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Results for “Lymphoproliferative Disorders”

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At least 19 recordsLinked to original sources
PubMed1990

Involvement of the gastrointestinal tract by Epstein-Barr virus--associated posttransplant lymphoproliferative disorders.

Posttransplant lymphoproliferative disorders (PTLD) are abnormal growths of lymphoid cells that occur in immunosuppressed organ transplant recipients. Most cases are of B-lymphocyte origin and are associated with Epstein-Barr virus infection. Twelve of 72 allograft recipients with PTLD in our series have had disease predominantly involving the gastrointestinal tract. The lesions are most often multiple and preferentially involve the distal small bowel. The appearance of the lymphoid cells ranges from nonuniform (polymorphic) to uniform (monomorphic). Most tumors contain a clonal component of B-lymphocytes, with or without a nonclonal background. Appropriate primary treatment includes surgical resection and reduction of immunosuppression. Occasional PTLD of the gastrointestinal tract do not respond to this regimen, these represent a more advanced state of tumor progression. Currently, 11 of 12 patients are alive 10-13 months after diagnosis. The surgical pathologist must be aware of the appropriate setting in which to consider a diagnosis of PTLD and be able to distinguish this condition from other lymphoproliferative disorders of the gastrointestinal tract.

Adolescent↗
PubMedDate not supplied

Lymphoproliferative disorders of the head and neck.

Lymphoproliferative disorders are the frequent cause of indeterminate processes in the head and neck region for which otolaryngologists are often consulted by colleagues seeking a diagnosis. Because a wide spectrum of diseases may be represented, tissue diagnosis is often required. Recent advances in tissue immunotyping and DNA probes permit more precise identification and classification of these disorders. Lymphoproliferative disorders may be subdivided into five categories: Hodgkin's disease, non-Hodgkin's lymphoma, histiocytosis X, benign reactive lymphoproliferative disorders, and plasma cell neoplasms. Representative cases are presented, along with a brief discussion of each category.

Adult↗
PubMed1989

Pulmonary lymphoproliferative disorders.

Nonlymphomatous pulmonary lymphoproliferative disorders include plasma cell granuloma, Castleman's disease, pseudolymphoma, lymphocytic interstitial pneumonitis, angioimmunoblastic lymphadenopathy, and lymphomatoid granulomatosis. They are thought to represent a hyperplasia of the pulmonary immune system in response to chronic antigenic stimulation. A description of the variable clinical, radiographic, and pathologic features of each entity is presented.

Humans↗
PubMed1988

Rearrangement of T-cell delta locus in lymphoproliferative disorders.

Studies of lymphoproliferative disorders using immunoglobulin and T-cell receptor genes have contributed to our understanding of clonality and lineages of these disorders. In this study, we examined the rearrangement of the recently discovered T-cell delta chain genes in a variety of lymphoproliferative diseases. We show here that six of 14 T-cell lymphomas and five of 23 B-cell lymphomas or B-cell leukemia cell lines have rearranged the delta loci, while two of two hyperimmune reactions retain germline configuration within these genes. Seven of ten cases of AILD were rearranged, and Lennert's lymphoma, which has been previously described as a T-cell malignancy, also contains rearrangements in the delta chain genes (three of five). Large cell anaplastic lymphomas positive for the activation antigen CD 30 also contain rearrangement in about one-half (five of 11) of the tumors examined. Two of seven of the Hodgkin's lymphomas studied contained a rearrangement for this gene. This study indicates that this newly identified T-cell delta gene is useful in evaluating clonality but is not lineage specific. However, with only one exception (in 28 rearrangements), this gene rearranges in tumors with gamma and beta chain gene rearrangements, indicating that when used in conjunction with the other TcR genes, delta rearrangement may also be useful in evaluating lineages.

B-Lymphocytes↗
PubMed1990

Effects of interferon alpha on autocrine growth factor loops in B lymphoproliferative disorders.

