Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary splenic lymphoma is uncommon, constituting only 1-2% of all patients with malignant lymphoma. Despite the rarity of this malignancy, the number of primary splenic lymphoma being reported has increased due to its ambiguous definition used in the literature. We describe a case of a 41-year-old man with chronic hepatitis C virus infection presenting abdominal discomfort in the upper left quadrant, weakness, nausea and vomiting. Abdominal computed tomography revealed nodules in the congested splenic parenchyma. Splenectomy was performed and an analysis of the spleen diagnosed B-cell non-Hodgkin's lymphoma. Biopsy of the liver showed evidence of hepatitis C virus. Bone marrow biopsy revealed no tumor infiltration. The patient has been followed to date, has progressed quite well and remains essentially asymptomatic. Recently, an etiologically important role has been suggested for hepatitis C virus infection in the development of B-cell non Hodgkin's lymphoma. Lymphotropism of hepatitis C virus may play a pathological role in the development of non Hodgkin's lymphoma. It is important to add lymphoma to the list of differential diagnosis of extrahepatic disorders in patients with chronic hepatitis C virus infection.
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PMID:Primary splenic lymphoma in patient with hepatitis C virus infection: case report and review of the literature. 1132 5

We report a chronic hepatitis B virus (HBV) carrier with non-Hodgkin lymphoma (NHL) who developed HBV hepatitis following conventional dose chemotherapy and was successfully treated with lamivudine and glycyrrhizin. A 55 year-old male patient with primary testicular NHL (diffuse large B-cell type) relapsed. During the salvage chemotherapy, the patient showed elevated serum levels of transaminase and HBV-DNA due to HBV reactivation. Treatment with lamivudine, an antiviral nucleoside analog, was started at a dose of 100mg/day. Shortly after the treatment the HBV-DNA level was suppressed, and sustained elevation of transaminase levels were normalized after additional treatment with glycyrrhizin. This experience suggests that lamivudine combined with glycyrrhizin may be effective for controlling HBV replication and treating chemotherapy-induced HBV hepatitis in chronic HBV carriers with NHL.
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PMID:Lamivudine and glycyrrhizin for treatment of chemotherapy-induced hepatitis B virus (HBV) hepatitis in a chronic HBV carrier with non-Hodgkin lymphoma. 1134 73

Two male patients, aged 54 years and 17 years respectively, were treated with chemotherapy for non-Hodgkin lymphoma. Both patients were chronic hepatitis-B-virus (HBV) carriers prior to the chemotherapy. One patients died as a result of the virus exacerbating during chemotherapy; the other patient received the antiviral drug lamivudine prior to the chemotherapy and finished the cures without any problems. Exacerbations of HBV replication followed by an increase in serum transaminase activity levels ('flares') occur naturally during the course of the viral infection. However, there is an elevated risk when a patient receives high doses of corticosteroids for a short period, as is the case in chemotherapy for non-Hodgkin's lymphoma. Lamivudine is registered for the treatment of chronic hepatitis B and can be used as a prophylactic prior to chemotherapy or to treat an exacerbation of the hepatitis. It is advisable to systematically test all patients with lymphoma for the presence of the HBsAg. If this is positive, prophylactic administration of lamivudine 100 mg once daily is strongly recommended if chemotherapy is indicated.
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PMID:[Lamivudine for the prevention of chronic hepatitis B exacerbations during chemotherapy for non-Hodgkin's lymphoma]. 1209 7

Hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Studies of HCV replication and pathogenesis have so far been hampered by the lack of an efficient tissue culture system for propagating HCV in vitro. Although HCV is primarily a hepatotropic virus, an increasing body of evidence suggests that HCV also replicates in extrahepatic tissues in natural infection. In this study, we established a B-cell line (SB) from an HCV-infected non-Hodgkin's B-cell lymphoma. HCV RNA and proteins were detectable by RNase protection assay and immunoblotting. The cell line continuously produces infectious HCV virions in culture. The virus particles produced from the culture had a buoyant density of 1.13 to 1.15 g/ml in sucrose and could infect primary human hepatocytes, peripheral blood mononuclear cells (PBMCs), and an established B-cell line (Raji cells) in vitro. The virus from SB cells belongs to genotype 2b. Single-stranded conformational polymorphism and sequence analysis of the viral RNA quasispecies indicated that the virus present in SB cells most likely originated from the patient's spleen and had an HCV RNA quasispecies pattern distinct from that in the serum. The virus production from the infected primary hepatocytes showed cyclic variations. In addition, we have succeeded in establishing several Epstein-Barr virus-immortalized B-cell lines from PBMCs of HCV-positive patients. Two of these cell lines are positive for HCV RNA as detected by reverse transcriptase PCR and for the nonstructural protein NS3 by immunofluorescence staining. These observations unequivocally establish that HCV infects B cells in vivo and in vitro. HCV-infected cell lines show significantly enhanced apoptosis. These B-cell lines provide a reproducible cell culture system for studying the complete replication cycle and biology of HCV infections.
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PMID:Establishment of B-cell lymphoma cell lines persistently infected with hepatitis C virus in vivo and in vitro: the apoptotic effects of virus infection. 1252 48

