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PubMed1987

Polyclonal polymorphic B-cell lymphoproliferative disorder with prominent pulmonary involvement in children with acquired immune deficiency syndrome.

Four cases of pediatric Acquired Immune Deficiency Syndrome (AIDS) with lymphoproliferative disorder are described and other lymphoid lesions in previously reported cases of pediatric AIDS are reviewed. The lymphoproliferative disorder was characterized by polyclonal, polymorphic B-cell content without evidence of cellular atypia, necrosis or prominent mitotic activity but with predominantly extranodal systemic and prominent pulmonary involvement. Since the lesion has overlapping features it is considered to be intermediate between benign and malignant lymphoproliferations and designated as polyclonal, polymorphic B-cell lymphoproliferative disorder (PBLD) of pediatric AIDS. The PBLD is part of a spectrum of lymphoid lesions in pediatric AIDS consisting of follicular lymphoid hyperplasia of nodal and extranodal sites, pulmonary lymphoid hyperplasia/lymphoid interstitial pneumonitis complex (PLH/LIP complex) in cases previously reported by the authors, and also malignant lymphoma reported by others. It is possible that Epstein-Barr virus (EBV) by itself or in synergism with human T-lymphotropic virus-type III (HTLV-III) is related to pathogenesis of PBLD in children with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Prognostic impact of p27KIP1 expression in cyclin D1 positive lymphoproliferative disorders.

Nodal mantle cell lymphoma (MCL) is a well-defined entity, but non-nodal leukemic cyclin D1 positive lymphoproliferative disorders have been reported and their relationship with MCL remains controversial and their prognosis heterogeneous. We prospectively studied the expression of cyclin D1 in CD5 positive leukemic B lymphoproliferative disorders at diagnosis and identified 65 cases overexpressing cyclin D1. We did not distinguish any clinical or biological criteria allowing one to identify a non-MCL group. Multivariate analysis identified age, anemia and p27kip1 expression as independent prognostic factors of survival. By univariate analysis, p27kip1 high expression proved to be the strongest predictor of prolonged survival. The median survival of p27 low expressors was 30 months, while it was not reached for p27 high expressors. A high level of p27 expression was often found associated with the absence of nodal involvement and the presence of somatic mutations, but neither of them was restricted to the p27 high expression group. In conclusion, we hypothesize that MCL and these cyclin D1 positive leukemic lymphoproliferative disorders represent a continuous spectrum of diseases. Determination of p27 expression level appears as a routine applicable test allowing identification of a subset of patients who could be considered for different therapeutic approaches.

Adult↗
PubMed1994

Glomerulopathies of dysproteinemias, abnormal immunoglobulin deposition, and lymphoproliferative disorders.

The glomerulopathies associated with dysproteinemias and lymphoproliferative disorders exhibit diversity in their morphologic appearance and underlying pathophysiology. Some entities, such as amyloidosis, light-chain nephropathy, and monoclonal immunoglobulin deposition disease, are now well-recognized clinical entities. The disease processes of fibrillary glomerulonephritis and immunotactoid glomerulopathy, which may be associated with these disorders, are becoming increasingly recognized and established entities as reports on significant series of patients continue to be published. Most new information about the pathogenesis of these entities comes from structural, biochemical, and synthetic studies of individual pathogenic paraproteins. The ability to use individual pathogenic human paraproteins to recreate disease in experimental animals is a development that may allow better understanding of disease pathophysiology. The determination of effective therapeutic strategies for the management of these disorders continues to be elusive.

Animals↗
PubMed2001

Ocular involvement in patients with posttransplant lymphoproliferative disorder.

