Cases reported "Lymphocytosis"

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1/7. Barrett's adenocarcinoma of the esophagus with lymphoid stroma.

    We report a case of Barrett's adenocarcinoma of the esophagus with lymphoid stroma. We believe this is the first reported case of this entity, although six previous cases of esophageal lymphoepithelioma-like carcinoma have been reported. The esophageal tumor from a 58-year-old man was examined histologically. In situ hybridization to detect Epstein-Barr virus (EBV) was also performed. The tumor consisted of a poorly differentiated adenocarcinoma with dense lymphoid cell infiltration in the invasive portions and a well-differentiated adenocarcinoma without lymphoid stroma in the mucosa. Barrett's epithelium was observed adjacent to the carcinoma. No positive signals for EBV were detected in the tumor cells. Six previously reported patients with esophageal lymphoepithelioma-like carcinomas, and the current patient, all survived for longer than 24 months, a better outcome than that of patients with esophageal squamous cell carcinomas of usual type. The data suggest that this tumor arose as a mucosal, well-differentiated adenocarcinoma without lymphoid stroma and that EBV had no relation to either its pathogenesis or progression.
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2/7. Is persistent polyclonal B lymphocytosis caused by Epstein-Barr virus? A study with polymerase chain reaction and in situ hybridization.

    Previous reports of patients with persistent polyclonal B lymphocytosis have found associations with female sex, cigarette smoking, HLA-DR7 phenotype, and moderate elevation of peripheral blood polyclonal B lymphocytes. The presence of binucleated cells and atypical lymphocytes in the peripheral blood of these patients was highly suggestive of a viral infection, such as with the Epstein-Barr virus. We report a 47-year-old asymptomatic woman who was incidentally found to have persistent polyclonal B lymphocytosis and serum IgG against virus capsid antigen (VCA) and Epstein-Barr virus (EBV)-associated nuclear antigen (EBNA) of EBV. The presence of EBV was investigated in the peripheral blood lymphocytes from this patient by in situ hybridization and polymerase chain reaction methods. EBV dna was demonstrated in the lymphocyte fraction by polymerase chain reaction, and it was further located in lymphoid cells by in situ hybridization. These results indicate that persistent polyclonal B lymphocytosis is strongly associated with EBV.
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3/7. Variant lymphoproliferative disorder of granular lymphocytes (LDGL) following Hodgkin lymphoma.

    A 41-year-old Caucasian female was diagnosed with a CD3( ) CD4( ) CD8( ) variant of lymphoproliferative disorder of granular lymphocytes (LDGL) in the third year of remission following treatment of stage III-B Hodgkin lymphoma (HL). The patient was asymptomatic at diagnosis, without clinical evidence of immune disorder or recurrence of HL. diagnosis was made incidentally, secondary to lymphocytosis discovered on a routine follow-up post HL therapy. Clonal chromosomal abnormalities were seen in 20% of peripheral blood lymphocytes with a karyotype 46, XX, t(2;6;2;11) (p13;q23;q24;q23). The breakpoint on 11q23 is distal to the MLL gene as shown by fluorescence in situ hybridization (FISH) analysis. To our knowledge, this is the first report of variant LDGL in association with HL treatment with documented clonal chromosomal abnormalities.
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4/7. Histological varieties of Epstein-Barr virus-related lymph node lesion resembling autoimmune disease-like clinicopathological findings in middle-aged and elderly patients: a study of six cases.

    Six cases were studied to further clarify clinicopathological findings of Epstein-Barr virus (EBV)-related lymph node lesions showing autoimmune disease-like clinicopathological findings (EBVAID) in middle-aged and elderly patients. The patients, four males and two females, ranged in age from 53 to 74 years, with a median age of 62 years. Clinically, they were characterized by systemic lymphadenopathy, "B"symptoms, polyclonal hypergammaglobulinemia, elevated serum lactate dehydrogenase and a transient presence of various autoantibodies, as well as an infrequent presence of atypical lymphocytosis in peripheral blood. Two cases were associated with idiopathic thrombocytopenic purpura. The clinical course was self-limiting. Histologically, three patterns could be delineated: pattern A, follicular hyperplasia with pronounced arborizing vasculature in the expanded paracortex (n=3); pattern B, follicular hyperplasia with pronounced interfollicular B-immunoblastic/plasma cell proliferation (n=2); and pattern C, paracortical hyperplasia containing numerous large transformed lymphocytes (n=1). in situ hybridization demonstrated a varying number of EBV-infected lymphocytes in the germinal center and in the interfollicular area. polymerase chain reaction analysis demonstrated that neither clonal rearrangement of T-cell receptor gamma-chain nor immunoglobulin heavy-chain rearrangement was detected in the three cases examined. Although EBVAID appears to be rare in middle-aged and older adults, EBVAID exhibits histological variations and should be added to the differential diagnosis of various atypical or malignant lymphoproliferative disorders, in particular autoimmune-disease-associated lymphadenopathy and angioimmunoblastic T-cell lymphoma with a hyperplastic germinal center in middle-aged and elderly patients.
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5/7. Lymphoproliferative disease of granular lymphocytes in a patient with concomitant hepatitis b virus infection of CD4 lymphocytes.

