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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported the first case of angiotropic lymphoma diagnosed by adrenal biopsy in Japan. Immunohistochemical study and southern blot hybridization analysis proved it to be B-lymphocyte origin. A 61-year-old man with history of mild hypertension and diabetes mellitus was admitted to our department because of recurrent minor stroke. On admission, general physical findings were normal. Laboratory investigations showed an elevated erythrocyte sedimentation rate and increased serum lactic dehydrogenase (LDH) level. The serial computed tomographic (CT) scan of the brain showed multifocal abnormal density lesions in bilateral hemispheres. Magnetic resonance imaging (MRI) of the brain demonstrated multiple lesions of increased signal intensity in the brainstem and bilateral hemispheres. A subsequent CT scan of the abdomen revealed swelling of bilateral adrenal glands. Adrenal biopsy was performed. Biopsy samples showed the intravascular proliferation of malignant lymphoma cells, non-Hodgkin, diffuse large cell type. These cells had the immunophenotype of a B cell lymphoma (reactive with the antileukocyte common antigen, anti-MB-1, anti-MB-2 and anti-MX-pan B, and unreactive with the anti-MT-1, anti-UCHL, anti-Ki, anti-kappa, anti-lambda and antifactor-VIII). Southern blot hybridization analysis showed monoclonal rearrangements of the immunoglobulin heavy-chain gene, which strongly suggested a B-lymphocyte origin. Thus, a diagnosis of angiotropic lymphoma was made. As soon as chemotherapy was begun, the patient fell into deep coma. A repeat CT scan of the brain was normal. His clinical status gradually deteriorated, and he died 18 months after his initial symptom. Autopsy, which was limited to the body, revealed characteristic systemic intravascular stagnation of lymphoma cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of angiotropic lymphoma diagnosed by adrenal biopsy]. 129 Nov 69

This is the case report of a 4-year-old white boy who was diagnosed as having acute lymphoblastic leukemia (ALL) in November 1985. While in remission and on maintenance chemotherapy, he developed a primary Epstein-Barr virus (EBV) respiratory infection in October 1986. On October 27, 1986 a plain abdominal radiograph taken for abdominal distention showed free air. At celiotomy, multiple nodules were noted to stud the small bowel. Central necrosis of these nodules with perforations were present in the distal small bowel. Resections and end-to-end anastomoses were performed. Three days later the patient again had a similar acute abdominal episode. At reexploration, similar lesions in the liver, kidney, duodenum, proximal jejunum, and colon were found. Liver biopsy as well as intestinal resections and end-to-end anastomoses were performed, along with a loop ileostomy. Polymorphic B-cell lymphoma positive for EBV was found in the specimens. After cessation of chemotherapy and institution of abdominal radiotherapy, the hepatic and renal lesions were seen to resolve on computed tomography scan. The patient's course was complicated by the development of cervical and mediastinal abscesses that were drained, and E coli sepsis accompanied by chronic diarrhea requiring intravenous hyperalimentation. By January 1988, he appeared to be recovering. His ileostomy was closed in March 1988. Despite cessation of chemotherapy since October 1986, the patient is now well and in complete remission.
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PMID:Multiple small bowel perforations in leukemia secondary to Epstein-Barr virus lymphoma with survival: a case report. 217 5

A 52-year-old man, who had been diagnosed as having alcoholic liver cirrhosis, presented a chronic nephritic syndrome due to hepatic glomerulosclerosis. Ten months before death, massive proteinuria exceeding 40 g/day was noted. A renal biopsy revealed diffuse mesangial sclerosis, associated with an IgA deposition consistent with hepatic glomerulosclerosis. Although the nephrotic syndrome subsided with immunosuppressive therapy, he died of hepatic failure. Postmortem examinations disclosed a diffuse, medium-size B-cell lymphoma, involving the peritoneal and retroperitoneal organs and an IgA-positive plasmacytosis. His massive proteinuria seems to have been caused by the paraneoplastic syndrome of a malignant lymphoma.
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PMID:[An autopsied case of a malignant lymphoma with a severe nephrotic syndrome overlapped by cirrhotic glomerulosclerosis]. 329 70