OBJECTIVES: To describe ocular disease in 3 patients with posttransplant lymphoproliferative disorder (PTLD) and to identify the frequency of such ocular involvement. METHODS: Medical record reviews. Using Kaplan-Meier analysis, we calculated the frequency of ocular involvement among pediatric patients with systemic PTLD after liver transplantation. RESULTS: Each patient had bilateral anterior chamber cells. Biopsy of an iris nodule from a patient who had undergone cardiac transplantation confirmed the diagnosis of PTLD, but no signs of systemic PTLD were found. The other 2 patients had systemic PTLD after liver transplantation; 1 presented with iris nodules in both eyes and a subretinal mass in the left eye, while the other had bilateral anterior chamber cells only. Ocular signs improved slowly after reduction of immunosuppressive drug therapy. Ophthalmological examinations were performed on 22 of 25 pediatric patients with PTLD after liver transplantation; 2 had ocular disease. Kaplan-Meier analysis indicated a 20% risk of ocular involvement at 3 years after development of PTLD (95% confidence intervals, 0%-50%). CONCLUSIONS: Posttransplant lymphoproliferative disorder should be considered in the differential diagnosis of uveitis after organ transplantation. Anterior chamber cells and iris nodules are the most common ocular signs, but the posterior segment can be involved. Ocular involvement can occur without evidence of systemic disease and can be asymptomatic. Reduction of immunosuppressive drug therapy is an appropriate treatment.

Adolescent↗
PubMed2000

Polymorphism analysis of Epstein-Barr virus isolates from patients with cutaneous natural killer/T-cell lymphoproliferative disorders: A possible relation to the endemic occurrence of these diseases in Japan.

Certain forms of cutaneous lymphomas in Asia are associated frequently with Epstein-Barr virus (EBV) infection, whereas such cases are less common in western countries. The virus-related peptides, EBV-determined nuclear antigen (EBNA)-2 and the latent membrane protein (LMP)-1, play an essential role in cell transformation. The polymorphisms of these EBV genes may be related to their transforming abilities. In order to clarify the viral subtype that may be involved in the incidence of EBV-associated lymphomas, we analyzed the EBNA-2 and LMP-1 gene polymorphisms and mutations in healthy adults and in patients with EBV-associated cutaneous natural killer(NK)/T-cell lymphoproliferative disorders in Japan. In EBV-related cutaneous lymphoproliferative disorders, EBV subtype 1 was found in all 15 cases, and 1 sample contained a dual infection with subtypes 1 and 2. All EBV isolates from our patients lost a Xho-1 site in exon 1 of the LMP-1 gene, and 7 of 13 cases had a Nco-1 site within the promoter region. All isolates without the LMP-1-Xho-1 site had a 30 bp deletion in the carboxy terminus of the LMP-1 gene, except for the isolate from a patient with angioimmunoblastic lymphadenophathy-like T-cell lymphoma in which a novel Nco-1 site was present in exon 1. Eleven of fourteen throat washings from healthy adults which contained EBV-DNA harbored EBV subtype 1, and the EBNA2 region was not amplified in the other 3 samples. The Xho-1 site was lost in 12 (86%) of 14 isolates and the 30 bp deletion was present in 11 (78%) of 14 isolates from the throat washings. The findings indicate that the predominant EBV isolate from Japanese healthy adults and patients with cutaneous NK/T-cell lymphoproliferative disorders is subtype 1 with a 30 bp deletion and loss of a Xho-1 site in the LMP-1 gene. Since previous data indicated that either subtype 1 or the 30 bp deletion variant possesses high tumorigenic activity, the prevalence of subtype 1 containing these mutations might be responsible for the high incidence of EBV-associated lymphoproliferative disorders in Japan.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Angiogenesis in lymphoproliferative disorders.

In this review, the cellular and molecular mechanisms underlying angiogenesis in lymphoproliferative disorders are summarized, alongside with possible therapeutic applications. Although most of the initial studies in angiogenesis were done on solid tumors, recent data demonstrate the importance of angiogenesis in hematological malignancies including leukemia, lymphoma, and multiple myeloma. Expression of angiogenic polypeptides vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) correlate with clinical characteristics in leukemia and lymphoma, and their serum concentrations serve as predictors of poor prognosis. Antiangiogenic drugs, including thalidomide, arsenic trioxide, endostatin, vasostatin, and neutralizing antibodies to VEGF receptors, used alone or in combination with established chemo- or immunotherapy regimens, constitute a promising approach for the treatment of lymphoproliferative disorders.