    In this report we studied a 35-year-old male who developed an abnormal expansion of granular lymphocytes (GL) which spontaneously regressed over a period of 2 years. The immunological and molecular characterizations of expanded cells showed the CD3 ,CD8 ,HNK-1 phenotype, a polyclonal organization of the T-cell receptor beta-chain gene and normal natural killer activity. At the time of presentation, spot and blot hybridization techniques revealed the presence of viral hepatitis b virus (HBV) dna sequences only in highly enriched CD4 T cells, while proliferating GL were negative. With this as a background, we addressed the question of whether in our case the polyclonal GL proliferation represented an immunoreactive response against CD4 infected cells. In particular, we tested the possibility that expanded GL could be cytotoxic against autologous infected CD4 cells. At the time of the first determination, when several of the CD4 cells harbored HBV, GL showed a minimal degree of cytotoxicity against 51Cr-labeled CD4 cells; 2 years later, when GL became capable of lysing these targets, the appearance of the specific cytotoxicity was concomitant with the disappearance of the HBV-infected CD4 cells and with the recovery of granular lymphocytosis. Taken together, our data suggest that in this case GL proliferation could represent an immunoreactive process against CD4 cells.
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6/7. Human T-lymphotropic virus type I-associated benign transient immature T-cell lymphocytosis.

    We describe a case of human T-lymphotropic virus type I (HTLV-I)-associated transient benign immature T-cell lymphocytosis in a black female patient, which over the course of several months underwent spontaneous complete remission. The patient presented with a white blood cell count of 20,000/microliter and a T4/T8 ratio of 1.7:1. The majority of cells appeared to be lymphoid in origin, and cell marker analyses established that the circulating lymphocytes were predominantly immature T-cells. HTLV-I was detected at this time by a p19 indirect immunofluorescent slide assay. Over a 1-month period of time the patient's clinical status evolved into a mature T-lymphocytosis with a T4/T8 ratio of 4.5:1. HTLV-I was detected by anti-p19 immunofluorescence by cell sorter analyses and by dot-bloc nucleic acid hybridization. Serological testing demonstrated that the patient had anti-htlv-i antibodies and antimembrane antibodies specific for an HTLV-I producing cell line. In a competitive HTLV-I ELISA assay only HTLV-I proteins could effectively compete out the seroreactivity. The patient also had a high serum level of soluble interleukin-2 (IL-2) receptors, which is associated with HTLV-I infection. This is the first reported case of immature T-lymphocytosis in a patient infected with HTLV-I. The patient's HTLV-I markers disappeared with time, and her lymphocytosis subsequently spontaneously resolved. She remains disease free and virus negative after 2 years of follow-up study.
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7/7. Common clonal origin of lymphocytes and plasma cells in splenic lymphoma with villous lymphocytes.

    In two-thirds of patients with splenic lymphoma with villous lymphocytes (SLVL) a small amount of M-protein can be detected in association with the presence of plasma cells in the peripheral blood (PB) and/or bone marrow (BM). However, it is not known whether lymphoma cells and plasma cells originate from the same clone. In this report we describe a case of SLVL which was characterized by the presence of marked monoclonal gammopathy (IgG-kappa 90 g/l) and increased plasma cells in the BM. In an attempt to elucidate the origin of lymphoma cells and plasma cells, we performed morphological, cytogenetic and molecular studies on PB mononuclear cells (PBMNC) without plasma cells and BMMNC containing 10% plasma cells from this patient. Immunofluorescence showed that lymphoma cells and plasma cells were positive for cytoplasmic gamma heavy and kappa light chains. Well-developed endoplasmic reticulum was observed in the cytoplasmic organelles of PBMNC using an electron microscope. The mean IgG concentration in the 3 d supernatant cultures of PBMNC was 374 /- 24 microg/l. More than 50% PBMNC differentiated into plasmacytoid cells in 6 d of liquid culture with IL-3 and IL-6. Analysis by two-colour FISH revealed that karyotypic abnormalities of monosomy X and trisomy 17 existed simultaneously in both lymphoma cells and plasma cells. JH gene rearranged bands from PBMNC and BMMNC by Southern blot hybridization were identical, whereas DNAs from PBMNC failed to hybridize with the Cmu probe. These observations strongly suggest that lymphoma cells and plasma cells originate from the same clone, and that plasma cells, as well as lymphoma cells, which have undergone class switch recombination, could produce IgG type M-protein in this case.
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