The B lymphoproliferative disorders B chronic lymphocytic leukemia (B-CLL) and hairy cell leukemia (HCL) produce a number of autocrine growth factors, including tumor necrosis factor (TNF), interleukin 6 (IL-6), and IL-1, all of which may induce positive feedback growth loops. If such malignancies depend on these autocrine growth loops for survival, their interruption may be therapeutically valuable. Interferon alpha (IFN-alpha) abrogates TNF- or IL-6-induced proliferation of HCL and B-CLL cells in vitro and has therapeutic activity in these diseases. We have investigated the possibility that IFN-alpha may act by interrupting autocrine growth factor loops. If purified B-CLL or HCL cells are cultured in the presence of TNF, there is induction of mRNA for TNF, IL-1 alpha, IL-1 beta, and IL-6. However, culture in the presence of IFN-alpha in addition to TNF reduced the level of mRNA for all these cytokines, compared with cells cultured in TNF alone. While cytokine mRNA levels were diminished, levels of mRNA for the ribonuclease activator 2-5A synthetase were increased. Analysis of the kinetics of cytokine mRNA production showed that levels fall shortly after the rise of 2-5A synthetase mRNA. IFN-alpha may produce these effects by shortening the half-life of cytokine mRNA, since TNF mRNA half-life in B-CLL and HCL cells is substantially reduced when the cells are cultured with IFN-alpha. These data suggest that IFN-alpha may mediate its therapeutic effects in these malignancies by blocking autocrine growth factor loops.

Adult↗
PubMed1992

Posttransplant lymphoproliferative disorder: intrathoracic manifestations.

Posttransplant lymphoproliferative disorder (PTLD) is a serious complication of organ transplantation and immunosuppression. Early diagnosis and treatment greatly affect prognosis. Chest radiographs (n = 13), chest computed tomographic (CT) scans (n = 2), or both (n = 20) from 35 patients with intrathoracic PTLD were retrospectively studied to define the intrathoracic manifestations of this disorder. Intrathoracic abnormalities consisted of pulmonary nodules (16 patients), patchy air-space consolidation (three patients), mediastinal and hilar adenopathy (17 patients), thymic enlargement (two patients), pericardial thickening and/or effusions (two patients), and pleural effusions (four patients). Multiple, well-circumscribed pulmonary nodules with or without mediastinal adenopathy are highly suggestive of PTLD. However, pathologic examination is usually necessary for a definitive diagnosis.

Adolescent↗
PubMed1992

Study of the major phenotype of large granular T-cell lymphoproliferative disorder.

Six cases of large granular T-cell lymphoproliferative disorder with a selected immunophenotype (CD3+, CD4-, CD8+, CD16+) were studied to characterize a homogeneous group of patients. It was found that most of these patients did not exhibit the clinical features frequently described in large granular T-cell lymphoproliferative disorder--recurrent infection, rheumatoid arthritis, and splenomegaly. The laboratory tests usually positive in large granular T-cell lymphoproliferative disorder, including rheumatoid factor and anti-nuclear antibodies, also were frequently negative. The pathognomonic features were found to be neutropenia and large granular lymphocytosis with positive killer cell markers. All six cases showed T-cell receptor gene rearrangement that indicated a monoclonal proliferation of lymphoid cells, which were natural killer-like T cells by immunophenotyping. B cells were essentially absent in all cases. It should be emphasized that bone marrow aspirates are as informative as peripheral blood samples for the diagnosis of large granular T-cell lymphoproliferative disorder; indeed, phenotypes of blood and marrow in one case were identical in terms of percentages of markers. In this selected group of patients, the clinical courses were indolent with uncomplicated outcomes. In three patients, chemotherapy did not induce an obvious clinical response, but all patients' conditions remained stable with only supportive care.

Adult↗
PubMed1991

Hepatitis B surface antigenaemia in patients with malignant lymphoproliferative disorders.