Angiogenesis Inhibitors↗
PubMed2004

Progressive epidermotropic CD8+/CD4- primary cutaneous CD30+ lymphoproliferative disorder in a patient with sarcoidosis.

We describe a patient with a CD8+/CD4- primary cutaneous CD30(+) lymphoproliferative disorder with striking epidermotropic histology and coincident cutaneous and systemic sarcoidosis. This patient illustrates the spectrum of clinical and histologic features of CD30+ lymphoproliferative disorders and the need for adequate staging in such cases. This patient's CD30/CD8 coexpression is rare and has clinical and prognostic implications, including mucosally and acrally accentuated lesions and a potentially more aggressive course. Primary cutaneous CD30+ lymphoproliferative disorders have an excellent prognosis; therefore multiagent chemotherapy modalities are generally not indicated. The combination of T-cell lymphoma and sarcoidosis is also rare and may limit treatment options.

Adult↗
PubMed1992

Autoimmunity and auto-immune syndromes associated with and preceding the development of lymphoproliferative disorders.

In this report the association of autoimmunity and autoimmune syndromes with lymphoproliferative disorders (LPD) is described in 15 patients. Non-Hodgkin's lymphoma (NHL) developed in 10 patients, Hodgkin's disease (HD) in 3 and chronic lymphocytic leukemia (CLL) in two. In most instances clinical and laboratory phenomena preceded the development/diagnosis of these disorders. Manifestations ranged from the presence of autoantibodies in the serum to the presence of both ill defined or incomplete autoimmune syndromes including cold urticaria, Raynaud's phenomenon, cold agglutinin disease, thyroiditis, nephrotic syndrome and vasculitis to typical systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and even one of scleroderma. It is suggested that in some patients (in)complete clinical manifestations of autoimmunity may precede the development of lymphoid neoplasias. The link between autoimmunity and lymphoproliferative disorders is briefly discussed.

Autoimmune Diseases↗
PubMed1995

Discordant immunophenotype of chronic B-cell lymphoproliferative disorders in simultaneous specimens from bone marrow and peripheral sites.

This study consisted of 10 cases of chronic B-cell lymphoproliferative disorders that had simultaneous specimens obtained from both bone marrow and peripheral sites for flow cytometric immunophenotyping. The immunophenotyping results of peripheral sites from all 10 cases showed a monoclonal B-cell proliferation expressing monoclonal surface immunoglobulin, CD19, CD20, HLA-DR, and CD5 (except 1 case). Eight (80%) of the 10 cases, however, demonstrated discordant immunophenotypes with myeloid-associated marker expression (CD13, CD11b, and/or CD15) found only in the bone marrow. Patients with CD13 or CD11b marker expression in the bone marrow followed an aggressive clinical course with advanced Rai's stage and a diffuse or mixed bone marrow infiltration pattern or disease transformation. These results indicate that discordant immunophenotypes of malignant cells from different body sites occur in chronic B-cell lymphoproliferative disorders and are not uncommon. Additionally; myeloid-associated markers, which some investigators have described as being associated with an unfavorable clinical course, may be expressed only in bone marrow specimens in these disorders. Thus, bone marrow specimens may be preferential in determining myeloid-associated marker expression in chronic B-cell lymphoproliferative disorders.

Aged↗
PubMed1995

Posttransplantation lymphoproliferative disorders in solid organ recipients are predominantly aggressive tumors of host origin.

