females and 9 males, mean age 63.5 years. The pathogenesis is still unclear but half of the patients had a past history of chronic inflammatory liver disease (hepatitis B or C virus infection, ascaris infection, primary biliary cirrhosis) or malignant neoplasm. This tumor has a good prognosis; it is usually limited to the liver and surgical resection cures the patient in most cases.
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PMID:[Primary hepatic lymphoma of MALT-type: a tumor that can simulate a liver metastasis]. 1624 95

We describe the clinical, histological, and immunohistochemical features of primary hepatic low grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) in a liver transplant recipient with hepatitis B cirrhosis. MALT lymphomas arise in organs normally devoid of lymphoid tissue, which accumulates as a consequence of chronic antigenic stimulation associated with chronic infection or autoimmune disease. Primary hepatic MALT lymphoma is extremely rare; 13 cases have been reported worldwide to date. Our patient is the first case of primary hepatic MALT lymphoma associated with hepatitis B cirrhosis who was treated with orthotopic liver transplantation.
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PMID:Primary hepatic marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue type in a liver transplant patient with hepatitis B cirrhosis. 1638 33

The treatment of patients with non-Hodgkin's lymphoma (NHL) may be complicated by concomitant chronic hepatitis C virus (HCV) infection. Recent data suggest that HCV may also be a contributing factor to the development of this disease. Although antiviral treatment has occasionally been reported to result in the regression of lymphoma in patients with HCV infection, the importance of the control of this infection on the prognosis of lymphoma needs to be defined. Here we report a patient with diffuse large B-cell lymphoma who presented with a mass in her left breast. She had had HCV-related liver cirrhosis for 6 years. She was given rituximab monotherapy for three consecutive weeks, but treatment had to be discontinued as a result of hematological toxicity. HCV viral load also increased, but then decreased gradually after rituximab was stopped. She could be given no further therapy. Six months later she presented with spinal involvement with infiltration of the cauda equina. Though cranial-spinal radiotherapy and steroids were started, she died shortly thereafter. Though rituximab is an invaluable drug in the treatment of B-cell lymphomas, we believe that the use of such agents with potentially long-lasting effects on B lymphocytes requires extended vigilance for accelerated replication of hepatitis B and C viruses.
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PMID:Accelerated hepatitis C virus replication with rituximab treatment in a non-Hodgkin's lymphoma patient. 1670 40

Patients with hepatitis B virus (HBV) infection have a higher morbidity and mortality after heart transplantation (HT). HBV infection is endemic in Taiwan. We studied the effect of lamivudine treatment of HBV infection after HT. From July 1987 to July 2005, 252 patients underwent HT. All recipients and donors underwent routine screening of hepatitis B surface antigen (HBsAg), hepatitis B e antigen, antibody to hepatitis B surface antigen, antibody to hepatitis B core antigen, antibody to hepatitis B e antigen, and an alanine aminotransferase (ALT) level before HT. When ALT was two times greater than the upper limit of normal or serum bilirubin was higher than 3 mg/dL in HBsAg-positive patients, HBV-DNA were checked by a branched DNA assay or polymerase chain reaction. When HVB-DNA was greater than 100,000 copies/mL, lamivudine (100 mg per day) was prescribed indefinitely. There were 14 patients under lamivudine treatment after HT, among whom, none suffered severe adverse reactions from lamivudine. Four patients died: one due to end-stage cirrhosis while awaiting liver transplantation at 14 months after HT. Two died of sudden death at 54 months and 138 months after HT. Another died of diffuse B cell lymphoma at 62 months after HT. All the survivors have normal ALT and undetectable HBV-DNA after lamivudine treatment. But the YMDD mutant was detected in two patients. With successful treatment of HBV infection in HT, it is not necessary to exclude HBV infection patients from HT.
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PMID:Successful treatment of hepatitis B virus infection with Lamivudine after heart transplantation. 1698 24

The chimeric anti-CD20 monoclonal antibody, rituximab, is a promising treatment for cutaneous B-cell lymphomas. Classically used in combination with a multiagent-chemotherapy regimen, it can sometimes give excellent results alone. Because of its selective action on B lymphocytes, it is considered a moderate immunosuppressant in terms of infection. We describe a woman with relapsed cutaneous follicular centre B-cell lymphoma and secondary lymph-node involvement treated with rituximab alone, which induced a complete remission. One year later, she experienced a fatal hepatitis B virus (HBV) reactivation. Several such HBV reactivations were reported after combined rituximab and multiagent chemotherapy for B-cell lymphomas. This is the first case of HBV reactivation occurring during the year following rituximab monotherapy in the absence of any other immunosuppressive factor.
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PMID:Late lethal hepatitis B virus reactivation after rituximab treatment of low-grade cutaneous B-cell lymphoma. 1703 41