One hundred and four patients with malignant lymphoproliferative disorders and 5,690 control subjects were screened for the presence of Hepatitis B surface antigen (HBsAg) in their sera. Lymphoproliferative disorders included in the study were acute lymphoblastic leukaemia (ALL), non Hodgkin's Lymphoma (NHL), chronic lymphocytic leukaemia (CLL), Hodgkin's disease (HD), Burkitt's lymphoma (BL) and multiple myeloma (MM). Screening was done by the Reverse Passive Haemagglutination method using the Welcome kit. The percentage antigenaemia in the patients and control subjects were 35.6 and 7.7% respectively (p less than 0.0001). Using the Odds ratio the relative risk was found to be 6.75. The Odds ratio for individual disorders ranged from 2.8 to 9.17. The results suggest an association between Hepatitis B surface antigenaemia and malignant lymphoproliferative disorders and highlights the risk involved in handling specimens from the patients.

Adolescent↗
PubMedDate not supplied

Immunological and genotypic analysis of human T gamma-lymphoproliferative disorders.

T gamma-lymphoproliferative disorders (T gamma-LPD) are rare diseases characterized by expansion of circulating elements with resemblance to large granular lymphocytes (LGL). We have studied 12 patients with T gamma-LPD. Morphological evaluation revealed 79-88% of LGL in non-adherent peripheral blood lymphocytes as assessed by light and electron microscopy. The most common features of the membrane phenotype included expression of T3, HNK-1 and AB8.28 (anti-Fc gamma); other surface markers of LGL (OKM1, B73.1, N901) were variably expressed or absent. Patients' LGL usually had little or no NK activity, with the exception of two patients who had values comparable to those of normal donors; in addition, cell preparations from all patients mediated antibody-dependent cellular cytotoxicity. The recent availability of the T cell receptor beta chain probes allowed us to investigate the lineage and the clonality of T gamma-LPD. Of the 12 patients analyzed, 10 displayed clonal rearrangements of T beta locus and expression of the T3 antigen, whereas the two remaining cases displayed a germ-line configuration of the T beta gene and no expression of the T3 antigen. We suggest that individual T gamma-LPD cases represent the clonal expansion of cells frozen at different stages of differentiation/activation within an individual hematopoietic LGL/NK lineage. These data suggest that either a subset of LGL or a particular step of differentiation may be related to the T cell lineage.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1979

Membrane receptors and their redistribution in lymphoproliferative disorders.

Lymphoid cells from 20 patients with lymphoproliferative disorders, including chronic lymphocytic leukemia, hairy cell leukemia, Sezary syndrome, lymphoma, and lymphadenitis, were studied for redistribution of surface membrane immunoglobulins (SmIg) and concanavalin A (Con-A) receptors. Fluorescein-labeled polyvalent goat anti-human immunoglobulin and fluoresceinated concanavalin A were used as ligands. Results were similar with both ligands. The highest percentage of capping of ligand-membrane receptors was noted in mononuclear cells from patients with "hairy" cell leukemia: from 24% to 90%. These cells showed moderate to marked fluorescein activity and were able to cap within 15 min at 4 degrees C. Chronic lymphocytic leukemia cells showed a weak fluorescein stain with a very low percentage of cells (0%--16%) capping. Lymph node cells from patients with lymphoma demonstrated moderate to strong fluorescein activity with only an average of 3% of the cells capping; while lymphoid cells from patients with lymphaedenitis showed an average of 27.5% capping and moderate fluorescein activity. Capping of Con-A receptors in mononuclear cells from patients with Sezary syndrome was poor (0%--14%) with moderate fluorescein intensity. This report demonstrates difference in density and mobility of binding sites for SmIg and Con-A on the surface membrane of lymphoid cells from various subclasses of lymphoproliferative disorders. These differences may assist in the differential diagnosis and classification of these conditions.

Cell Membrane↗
PubMed1987

Present nosography of lymphoproliferative disorders.

The present nosography of lymphoproliferative disorders is continuously in progression. Until now, a number of data regarding cytomorphological, cytochemical, immunological and molecular biological findings demonstrated importance in diagnostic and prognostic evaluation.

Deltaretrovirus Infections↗
PubMed1990

Increased incidence of lymphoproliferative disorder after immunosuppression with the monoclonal antibody OKT3 in cardiac-transplant recipients.