The association of hepatitis C and certain hemotological diseases (non-Hodgkin B-cell lymphoma, villous splenic lymphoma.) is a debated question which remains open due to discordant epidemiological data. We report the case of a new patient with chronic hepatitis C and tricholeukocyte leukemia.
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PMID:[Hepatitis C and tricholeukocyte leukemia: a fortuitous association? A case report]. 1274 51

The results of lamivudine therapy in 4 patients with chemotherapy-induced hepatitis B virus (HBV) reactivation are reported. Cancer chemotherapy-induced reactivation is a known complication in patients with chronic HBV infection or history of HBV infection with recovery. Reactivation of HBV infection has a broad spectrum of manifestations ranging from mild elevation of aminotransferase levels to fatal fulminant hepatitis. Lamivudine is a nucleoside analogue and a potent inhibitor of HBV reverse transcription. The 4 patients treated with lamivudine included 1 woman with breast cancer and 3 men with non-Hodgkin lymphoma, ranging from 41 to 63 years of age. All 4 patients were undergoing standard, multi-agent chemotherapy when they presented with HBV reactivation manifested by sudden onset of fatigue, jaundice, and HBV serology consistent with active HBV infection (detectable serum HBV DNA) in the absence of other known causes of acute hepatitis. Lamivudine therapy (100 mg/d in 3 patients and 150 mg/d in 1 patient) was initiated from 1 to 18 days following the diagnosis of HBV reactivation. All 4 patients showed rapid decrease in aminotransferase levels within 2 weeks after initiating lamivudine therapy. Unfortunately, hepatic synthetic function failed to improve in 2 patients, who both died. The remaining 2 patients had suppression of HBV DNA to undetectable levels after 1 and 4 months of treatment and had biochemical and clinical improvement. The 2 patients who died received lamivudine therapy for 8 days and for 3 weeks. There have been no randomized clinical trials to study the role of lamivudine for prophylaxis or treatment of HBV reactivation associated with chemotherapy. However, based on our limited experience, lamivudine may be efficacious in suppressing potentially fatal HBV reactivation secondary to chemotherapy in patients with chronic HBV infection or prior infection with recovery. Patients who undergo chemotherapy should be screened for the presence of markers of chronic hepatitis B infection or previous HBV infection. We recommend that patients with chronic HBV infection (positive HBV DNA and/or positive HBsAg) or history of HBV infection with recovery (positive hepatitis B core antibody with or without HBsAb) be considered for prophylactic lamivudine use to prevent chemotherapy-induced HBV reactivation.
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PMID:Prophylaxis against chemotherapy-induced reactivation of hepatitis B virus infection with Lamivudine. 1281 Dec 13

Patients who will receive chemotherapy require careful assessment of liver function prior to treatment to determine which drugs are not appropriate, and which drugs need dose modification. However, if the hepatic parenchymal abnormalities are caused by an underlying neoplasm and the neoplasm is sensitive to the drugs, it may not be necessary to reduce the dose. Clearly, this is an area where clinical judgment must be used to assess the risk/benefit ratio. Treatment of chronic hepatitis B virus (HBV) involves either the nucleoside analogue lamivudine or interferon alpha. The advantage of lamivudine includes limited adverse effects and the fact that histological improvement has been documented in the majority of patients. Primary prophylaxis with lamivudine may be a well tolerated and effective method to reduce the frequency of chemotherapy-induced HBV reactivation in chronic HbsAg carriers. HbsAg screening is necessary before beginning chemotherapy for non Hodgkin's lymphoma patients. However, the main problem with long-term lamivudine therapy is the emergence of genotypic resistance because of base pair substitution at specific sites within the YMDD locus of the DNA polymerase gene. Significant hepatic dysfunction is uncommon among hepatitis C virus (HCV) infected patients treated with chemotherapy for hematological malignancies. However, infection with elevated AST levels is a significant risk factor for veno-occlusive disease after hematopoietic stem cell transplantation. Clinical judgment and a high index of suspicion remain critical tools in preventing and treating hepatic manifestations of cancer chemotherapy.
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PMID:[Hepatotoxicity of chemotherapy]. 1285 43