Non-Hodgkin's lymphoma is a common complication in patients with human immunodeficiency virus infection that most frequently affects the gastrointestinal tract. We describe the first case report of non-Hodgkin's lymphoma primarily involving the pancreas in a 27-yr-old white man who presented with epigastric pain, weight loss, and jaundice (and was later found to be HIV seropositive). Endoscopic ultrasound and CT scan of the abdomen showed a large mass arising from the body and head of the pancreas obstructing the common bile duct. An attempted ERCP was unsuccessful due to extrinsic compression and distortion of the second part of the duodenum. A percutaneous CT-directed true-cut needle biopsy of the pancreas revealed a small noncleaved B-cell lymphoma. The patient was started on combination chemotherapy. His pancreatic mass, epigastric symptoms, and jaundice resolved completely. This case report illustrates an otherwise rare presentation of isolated pancreatic involvement of non-Hodgkin's lymphoma in a patient with acquired immunodeficiency syndrome. An approach to its diagnosis and management is summarized.
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PMID:AIDS-related non-Hodgkin's lymphoma of the pancreas. 904 Feb 19

The MHC class II molecule I-Ad has been reported to bind peptides containing a motif of six consecutive amino acids. We demonstrate that binding of the murine IgG2ab heavy chain allopeptide gamma 2ab 435-451 (Kabat numbering) to I-Ad is strongly enhanced by a novel first primary anchor (P1) three residues N-terminal to this hexamer. This is based on flow cytometric assessment of the I-Ad binding capacity of gamma 2ab peptide analogues, their antigenicity for I-Ad-restricted T cell clones and molecular modelling. The P1 pocket is broadly specific since allphatic, aromatic, acidic, the basic histidine and small polar side chains all allowed good binding. By contrast, asparagine, arginine and glycine reduced the binding capacity 10-, 16- and > 100-fold respectively. Truncation or glycine substitution at P1 decreased antigenicity by a factor > 1000. Nevertheless, I-Ad-restricted T cells are not completely dependent on this anchor since high concentrations of a peptide with glycine-substituted P1 elicited maximal responses. Additional anchoring side chains are found at P4, P6 and P9. The autologous IgG2aa heavy chain shares prominent epitopic residues with gamma 2ab 435-451 at P3, P5 and P8. However, the lysine of gamma 2aa at P9 impairs binding to I-Ad, which may explain why the gamma 2ab allopeptide-reactive T cells escaped negative selection. The data rationalize our observation (Bartnes, K. and Hannestad, K. 1997. Eur. J. Immunol. 27:1124) that these T cells recognize a syngeneic B cell lymphoma, provided its presentation of intrinsic gamma 2aa is enhanced by surface IgG2aa ligation.
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PMID:A novel first primary anchor extends the MHC class II I-Ad binding motif to encompass nine amino acids. 926 16

Renal lymphoma is most frequently due to secondary lymphomatous infiltration of the kidneys in advanced stage disease. Rarely, are the kidneys the tissue of origin. We describe a 15-year-old male presenting with hypercalcemia and acute renal failure, due to a bilateral "primary B-cell lymphoma of the kidneys". The diagnosis was established by percutaneous needle biopsy of the right kidney. His disease was metastatic to multiple bones. His presenting features radiological findings and biopsy results are unique. We report his case, and review the pediatric literature.
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PMID:Primary renal lymphoma and hypercalcemia in a child. 1214 99

Addison's disease due to adrenal lymphoma usually manifests as bilateral adrenal enlargement. We report a patient with Addsion's disease in whom the initial overt primary adrenal insufficiency was accompanied by an only slightly enlarged right adrenal gland. The 80-year-old man presented with nausea, anorexia, weight loss, and hyperpigmentation of the skin and buccal mucosa. Addison's disease was diagnosed based on this clinical presentation and laboratory findings of low cortisol and high adrenocorticotropin levels. Computerized tomography (CT) of the adrenal glands revealed a small right adrenal tumor. His family refused to allow percutaneous or surgical biopsy to determine the nature of the tumor. His general condition improved after steroid supplementation. However, about 1 year later, dizziness, fever, night sweats, and edema of the lower legs developed, and adrenal CT scanning revealed that the left adrenal gland had enlarged and now exceeded the size of the right one. Left adrenalectomy was performed and pathology showed a diffuse large B-cell lymphoma. Staging work-up using whole-body CT scanning suggested a stage IIIb lymphoma. Chemotherapy was given, but the disease still progressed and the patient died 4 months after diagnosis. Primary adrenal lymphoma should be considered in the differential diagnosis of Addison's disease, even if only slight enlargement of the adrenal glands is found initially.
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PMID:Adrenal lymphoma and Addison's disease: report of a case. 1263 19