BACKGROUND: A sudden increase in the incidence of post-transplantation lymphoproliferative disorder among the patients in our cardiac-transplantation program was temporally related to introduction of the immunosuppressive drug OKT3. This monoclonal antibody has come to be widely used in recent years both to prevent and to treat rejection after cardiac transplantation. METHODS: In order to identify variables that predict the development of post-transplantation lymphoproliferative disorder, we analyzed retrospectively a series of 154 consecutive cardiac-transplant recipients at a single institution. Univariate analyses and multivariate analysis by logistic regression were performed. RESULTS: Among 75 patients who did not receive OKT3, post-transplantation lymphoproliferative disorder developed in 1 (1.3 percent), as compared with 9 of 79 patients who received the drug (11.4 percent); the incidence among the OKT3-treated patients was ninefold higher (odds ratio, 9.5; 95 percent confidence interval, 1.6 to 54.7). According to multivariate analysis, the only factor significantly associated with the development of post-transplantation lymphoproliferative disorder was the use of OKT3 (P = 0.001). A significant increase in risk with increasing doses was also apparent: 4 of 65 patients who received a cumulative dose of 75 mg of OKT3 or less (6.2 percent) had post-transplantation lymphoproliferative disorder, whereas 5 of 14 patients who received more than 75 mg had the disorder (35.7 percent; P less than 0.001). CONCLUSION: The addition of OKT3 to the immunosuppressive regimen increases the incidence of post-transplantation lymphoproliferative disorder after cardiac transplantation, and the risk increases sharply after cumulative doses greater than 75 mg. We suggest that the risks and benefits of prophylactic OKT3 administration be reassessed in the light of these findings, particularly since the value of prophylactic immunotherapy in cardiac-transplant recipients remains to be clearly established.

Antibodies, Monoclonal↗
PubMed1987

Transferrin receptor expression in the leukaemias and lymphoproliferative disorders.

The expression of the transferrin receptor (TfR) was studied in the acute leukaemias and lymphoproliferative disorders by means of indirect immunofluorescence and/or the enhanced alkaline phosphatase anti-alkaline phosphatase (APAAP) techniques using monoclonal antibodies to the receptor. A total of 174 cases of acute leukaemia and lymphoproliferative disorder were studied. The results indicate that the receptor is expressed with increased density in the majority of positive cases of acute leukaemia. The lymphoproliferative disorders, however, only expressed the receptor in a minority of cases and did so with weak density. It is proposed that this weak expression in the lymphoproliferative disorders may be of use as an indicator of an increase in cell activity.

Acute Disease↗
PubMed1992

A familial lymphoproliferative disorder presenting with primary pulmonary manifestations.

A familial lymphoproliferative disorder presented in three male siblings with primary pulmonary involvement manifested as either lymphoid interstitial pneumonia or an angiodestructive polymorphous infiltrate morphologically resembling lymphomatoid granulomatosis. The polymorphous infiltrate consisted chiefly of mature T-cells with a few B-cells and plasma cells, and gene rearrangement studies failed to show clonality. Epstein-Barr virus, frequently associated with proliferative lesions in males in the X-linked lymphoproliferative syndrome, was not demonstrated in any of the pulmonary lesions. An HLA haplotype shared among the affected siblings was A1, B8, DR4. The unusual clinical presentation plus the lack of involvement by EBV in the pulmonary lesions suggests that this is a previously undescribed familial lymphoproliferative disorder.

Adolescent↗
PubMed1978

Bone-marrow mast cells in lymphoproliferative disorders.

Increased bone-marrow mast-cell content and lymphoproliferative disorders have been previously linked. Using a semiquantitative method we examined bone-marrow mast-cell content in 120 marrow specimens from patients with multiple myeloma, chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and reactive lymphocytosis. Results indicated a statistically significant increase of marrow mast-cell content in patients with chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and reactive lymphocytosis when compared with iron-deficient control subjects (p less than or equal to 0.0005). Patients with multiple myeloma had decreased marrow mast-cell content, clearly separating them from patients with lymphoproliferative disorders and reactive lymphocytosis. Linear regression plot of marrow mast-cell content against percentage of marrow lymphocytes showed a direct relation, indicating that marrow mast-cell density may be related more to the degree of lymphoid proliferation than to the specific lymphoproliferative process. Marrow mast-cell content may therefore be reproducibly determined and used to support the morphologic diagnosis of lymphoproliferative disorders and differentiate them from atypical myelomas.