Patients immunosuppressed after organ transplantation have an increased frequency of lymphoproliferative disorders, known as posttransplantation lymphoproliferative disorders (PTLDs). In recipients of bone marrow allografts. PTLDs are often of donor origin. In only a few cases of lymphoma arising in solid-organ transplant recipients has the origin from host or donor lymphocytes been established. The authors have analyzed 11 cases of PTLD from Massachusetts General Hospital, arising in seven male and four female patients, aged 8 to 63, five with renal, four with cardiac, and two with hepatic allografts. Using the polymerase chain reaction (PCR) to investigate genetic polymorphism at the D4S174 locus on chromosome 4, the Rb1.20 locus on chromosome 13, and the D19S178 locus on chromosome 19, only one tumor (previously reported) was of donor origin, whereas 10 were of host origin. Follow-up revealed that six patients died of PTLD, one was alive with recurrent PTLD, and four were alive and well or had died of other causes, including the patient with donor-origin PTLD. Based on these cases and on a review of previously reported cases, the authors conclude that the majority of PTLDs in solid organ recipients are of host origin. There appears to be a trend toward a greater likelihood of persistent or recurrent PTLD among solid organ recipients with host-origin tumors than among those with donor-origin tumor.

Adolescent↗
PubMed1995

Unusual lymphoproliferative disorders in nine adults with HIV or AIDS: CT and pathologic findings.

PURPOSE: To identify characteristic computed tomographic (CT) findings in unusual pulmonary lymphoproliferative disorders seen in adults with the human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS). MATERIALS AND METHODS: The authors retrospectively reviewed the CT scans and pathologic specimens from nine patients with pulmonary lymphoproliferative disorders. CT scans were evaluated for nodules, reticulation, areas of ground-glass attenuation, consolidation, and bronchial disease. Changes seen in pathologic specimens were classified as consistent with classic lymphocytic interstitial pneumonitis (LIP), mucosa-associated lymphoid tissue lymphoma (MALTOMA), or atypical lymphoproliferative disorder (ALD). Immunopathologic results were reviewed when available. RESULTS: Eight patients had AIDS. Five patients had classic LIP. One patient had MALTOMA, and three patients had ALD. Altogether, 2-4-mm-diameter nodules were the predominant CT finding in eight patients; these were peribronchovascular in four patients. The presence of interstitial nodules correlated with the pathologic finding of nodular disease in seven patients. CONCLUSION: Familiarity with these AIDS-related disorders and their CT appearance should assist in the differential diagnosis.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Lymphocyte markers and clinical expression of lymphoproliferative disorders with moderate lymphocytosis.

Lymphoproliferative syndrome with well differentiated lymphocytes and moderate lymphocytosis in the peripheral blood includes a heterogeneous group of disorders, that present often difficulties in classification. We have studied the lymphocyte markers (ER, EMR, sIg and T3, T4, T8 antigens) in 36 cases who had lymphocytic infiltration in the bone marrow and peripheral lymphocyte counts less than 15 X 10(9) l-1. Four cases (11.1%) had the characteristics of T8 lymphocytosis and 31 had a B cell monoclonal proliferation in the peripheral blood. Of these, four were sIg-, EMR+, 19 were sIg+, EMR+ and 8 were sIg+, EMR-. Most patients (17/32) had the clinical picture of stage 0 and I B-CLL. Six cases presented as pure splenomegalic form of CLL, three had the features of immunocytic lymphoma and five had the features of lymphocytic lymphoma. It is concluded that the majority of lymphoproliferative disorders presenting with moderate lymphocytosis represent early forms of B-CLL. Occasionally cases of lymphocytic or immunocytic lymphoma may present problems of differential diagnosis since there may be a dissociation of phenotypic characteristics of lymphocytes between tissues and peripheral blood.

Aged↗
PubMed1996

First report of a B cell lymphoproliferative disorder arising in a patient treated with immune suppressants for severe aplastic anemia.

