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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Giant-cell hepatitis is a frequent pattern of liver injury in the neonate, but it is rare after infancy. Such cases have been attributed to autoimmune disease, to non-A, non-B hepatitis and, most recently, to paramyxovirus infection. To better define the entity of postinfantile (syncytial) giant-cell hepatitis, we reviewed 24 biopsy specimens from 20 patients with this finding, either alone or in combination with other diagnoses. The number of multinucleated giant cells varied greatly from one specimen to another. Varying degrees of portal inflammation appeared in all but one of the patients, and all had hepatitislike acinar inflammation associated with hepatocellular injury. Fibrosis was a common finding, varying from mild periportal fibrosis to established cirrhosis (33%). The changes were interpreted as acute giant-cell hepatitis in 25%, as CAH in 42% and as active cirrhosis in the remainder. The patients ranged in age from 2 to 80 yr, with a mean of 35 yr and a male/female ratio of approximately 1:1. The signs and symptoms of liver disease were present for more than 1 mo in most patients. A positive antinuclear antibody titer was found in seven of the patients. Three patients had a direct Coombs reaction and anemia. Overall, evidence of autoimmune disease was found in 40% of the patients. One patient had non-Hodgkin's lymphoma involving the liver. Only one patient had a history of blood transfusion or risk factors for hepatitis C. No patient underwent serological study for paramyxovirus antibodies. Liver tissue from one patient was examined ultrastructurally, but no viral particles could be identified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postinfantile giant-cell transformation in hepatitis. 163 41

We conducted a pilot study in 20 patients with high-risk or recurrent/refractory non-Hodgkin's lymphoma (NHL) using high-dose sequential chemotherapy (HDSC) and autologous hematopoietic cell transplantation (AHCT). After cytoreduction with standard salvage therapy, HDSC/AHCT was administered in 4 phases at 2- to 4-week intervals. Phase 1 consisted of cyclophosphamide 7 g/m2 followed by granulocyte colony-stimulating factor (G-CSF) at 10 microg/kg per day and leukapheresis upon recovery from white blood cell nadir. The hematopoietic cell product was enriched by Percoll gradient separation and purged with a B-cell or T-cell monoclonal antibody panel and complement. Phase 2 consisted of methotrexate 8 g/m2 with leucovorin rescue and vincristine 1.4 mg/m2. Phase 3 was etoposide 2 g/m2 with G-CSF 5 microg/kg per day. In phase 4, the preparative regimen of mitoxantrone 60 mg/m2 and melphalan 180 mg/m2 was administered followed by AHCT. The NHL histologies were diffuse large cell, follicular/diffuse mixed, small noncleaved cell, T-cell-rich B-cell, lymphoblastic, and peripheral T cell. The remission status was first partial remission (PR1; n = 1) or beyond first complete remission (post-CR1; n = 19). Of the 20 patients enrolled, 11 proceeded through all 4 phases. Nine were removed from the study after the first or second phase because of progressive disease (n = 5), poor hematopoietic cell mobilization (n = 1), excessive toxicity (n = 2), and chronic active hepatitis C (n = 1). Treatment-related toxicities in the remaining 11 transplant recipients were cardiomyopathy, hemorrhagic cystitis, persistent cytopenias, acute renal failure, abnormal liver function test results, and infectious complications. There were no treatment-related deaths. Eight of the 11 transplant recipients were alive, 6 without disease, at a median follow-up of 2.7 years. The estimated median 2-year event-free survival was 55%, and overall survival was 70%. We conclude that HDSC/AHCT in refractory/recurrent NHL is associated with considerable acute and chronic toxicities. Given the toxicity profile, efficacy data were not sufficiently promising to warrant further study.
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PMID:Toxicity of high-dose sequential chemotherapy and purged autologous hematopoietic cell transplantation precludes its use in refractory/recurrent non-Hodgkin's lymphoma. 1107 Dec 61

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

The relationship between the occurrence of cryoglobulins and hepatitis C virus (HCV) productive infection in peripheral blood and bone marrow-derived lymphocytes was explored. HCV minus strand RNA, the viral replicative intermediate, was searched for by a polyA(+) tract strand-specific Tth-based reverse transcriptase-polymerase chain reaction (RT-PCR) in lymphoid cells of 46 patients with acute and chronic infection. The HCV minus strand was demonstrated in RNA extracted from six (13%) and five (11%) peripheral blood and bone marrow-derived lymphocytes, respectively. The HCV replicating form in lymphoid cells was associated strictly with mixed cryoglobulinaemia (MCG), in that it was found in six of 13 (46%) MCG patients, including two with B cell non-Hodgkin's lymphoma (NHL). No traces of HCV-negative strand RNA were found in four patients with acute hepatitis C, in 15 with chronic active hepatitis without extrahepatic disorders, in seven with monoclonal gammopathy of undetermined significance, and in seven with B-NHL without MCG. These results emphasize the direct role of the virus in the pathogenesis of MCG and support the contention that HCV is not specifically lymphotropic, its entry and replication in lymphoid cells being determined largely by selective interactions.
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PMID:Hepatitis C virus productive infection in mononuclear cells from patients with cryoglobulinaemia. 1722 64