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PubMed2005

Lymphoproliferative disorder of the airway of an adolescent without immunodeficiency.

Epstein-Barr virus (EBV) is a ubiquitous viral pathogen in humans that has a unique ability to immortalize B-cells. In immunosuppressed individuals, EBV can produce non-neoplastic lymphoproliferative disorders involving various organs. We describe a case report of EBV-associated lymphoproliferative disorder in an immunocompetent 14-year-old male. The case provides a description of EBV-associated lymphoproliferation affecting the upper and lower respiratory tract. The massive submucosal infiltration of B-cells in the lingual tonsils, trachea, and bronchi produced near-complete airway obstruction resulting in tracheotomy. Neither surgical reduction of lingual tonsils nor treatment with steroids was of benefit. An extensive evaluation for immunodeficiency and neoplasia was normal. Treatment with rituximab, an anti-CD20 antibody, resulted in near-complete resolution of the infiltrative process, sufficient to allow decannulation. Rituximab is a treatment option for the rare occurrence of non-neoplastic, EBV-associated, lymphoproliferative disorders.

Adolescent↗
PubMed2003

Recombinant adenovirus-mediated cytotoxic gene therapy of lymphoproliferative disorders: is CAR important for the vector to ride?

The literature has seen an incredible booming of publications related to the use of recombinant adenoviruses as therapeutic tools for lymphoproliferative disorders over the last decade. Several approaches of adenovirus-mediated gene expression have been used to transfect cell lines that are derived from lymphoid tumors and would have otherwise been refractory to other transfection methods. The identification of high-affinity receptor for human adenoviruses serotype 2 and 5, the coxsackie-adenovirus receptor (CAR), has raised the question about its relevance for the efficacy of recombinant adenovirus-mediated gene therapy. We review published studies that have analyzed the use of recombinant adenovirus vectors expressing cytotoxic genes for gene therapy in lymphomas, chronic lymphocytic leukemia and multiple myeloma. For simplicity, we group all these diseases under the term lymphoproliferative disorders. We analyze the use of recombinant adenovirus-mediated cytotoxicity by assessing the importance of the biochemical and intrinsic signaling pathways interacting with the products of the exogenous viral-mediated expression. Ultimately, we discuss studies that have been finalized to by-pass the limitations of the biodistribution of CAR by modifying or targeting adenovirus to other membrane proteins in cells derived from lymphoproliferative disorders.

Adenoviruses, Human↗
PubMed1997

Quantitative polymerase chain reaction for human herpesvirus diagnosis and measurement of Epstein-Barr virus burden in posttransplant lymphoproliferative disorder.

Human herpesviruses can cause acute diseases such as chicken pox or mononucleosis, but also may reactivate during immunosuppression and result in severe or life-threatening illnesses such as shingles or lymphoproliferative disorders. We report the development and validation of a quantitative PCR method to measure viral burden for all eight human herpesviruses (HSV1, HSV2, VZV, EBV, CMV, HHV6, HHV7, and KSHV) in patients' samples. The method uses an internal standard that is coamplified with the viral target, allowing quantification of viral genomes in absolute terms (e.g., viral targets/mL of blood) and ruling out false-negative results. We demonstrate that transplant patients with lymphoproliferative disorder carry an EBV viral burden 3 logs higher than nontransplant patients. EBV titers in transplant patients without a lymphoproliferative disorder are between these values. This quantitative PCR method may aid in differentiating clinically significant vs latent viral burden in immunosuppressed patients.

Herpesviridae Infections↗
PubMed2000

Rituximab (anti-CD20 monoclonal antibody) for the treatment of patients with clonal lymphoproliferative disorders after orthotopic liver transplantation: a report of three cases.