Aplastic anemia is a disorder characterized by pancytopenia and bone marrow hypocellularity. There is some evidence that aplastic anemia may be due to suppression of hematopoiesis by activated T-suppressor cells. Thus, immunosuppressive agents have been used as an alternative to bone marrow transplantation for treatment. We report on a unique case of a patient with aplastic anemia who was treated with a course of immunosuppression including cyclosporine (CSA), anti-thymocyte globulin (ATG), and prednisone. Five months after this treatment, the patient developed a B cell lymphoproliferative disorder which was successfully treated with radiation therapy. Prior reports of CSA-associated lymphoproliferative disorders have appeared in the literature as potential side effects of immunosuppression following transplantation. This is the first report of a lymphoproliferative disorder associated with immunosuppressive treatment of aplastic anemia in a nontransplant setting. Thus, when presenting options for treatment of aplastic anemia, lymphoproliferative disorders should be included as a rare complication of immunosuppressive therapy.

Adolescent↗
PubMed2002

Are activation markers (CD25, CD38 and CD103) predictive of sensitivity to purine analogues in patients with T-cell prolymphocytic leukemia and other lymphoproliferative disorders?

T-cell prolymphocytic leukemia (T-PLL) is a rare lymphoproliferative disorder with distinctive clinical and laboratory features. It is often resistant to conventional chemotherapy, but complete or partial responses have been documented with the use of purine analogues. We report on two cases of T-PLL with a slightly different immunophenotype but a remarkably different response to pentostatin. We discuss the possible therapeutic implications of this finding and establish a comparison between immunophenotype and sensitivity to purine analogues in patients with T-PLL and other chronic lymphoproliferative disorders.

ADP-ribosyl Cyclase↗
PubMed1997

Epstein-Barr virus lymphoproliferative disorders after liver transplantation.

Post-transplant lymphoproliferative disorders (PTLD) represent a spectrum of histological and immunological abnormalities, ranging from benign polyclonal B-cell hyperplasia to monoclonal malignant lymphoma. The important role of Epstein-Barr virus (EBV) in PTLD in liver transplant patients, particularly in pediatric recipients, is reviewed. Understanding the risks of EBV infection, the clinical presentations and diagnosis of PTLD, and its pathophysiology are crucial to the management of these disorders. Current treatment methods have resulted in better outcomes of these disorders, which in the past were uniformly fatal.

Adult↗
PubMed1992

Demonstration of passenger leukocytes in a case of Epstein-Barr virus posttransplant lymphoproliferative disorder using restriction fragment length polymorphism analysis.

Lymphocytic populations of the posttransplant lymphoproliferative disorder in a completely matched renal allograft and a recipient's regional lymph node were examined, using restriction fragment length polymorphism analysis with probe YNH24 to the variable number tandem repeat D2S44. The donor's DNA was found in lymphocytes extracted from both the grafted kidney and the recipient's lymph node 26 days after engraftment. In both these organs, the results of in situ hybridization with a terminally biotin-labeled oligonucleotide probe to the Not I tandem repeat region of the Epstein-Barr virus (EBV) genome, as well as those of Southern blot hybridization to the EBV nuclear antigen region of the EBV genome, were positive. These findings confirmed the presence of the donor's lymphocytes ("passenger leukocytes") in the host nodal tissue in human renal transplantation and implicated EBV as playing a role in the development of posttransplant lymphoproliferative disorder. It is speculated that the EBV proliferative stimulus contributed to the recipient and the donor lymphocyte expansions. Alternatively, the proliferation of both lymphocyte populations could result from a mutual stimulation by minor histocompatibility or other antigens.

Cell Division↗
PubMed2006

Hepatitis C virus related lymphoproliferative disorder in a renal transplant recipient.

Posttransplant lymphoproliferative disorders (PTLD) are commonly caused by Ebstein-Barr Virus infection. The role of hepatitis C virus (HCV) in the genesis of lymphomas has been recognized recently. We report a HCV infected renal transplant recipient who developed PTLD 11 months after transplantation. Reduction of immunosuppression led to disappearance of viremia and clearance of PTLD. This is the first such report in the world literature.

Adult↗