In rituximab-containing regimen for lymphoma, the role of lamivudine therapy has not been well established. Therefore, in this nonrandomized phase II clinical study, hepatitis B virus (HBV) carriers with B-cell lymphoma who received rituximab-containing regimen were treated with oral administration of lamivudine. The incidence and severity of hepatitis along with other adverse clinical outcomes were analyzed. Between January 2003 and March 2006, 29 consecutive patients were enrolled. Four of the 29 patients (13.8%) developed hepatitis during chemotherapy, none of which was attributed to HBV reactivation. According to WHO acute toxicity assessment criteria, the severity of hepatitis was grade I in two patients (6.9%) and grade II in two patients (6.9%). In these four patients, only one (3.5%) had interval delay in chemotherapy. No patient had total abnormal bilirubin. No patient had died as the result of hepatitis during the treatment. Interestingly, one of the 29 patients developed HBV activation 5.1 months after the withdrawal of lamivudine. This patient recovered after reinstallation of lamivudine therapy and is still alive. Consequently, our study confirmed previous reports that prophylactic lamivudine therapy can prevent HBV reactivation in HBV carriers who were receiving rituximab-containing regimen for lymphoma.
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PMID:The effectiveness of lamivudine in preventing hepatitis B viral reactivation in rituximab-containing regimen for lymphoma. 1880 36

In a 56-year-old white male patient, a membranoproliferative glomerulonephritis Type I was diagnosed after a 12-month history of low grade B cell lymphoma (Binet A). HIV, Hepatitis B and C serology were negative. Due to an impairment of renal function despite chemotherapy with COP, an immunochemotherapy consisting of rituximab (6 cycles) and bendamustine (4 cycles) was given. This therapeutic approach caused a complete remission of the nephrotic syndrome. Renal function and arterial hypertension improved markedly. In addition, urinary sediment became normal and proteinuria disappeared completely.
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PMID:Remission of a B cell CLL-associated membranoproliferative glomerulonephritis Type I with rituximab and bendamustine. 1839 3

The etiology of most lymphoproliferative disorders remains unclear, though several hypotheses have been proposed. One of the conjectured mechanisms is infection of a tumor clone by an oncologic virus. Recently, evidence has arisen implicating both hepatitis B and, even more so, hepatitis C viruses in the pathogenesis of lymphoproliferative disease. Based on this information, we surveyed the prevalence of hepatitis B and C virus in patients with lymphoproliferative disease. A total of 334 newly-diagnosed lymphoproliferative disease patients (200 males, 134 females) and 1,014 (133 females, 881 males) healthy controls were randomly recruited from the university blood bank. Serologic evaluation for hepatitis B and C viruses was conducted and confirmed using PCR analyses. Those with hepatitis B and/or C, controls, and subgroups of patients with lymphoproliferative disease were compared using Pearson Chi-square analysis. Among patients with lymphoid tumors, the seropositivity of HbsAg and/or anti-HCV was 8.7% (29/334), and among the controls 6.1% (49/802), however this difference did not achieve statistical significance (P = 0.23, OR: 1.36, 95% CI: 0.82-2.26). We found no significant gender- or age-related differences for either hepatitis B or C seropositivity. There were no significant differences between the seropositivity rates of hepatitis B, C, or both in either NHL or Hodgkin's lymphoma. However, in the diffuse large cell lymphoma and follicular lymphoma subgroups, the HbsAg seropositivity rate was significantly higher than that in the controls (P = 0.017, P = 0.048, respectively), as was the seropositivity rate for hepatitis C in those with diffuse B cell lymphoma versus controls (P = 0.008). We did not identify any significant difference in the combined prevalence of hepatitis B or C seropositivity between patients with lymphoproliferative disorders and controls. However, significant differences were revealed among certain patient subgroups versus the controls. These two viruses could play a role in the development of certain specific lymphoproliferative disorders. Nevertheless, larger epidemiological studies are necessary and should focus, particularly on specific patient subgroups.
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PMID:Prevalence of hepatitis B and C viruses in patients with lymphoproliferative disorders. 1883 91

Hepatitis C virus (HCV) and hepatitis B virus (HBV) have been associated with hematopoietic malignancies, but data for many subtypes are limited. From the U.S. Surveillance, Epidemiology, and End Results-Medicare database, we selected 61,464 cases (> or = 67 years) with hematopoietic malignancies and 122,531 population-based controls, frequency-matched by gender, age, and year (1993--2002). Logistic regression was used to compare the prevalence of HCV, HBV, and alcoholic hepatitis in cases and controls, adjusted for matching factors, race, duration of Medicare coverage, and number of physician claims. HCV, HBV, and alcoholic hepatitis were reported in 195 (0.3%), 111 (0.2%), and 404 (0.7%) cases and 264 (0.2%), 242 (0.2%), and 798 (0.7%) controls, respectively. HCV was associated with increased risk of diffuse large B-cell lymphoma [odds ratio (OR) 1.52, 95% confidence interval (95% CI) 1.05-2.18], Burkitt lymphoma (OR 5.21, 95% CI 1.62-16.8), follicular lymphoma (OR 1.88, 95% CI 1.17-3.02), marginal zone lymphoma (OR 2.20, 95% CI 1.22-3.95), and acute myeloid leukemia (OR 1.54, 95% CI 1.00-2.37). In contrast, HBV was unrelated to any hematopoietic malignancies. Alcoholic hepatitis was associated with decreased risk of non-Hodgkin lymphoma overall, but increased risk of Burkitt lymphoma. In summary, HCV, but not other causes of hepatitis, was associated with the elevated risk of non-Hodgkin lymphoma and acute myeloid leukemia. HCV may induce lymphoproliferative malignancies through chronic immune stimulation.
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PMID:Hematopoietic malignancies associated with viral and alcoholic hepatitis. 1895 21


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