Adolescent↗
PubMed1987

Posttransplantation cyclosporine-induced lymphoproliferative disorders: clinical and radiologic manifestations.

Fifteen allograft transplant recipients acquired lymphoproliferative disorders after immunosuppressive therapy with cyclosporine and steroids. Many of these lymphoproliferative disorders regressed or disappeared completely after reduction of cyclosporine dose. This disease has several aspects that distinguish it from usual posttransplantation lymphomas that occur with regimens that do not contain cyclosporine. The time course from transplantation to onset of lymphoma is relatively short, with an average of approximately 8 months. Organs show a wide spectrum of abnormalities typical of other immunosuppression-associated lymphomas, but there is unique sparing of the central nervous system. The tumor is also unique in that it responds to a decrease in the cyclosporine dose.

Adolescent↗
PubMed1991

The expression of CD22 (Leu 14) and CD11c (LeuM5) in chronic lymphoproliferative disorders using two-color flow cytometric analysis.

The monoclonal antibodies (MoAbs) CD22 and CD11c recognize B-lymphocyte- and monocyte-associated antigens, respectively. Reports indicate that when these two MoAbs co-express, they represent a unique marker for hairy cell leukemia (HCL) although neither is specific for that disease. The authors evaluated the expression and diagnostic utility of CD22 and CD11C in specimens from 26 normal subjects, 29 patients, with various nonlymphoproliferative disorders (NLPDs), and 75 patients with different types of chronic lymphoproliferative disorders (CLDs) using two-color flow cytometric analysis of peripheral blood lymphocytes. Lymphocytes co-expressed CD22 and CD11c in less than or equal to 3% of the normal subjects and in less than or equal to 6% of the patients with NLPDs. These markers were expressed in greater than 10% of the lymphocytes of 46% (32/69) of the patients with B-cell CLDs: B-cell chronic-lymphocytic leukemia, 9/41; B-cell non-Hodgkin's lymphoma, 8/14; HCL, 11/11; B-cell lymphoproliferative disorder (NOS), 1/2; and B-cell prolymphocytic leukemia, 1/1. None (0/6) of the lymphocytes of patients with T-cell CLDs expressed greater than 10% CD22-positive (CD22+) or CD11c-positive (CD11c+) cells. The HCL cases demonstrated a unique CD22+CD11c+ fluorescence histogram pattern, distinct from other lymphoproliferative disorders, that was characterized by uniformly intense CD11c and CD22 fluorescence. Differences in the expression of the CD22+CD11C- and CD22+CD11C+ phenotypes between diagnostic groups were found, most notable was a paucity of CD22+CD11c+ cells in lymphocytes of patients with HCL. CD22 also had more variable expression than CD19 and HLA-DR in the cases of B-cell CLD. This study demonstrates that the CD22+CD11c+ phenotype is not unique to HCL but is a consistent feature of that disorder and that the immunofluorescence pattern of co-expression in HCL is diagnostically useful.

Antigens, CD↗
PubMed1987

B-cell lymphoproliferative disorders in children after bone marrow transplantation: radiologic manifestations.

The radiographic findings in five pediatric patients in whom unregulated B-cell lymphoproliferative disorders developed following bone marrow transplantation are described. Four patients received T-cell-depleted bone marrow from mismatched donors and one received nondepleted marrow from a matched sibling donor. These disorders are similar to B-cell lymphoproliferative disorders that have been described in other immunosuppressed hosts. They are associated with Epstein-Barr virus and range from polyclonal proliferation without cytogenetic abnormalities to monoclonal lymphoma with clonal cytogenetic changes. Unlike other postallograft lymphoproliferative processes, B-cell lymphoproliferative disorders in these patients have not responded to antiviral therapy, immunologic therapy, or chemotherapy. The radiographic patterns of disease include diffuse or focal hepatic involvement; gallbladder wall thickening; and pulmonary, soft-tissue, and basal-ganglion masses. These radiologic findings are not specific and evaluation of tissue histology is required for diagnosis.

Adolescent↗