BACKGROUND/AIMS: Post-transplant lymphoproliferative disorders (PT-LPD) are a well-known complication of organ transplantation. Their incidence after liver transplantation in adults ranges from 1.8 to 4%. Reduction of immunosuppression led to remission in a few cases. Other treatments include chemotherapy, interferon alpha therapy and/or intravenous-immunoglobulins, or antiviral drugs. However, monoclonal antibodies directed against B-cell specific antigens have rarely been used in those patients. Our aim was to study the feasibility and efficacy of Rituximab, a new, promising human chimeric antibody that recognizes the CD20 antigen, for the treatment of patients with clonal lymphoproliferative disorders after orthotopic liver transplantation. METHODS: Rituximab (IDEC-C2HB8; Roche Laboratories, Neuilly-sur-Seine, France) was administered at a 375 mg/m2 dose on days 1, 8, 15, and 22, in an outpatient setting, in three patients with PT-LPD. The tumor was classified as polymorphic PT-LPD in two cases and PT-LPD with features of large cell lymphoma in one case. All the tumors expressed the CD20 antigen and were EBV-related, and the clonality was confirmed in all three cases. The 4 injections of the anti-CD20 monoclonal antibody were associated with reduced immunosuppression in the three patient. RESULTS: The treatment with Rituximab was well tolerated without any side effects. The two patients with polymorphic PT-LPDs underwent rapid complete remission, whereas the treatment modalities were ineffective in the patient with the large-cell non-Hodgkin-lymphoma. CONCLUSION: These results must be confirmed in a larger cohort of liver transplant recipients suffering from lymphoproliferation. However, they indicate rapid efficiency of Rituximab in association with reduced immunosuppression in these disorders.

Adult↗
PubMed1990

Nodal and extranodal lymphoproliferative disorders in Sjogren's syndrome: a clinical and immunopathologic study.

Sjogren's syndrome (SS) is frequently associated with both reactive and neoplastic lymphoproliferative disease. Over a 12-year period beginning in 1970, 21 of 138 patients with SS followed at two tertiary university medical centers had biopsies taken of enlarged lymph nodes (18) or extranodal lymphoid infiltrates (8). Many had immunologic studies performed on fresh tissue and all had paraffin-embedded tissue available for histochemical and immunoperoxidase studies. Eight of our patients had malignant lymphomas which were chiefly B cell neoplasms including two lymphoplasmacytic lymphomas and two follicular center cell lymphomas. The remaining 13 patients had either reactive adenitis (usually with follicular hyperplasia) or atypical lymphoid hyperplasia which failed to meet both histopathologic and immunopathologic criteria for malignancy. None of the nine patients with reactive hyperplasia has yet progressed to lymphoma, while one of four patients with atypical lymphoid hyperplasia progressed to overt lymphoma. Clinical features such as age, duration of disease, extent of lymphadenopathy, splenomegaly, or parotid swelling failed to identify those subsets of patients with lymphadenopathy at increased risk for lymphoma. Recognition of lymphoma in two patients was greatly facilitated by tissue immunologic studies demonstrating focal areas of monotypic B cell proliferation. In one patient in whom the histopathologic diagnosis was immunoblastic sarcoma of B cells, tumor cells were L26-negative and strongly UCHL1-positive suggesting T cell differentiation. In three patients with relatively homogeneous extranodal lymphoid infiltrates, B cell polyclonality on tissue immunoperoxidase studies, and the absence of cytologic atypia, precluded a diagnosis of malignant lymphoma; none of these three patients has progressed to overt lymphoma. Our results indicate that (1) patients with SS develop a variety of B cell lymphomas and other lymphoproliferative disorders, and (2) the nature of the lymphoproliferative disorder is best determined by multiparameter analysis including immunologic phenotyping.

Adult↗
PubMed1984

Immunohistology of lymphoproliferative disorders.