We report a case of primary hepatic non-Hodgkin's lymphoma in a 77-year-old man with chronic hepatitis C. Laboratory data revealed slightly elevated liver function parameters and positive antibody for hepatitis C virus (HCV). Abdominal ultrasonography showed a low-echogenic tumor, about 5 cm in diameter, in the left lateral segment. Abdominal computed tomography showed that the tumor was marginally enhanced in the early phase, but no enhancement was seen in the late phase. Magnetic resonance imaging showed that the tumor was hypointense in relation to the liver on T1-weighted images, but hyperintense on T2-weighted images. Hepatic angiography showed a homogeneously stained hypervascular tumor. Under the diagnosis of a liver tumor, thought to be a hepatocellular carcinoma, left lateral segmentectomy was performed. Histological examination confirmed a diagnosis of non-Hodgkin's diffuse large B-cell lymphoma that was positive for L-26 and CD79Alpha, but negative for CD3 and UCHL-1. The surrounding liver tissue showed signs of chronic active hepatitis. Multiple recurrent lesions were found in the liver, spleen, and iliac bones 4 months postoperatively. However, complete remission was achieved after five courses of systemic chemotherapy using pirarubicin, cyclophosphamide, vincristine sulfate, and prednisolone. The patient has been carefully followed up for about 1 year since his operation, and has been doing well. We review the literature on primary non-Hodgkin's lymphoma arising in the liver infected by HCV.
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PMID:Primary hepatic non-Hodgkin's lymphoma in a patient with chronic hepatitis C: report of a case. 1505 56

High and intermediate grade non-Hodgkin's lymphomas (NHL) require treatments with aggressive chemotherapy schedules. However, low grade NHLs display a low chemoresponsiveness and patients aged >65 years often do not tolerate anthracycline and corticosteroid-containing chemotherapy regimens. Therapeutic options in this subset of patients are watchful waiting, oral alkylating agents, purine nucleoside analogues, combination chemotherapy, interferon and monoclonal antibodies. The approval of rituximab, an unconjugated chimeric antibody against the CD20 antigen for the treatment of B-cell NHL marked a milestone in the development of antibody treatment. Moreover, promising results have also been found with oxaliplatin in patients with NHL and reversible, cumulative, peripheral sensory neuropathy is the principle dose-limiting factor of oxaliplatin therapy. On the basis of these considerations we have performed a feasibility study in NHL in patients aged >65 years using as schedule: 130 mg/m2 oxaliplatin every 21 days and 375 mg/m2 rituximab weekly. We have enrolled 8 patients, 2 males and 6 females (mean age 69.2+/-3.1 years; median, 67 years) affected by intermediate or high grade stage III/IV NHL. Six patients have cardiac abnormalities (myocardial function between 45 and 50%) and 1 increase of transaminasemia due to active chronic hepatitis. All the patients included in the study were treated for at least 3 cycles and 31 cycles were completed. We have recorded grade I/II (CTC) neurotoxicity in 30%, grade I anemia in 25% and grade I neutropenia in 20% of the patients. No infusional reactions, liver or renal toxicity neither nausea and/or vomiting were recorded. One complete response, 3 partial response and 3 minimal response were obtained at 11 months of median time follow-up. These results demonstrate the feasibility of this schedule which offers a suitable alternative regimen to treat elderly patients with NHL and shows a good efficacy and an acceptable toxicity profile.
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PMID:Oxaliplatin/rituximab combination in the treatment of intermediate-low grade non-Hodgkin's lymphoma of elderly patients. 1520 74

Following acute hepatitis C virus infection (HCV), a significant percentage of patients do not clear the virus and develop a chronic hepatitis C. The symptoms, when they exist, are usually unspecific. Besides, approximately one third of the patients present extrahepatic manifestations of the infection, basically due to the lymphotropism of HCV. Outstanding amongst these, due to their clear association with HCV, are mixed cryoglobulinaemia and the production of autoantibodies (autoAb). Other diseases such as non-Hodgkin lynphoma (NHL) or autoimmune thyroiditis do not have a clearly established association. Although the majority of patients with chronic hepatitis C have slight or moderately high levels and fluctuations of transaminases, as many as one third of those infected can show persistently normal levels of transaminases. The diagnosis of chronic HCV infection is based on serological tests, which detect the presence of antibodies against HCV, and on virological tests that detect RNA of the HCV, which confirm the existence of active infection. Finally, an important topic of chronic HCV infection, following diagnosis, is to ascertain the stage of fibrosis and the degree of inflammation, since both characteristics are very important for predicting the natural evolution and the need for treatment. Nowadays, this information can only be obtained through liver biopsy, which is recommended in patients with chronic HCV infection and high transaminases. Whether liver biopsy should be performed in patients with normal transaminases is still subject of controversy.
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PMID:[Chronic hepatitis C virus infection]. 1538 45


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