A 31-yr-old man presented with a 1-wk history of fever, chills, weakness, headaches, and a significant 20-lb weight loss over the preceding 2 months. His past medical history was relevant for liver amebiasis during childhood. Two days before admission, the patient noticed jaundice. He denied abdominal pain or other GI symptoms, and there was no history of alcohol intake, medications, or illicit drugs. His physical examination revealed generalized jaundice, hepatosplenomegaly, and bilateral leg edema. Neurologically, the patient was agitated, with periods of disorientation, and he had bilateral flapping. His blood tests revealed pancytopenia, renal failure, liver failure, and coagulopathy. Because the patient had a fever, hepatosplenomegaly, and pancytopenia, a further workup also included a bone marrow and liver biopsy. No conclusive diagnosis could be made from the above tests, and the patient died 5 days after admission. Postmortem evaluation, including flow cytometry and gene rearrangement in the tissue obtained from the liver, revealed large B cell lymphoma. This case illustrates an unusual presentation of hepatic non-Hodgkin's lymphoma. Current information regarding this entity is scant, mainly owing to its rarity. We present a review of the literature, including the incidence, presentation, treatment, and prognosis of primary hepatic lymphoma.
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PMID:Primary hepatic non-Hodgkin's lymphomas: case report and review of the literature. 1468 34

Hepatic lymphoma metastasis is rare, and should always be considered in the differential diagnosis of hepatic malignancy. A 52-year-old man presented with a four-day history of fever, fatigue, yellowish skin and nausea. His past medical history was unremarkable. There was no history of alcohol intake or medications. His physical examination revealed generalized jaundice and hepatomegaly. His blood tests showed liver failure and coagulopathy. Abdominal ultrasonography illustrated hepatomegaly. A further work-up included bone marrow and liver biopsy. The pathology report was B-cell lymphoma. He was treated with chemotherapy, and his laboratory findings during follow-up showed steady improvement. In conclusion, lymphoma metastasis to liver can be a cause of liver dysfunction. A high index of suspicion is required for the diagnosis. We emphasize the importance of obtaining tissue sample in all patients with suspicious lesion in any organ to avoid missing the rare but curable pathologies.
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PMID:Hepatic lymphoma metastasis presenting with severe acute liver failure: a rare case. 1533 18

We used gene targeting in mice to insert a His(6)-tagged mouse c-Myc cDNA, Myc(His), head to head into the mouse immunoglobulin heavy-chain locus, Igh, just 5' of the intronic enhancer, Emu. The insertion of Myc(His) mimicked both the human t(8;14)(q24;q32) translocation that results in the activation of MYC in human endemic Burkitt lymphomas and the homologous mouse T(12;15) translocation that deregulates Myc in certain mouse plasmacytomas. Beginning at the age of 6 months, Myc(His) transgenic mice developed B-cell and plasma neoplasms, such as IgM(+) lymphoblastic B-cell lymphomas, Bcl-6(+) diffuse large B-cell lymphomas, and CD138(+) plasmacytomas, with an overall incidence of 68% by 21 months. Molecular studies of lymphoblastic B-cell lymphoma, the most prevalent neoplasm (50% of all tumors), showed that the lymphomas were clonal, overexpressed Myc(His), and exhibited the P2 to P1 promoter shift in Myc expression, a hallmark of MYC/Myc deregulation in human endemic Burkitt lymphoma and mouse plasmacytoma. Only 1 (6.3%) of 16 lymphoblastic B-cell lymphomas contained a BL-typical point mutation in the amino-terminal transactivation domain of Myc(His), suggesting that most of these tumors are derived from naive, pregerminal center B cells. Twelve (46%) of 26 lymphoblastic B-cell lymphomas exhibited changes in the p19(Arf)-Mdm2-p53 tumor suppressor axis, an important pathway for Myc-dependent apoptosis. We conclude that Myc(His) insertion into Igh predictably induces B-cell and plasma-cell tumors in mice, providing a valuable mouse model for understanding the transformation-inducing consequences of the MYC/Myc-activating endemic Burkitt lymphoma t(8;14)/plasmacytoma T(12;15) translocation.
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PMID:Insertion of c-Myc into Igh induces B-cell and plasma-cell neoplasms in mice. 1573 16


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