Malignant lymphomas have come to be recognized as neoplasms of the immune system. These lymphoproliferative disorders demonstrate surface and cytoplasmic antigenic phenotypes that reflect qualitative and quantitative alterations or aberrant expression of genetic material. Traditionally, cell suspension studies have been used for phenotypic analysis. Alternative immunohistologic methods can be used to profile immunophenotypes in situ. Most lymphoproliferative disorders can be readily classified as T or B cell malignancies, and criteria have been evolved to differentiate neoplastic from reactive/physiologic expansions of lymphoid clones. However, antigenic phenotypic expression does not always correspond to known immunophenotypes of subsets of T or B cells and probably reflects the complexity of neoplastic transformation. Currently, frozen tissue sections, preferably in combination with cell suspension analysis using cytocentrifuge preparations and/or flow cytometry, can provide information to phenotype lymphomas classified by the International Formulation or other nomenclature. Their continued utility depends on development of and adherence to strict quality assurance programs.

B-Lymphocytes↗
PubMed1994

Epstein-Barr virus latent and replicative gene expression in post-transplant lymphoproliferative disorders and AIDS-related non-Hodgkin's lymphomas. French Study Group of Pathology for HIV-associated Tumors.

In acquired immunodeficiency, B-cell proliferation is usually associated with Epstein-Barr virus (EBV), implying the impairment of the normal control of EBV and EBV-infected cells. It has been assumed that EBV infection is latent in lymphoproliferative disorders. In order to determine the type of latency and to investigate whether any lymphoproliferative disorders enter into the lytic cycle, we analyzed the expression of latent and replicative EBV genes in 9 post-transplant lymphoproliferative disorders (PTLD) and in 23 EBV-positive AIDS-related non-Hodgkin's lymphomas (AR-NHL). The PTLD cases were categorized into polyclonal or monoclonal polymorphic tumors and monoclonal monomorphic tumors. The AR-NHL cases included large-cell/immunoblastic (LC/IB) and Burkitt's lymphoma (BL) groups. We demonstrated that varying patterns of latent-viral-gene expression are exhibited showing the 3 forms of latency. Polymorphic PTLD and LC/IB AR-NHL frequently expressed type II or III latency, whereas monomorphic tumors and BL AR-NHL showed type I latency. It is noteworthy that 3 cases of BL AR-NHL expressed latency II form. Induction of lytic cycle highlighted by the expression of BZLF1 occurred in 55.5% of PTLD, 36% of LC/IB and 22% of BL AR-NHL. In contrast, late viral proteins indicating productive cycle were present in 22% of PTLD, 14% of LC/IB, and were absent in BL cases. These data suggest that the impairment of EBV control permits disruption of latency, but the initiation of the lytic cycle may not always lead to viral production.

Gene Expression↗
PubMed1995

Immunosuppression-associated lymphoproliferative disorders in rheumatic patients.

The association between rheumatic disease and the occurrence of hematolymphoid neoplasms has been a subject of investigation for many years. Recently, we and others have reported the development in rheumatic patients of lymphoproliferative disorders that are similar to those occurring in patients with known immunocompromised states. The lymphoid neoplasms that develop in patients with immunosuppression are characterized by several features including the presence of EBV genome in the neoplastic cells. The fact that lymphomas with features of those occurring in immunosuppressed patients can occur in patients with rheumatic disease suggests that immune system impairment secondary to the rheumatic disease, the treatment given for the rheumatic disease, or to a combination of these factors, might play a role in the development of lymphoma in these patients. This review will first describe the characteristics of lymphoproliferative disorders that occur in patients with known immunocompromised states. It will then review general aspects of lymphomas in rheumatic patients with a focus on more recent reports that have described the development of immunosuppression-associated lymphoproliferative disorders in rheumatic patients. Studies that investigate the relative contribution of the rheumatic disease versus therapy for rheumatic disease in the development of lymphoma in this patient group are still needed.

Adult↗
PubMed1996

Purine Analogs for the Treatment of Low-Grade Lymphoproliferative Disorders.

PRIMARY PURPOSE: Low-grade lymphoproliferative disorders follow an indolent clinical course but are incurable with current therapy. Recently, three active agents for the treatment of these diseases have been identified: the purine analogs fludarabine, pentostatin and 2-chlorodeoxyadenosine. The purpose of this review is to summarize the current knowledge on the mechanism of action, clinical activity and toxicities of the purine analogs. METHODS: Articles, abstracts and letters to the editor appearing in English literature and involving the use of the purine analogs in the treatment of hairy cell leukemia, chronic lymphocytic leukemia, indolent non-Hodgkin's lymphoma, cutaneous T cell lymphomas and Waldenstrom's macroglobulinemia were reviewed. RESULTS AND CONCLUSION: Purine analogs have marked cytoreductive potential in the treatment of chronic lymphocytic leukemia, indolent non-Hodgkin's lymphoma and hairy cell leukemia. Major side effects include myelosuppression and infections. Profound lymphocytopenia can be sustained, predisposing patients to opportunistic infections. Although remissions achieved with these agents can be long-lasting, minimal residual disease frequently persists. Postremission strategies aimed at eradicating such microscopic diseases can potentially improve the results of purine analog therapy. Alternatively, the up-front combination of these agents with traditional chemotherapy may lead to higher response rates and more sustained remissions.

Journal Article↗
PubMed1995

Primary lymphoproliferative disorders of the breast.

Primary breast lymphoproliferative disorders are rare lesions and include both the malignant lymphomas and the benign pseudolymphomas. We reviewed 4,491 consecutive cases of breast cancer diagnosed and treated between 1973 and 1988. Patients with lymphoma in other sites and those with lymphomas limited to axillary nodes were excluded. RESULTS. Five patients (0.11%) presented with primary lymphoreticular lesions, of which three were primary non-Hodgkin's lymphoma and two were pseudolymphomas. Patients were followed clinically through to the present time or until death occurred. Surgical procedures included incisional or excisional biopsy in four patients and modified radical mastectomy in one. Two patients received chemo-therapy and one received radiotherapy. One patient with pseudolymphoma subsequently developed infiltrating ductal carcinoma of the same breast. Three patients with primary breast non-Hodgkin's lymphoma died within the follow-up period, with a mean survival of 33 months. CONCLUSIONS. We conclude that primary breast lymphoma is a rare and aggressive breast malignancy with a poor prognosis despite different treatment options.

Aged↗
PubMed1990

Hairy cell leukemia and other "hairy-cell" lymphoproliferative disorders (LPD-HC): the significance of morphologic, histologic and immunologic studies.

In this report the clinical, morphologic, histologic and immunologic findings of 41 patients with hairy lymphoid cells in peripheral blood and/or bone marrow are analyzed. In 27 patients the diagnosis of hairy cell leukemia was established. 14 patients had other variants of lymphoproliferative disorders: malignant lymphoma with hairy cells--7, chronic lymphocytic leukemia with hairy cells--5, and T cell lymphoproliferative disorder with hairy cells--2 patients, respectively. Several variants of malignant lymphoma with hairy cells were defined: lymphocytic, centrocytic and lymphoplasmacytic. The importance of combined use of bone marrow biopsy and immunophenotyping for the correct diagnosis of hairy cell leukemia and other "hairy-cell" lymphoproliferative disorders is stressed. The obtained data suggest relationship between characteristic clinical manifestation (isolated splenomegaly), presence of hairy cells and CD11c-antigen expression.

Acid Phosphatase↗
PubMedDate not supplied

Bone marrow leukemias and lymphoproliferative disorders: scanning electron microscope diagnosis.

This work considers the primary diagnosis of bone marrow leukemias and lymphoproliferative disorders by using the scanning electron microscope (SEM). A total of 14 cases are studied, including 2 demonstrating bone marrow hyperplasia only. The utility of employing the ordinary pathology glass microslide with routine stain is emphasized, as well as certain capabilities of the SEM, including backscattered electron image, secondary electron image, and measurement program. Bone marrow hyperplasias, myeloid leukemias, and lymphoproliferative disorders are analyzed by comparing specific ultrastructural features, such as cell sizes, nuclear chromatin configuration and composition, nucleoli, nuclear contour, and cytoplasmic constituents, including granule population with sizes of such granules. These features set apart the common bone marrow neoplasms and can be a determinant in case diagnosis.

Adult↗
PubMed1989

The routine diagnostic utility of immunoglobulin and T-cell receptor gene rearrangements in lymphoproliferative disorders.

Immunophenotypic studies have a well-documented role in the assignment of lineage in the lymphoproliferative disorders. With the exception of mature B-cell disorders, it is difficult to demonstrate clonality by immunophenotypic studies. The advent of specific DNA probes for immunoglobulin and T-cell receptor genes has greatly facilitated the detection of clonality and, to a lesser degree, lineage, in these cases. The authors have evaluated the diagnostic utility of these probes and compared them with standard immunophenotyping in 65 patients with a variety of lymphoproliferative disorders. Their results show a significant correlation (P less than 0.01) between lineage assignment as determined by phenotyping and gene rearrangement studies, with the latter far superior in determining clonality. Furthermore, analysis of gene rearrangements facilitated the documentation of lineage and/or clonality in six cases in which standard techniques had failed. Although the scientific basis of the study of gene rearrangements has been well established, the authors wish to emphasize the role that these techniques have in evaluating problem cases in the routine diagnostic laboratory.

DNA Probes↗
PubMed1979

T-lymphocyte colonies in normal blood, bone marrow and lymphoproliferative disorders.

The formation of T-lymphocyte colonies was studied in normal individuals and in different lymphoproliferative disorders, using the double layer technique of Lowenberg & de Zeeuw (1977). All normal peripheral blood and bone marrow samples formed colonies: range 102-270 (mean 177) and 55-245 (mean 138) per 1 X 10(5) cells, respectively. Bone marrows from acute leukaemias in complete remission showed normal or increased colony formation. The T cell nature of the colonies was shown by rosette formation with sheep and human red blood cells (RBC). Most lymphoproliferative disorders of T and B cell either failed to grow colonies or showed reduced colony numbers. This was of particular interest in the chronic T cell disorders in which a high proportion of T cells was plated. This technique may help in the further characterization of leukaemic cell populations and may also provide clues on the distribution of particular subsets of T-lymphocytes in peripheral blood and bone marrow.

Adult↗
PubMed1983

Biclonal IgM gammopathy in a lymphoproliferative disorder.

An unusual case of an IgM producing lymphoproliferative disorder is presented. Using immunofluorescent techniques, this study shows that the heavy chain is associated with kappa light chain in some cells, and with lambda light chain in other cells. This indicates the presence of two distinct malignant cell populations in this patient.

Aged↗
PubMed2006

Unusual manifestation of posttransplant lymphoproliferative disorder in the esophagus.

Early manifestations of posttransplant lymphoproliferative disorders (PTLD) are mainly associated with a primary Epstein-Barr virus (EBV) infection. Rapid increases in peripheral blood EBV DNA load are supposed to reliably predict PTLD. We report a boy who 6 months after living-related kidney transplantation presented with an extranodal esophageal manifestation of PTLD. Despite a primary EBV infection with tonsillitis, the peripheral blood EBV DNA remained low, hiding the progression to PTLD.

Adult↗
PubMed1997

Classification of the posttransplant lymphoproliferative disorders: from the past to the present.

Posttransplant lymphoproliferative disorders (PTLD) represent a histopathologic, immunophenotypic, genotypic, and clinical spectrum of disease seen in patients after solid organ and bone marrow transplantation. Because of their great heterogeneity, several classification schemes have been proposed over the past 15 years. Although originally based on morphology and limited immunophenotypic studies, more detailed immunophenotypic and genotypic studies have become increasingly important in the classification of the PTLD. The classifications proposed by Frizzera et al, Nalesnik et al, and Knowles et al are discussed. In addition, some specific types of PTLD recognized in the literature but not distinguished in any of the currently published classifications are presented.

Humans↗