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PubMed2003

Immunophenotype and ultrastructure of B-cell lymphoproliferative disorder with cytoplasmic projection.

To identify the knowledge of rare lymphoproliferative disorder, the clinical and biological features of three kinds of lymphoproliferative disorders with cytoplasmic projections were compared. The clinical manifestations, ultrastructure and immunophenotype were analyzed. The results showed that hairy cell leukemia (HCL), splenic lymphoma with villous lymphocyte (SLVL) and hairy cell leukemia-variant (HCL-V) had some common characters including splenomegaly, peripheral blood and bone marrow infiltration by villous lymphocyte and B lymphocyte immunophenotype; but these three disorders had specific features respectively. It was concluded that overall analysis of clinical and laboratory features might be contributive to the differential diagnosis of these three disorders.

Adolescent↗

PubMed2002

Risk factors for lymphoproliferative disorders after liver transplantation in adults: an analysis of 480 patients.

BACKGROUND: Posttransplant lymphoproliferative disorder (PTLD) is a well-known complication of organ transplantation that leads to death in more than 50% of cases. The aim of this work was to identify specific risk factors for lymphoproliferative disorders after liver transplantation in adults. METHODS: A total of 480 consecutive patients who underwent transplantation between 1986 and 1997 were studied (323 men, 157 women; mean age: 49.8+/-10.4 years). Demographics, the indication for transplantation, the immunosuppressive regimens, the incidence of rejection episodes, and Epstein-Barr virus infection were analyzed. Univariate and multivariate analysis were used to identify factors predictive of PTLD. RESULTS: Sixteen cases of PTLD (3.3%) occurred at a median of 5.5 (range, 1-39) months after liver transplantation. All 16 cases occurred in patients with evidence of exposure to Epstein-Barr virus before transplantation. In multivariate analysis, the use of antilymphocyte antibodies (P=0.007, relative risk [RR]=4.2, 95% confidence interval [CI]=1.5-11.7), age older than 50 years (P=0.037, RR=3.5, 95% CI=0.95-13.0), liver transplantation for hepatitis C virus cirrhosis (P=0.015, RR=8.7, 95% CI=1-78.3), and liver transplantation for alcoholic cirrhosis (P=0.015, RR=9.6, 95% CI=1.2-77.2) were independently associated with the onset of PTLD. CONCLUSION: Liver transplantation for hepatitis C virus-related and alcoholic cirrhosis and age older than 50 years are three additional risk factors for lymphoproliferative disorder independent of the use of antilymphocyte antibodies. The use of antilymphocyte antibodies after liver transplantation should be avoided in these categories of patients, especially those older than 50 years.

Adult↗

PubMed1996

Oral presentation of posttransplantation lymphoproliferative disorders. An unusual manifestation.

Cyclosporine, an immunosuppressive agent widely used in organ transplantation, has several undesirable side effects, including gingival hyperplasia, which occurs in up to 70% of patients. Another complication associated with use of cyclosporine and other immunosuppressants is an increased incidence of malignancies. Long-term use of cyclosporine also is associated with a spectrum of hyperproliferative disorders ranging from reactive lymphoid hyperplasia to aggressive malignant lymphomas. While cyclosporine-related lymphoproliferative disorders have been widely reported, they have not been described in the oral cavity as the first manifestation of this disease. We report on two cardiac transplantation patients with a history of cyclosporine use who presented initially with oral symptoms of lymphoproliferative disorder. Both had erythematous to cyanotic and hyperplastic gingiva. On gingivectomy, the fixed tissue was soft, glistening, and tan colored, in contrast to the usual firm, white, cyclosporine-associated, benign gingival fibrous hyperplasia. Histologically, a dense, diffuse infiltrate of lymphoplasmacytoid cells with vesicular nuclei, prominent nucleoli, a moderate amount of cytoplasm, and high mitotic activity was observed. Immunocytochemical studies confirmed that the cells were monoclonal for lambda light chains in one patient and kappa light chains in the other. The cells from one patient were positive for CD45, while both patients were negative for CD20 and all nonhematopoietic antigens tested. Both tissues were strongly positive for Epstein-Barr virus. Morphology and immunocytochemistry findings are consistent with a posttransplant lymphoproliferative disorder. These are the first two reported cases of cyclosporine-associated posttransplant lymphoproliferative disorders presenting as gingival hyperplasia.

Adult↗

PubMed2000

Natural killer-type receptors for HLA class I antigens are clonally expressed in lymphoproliferative disorders of natural killer and T-cell type.

In recent years, natural killer (NK) cells, as well as subpopulations of T cells, have been found to express diverse NK receptors (NKRs) for HLA class I molecules. We have characterized NKR phenotypes in lymphoproliferative disorders of NK or T-cell type. Peripheral blood of patients with lymphoproliferative disorders (n = 9) was analysed by multiparametric immunofluorescence flow cytometry with eight different antibodies against NKRs. Abnormal neoplastic cell populations from different types of NK or T-cell lymphoproliferative disorders lacked diversity in their NKR repertoires, i.e. all or none of the abnormal cells expressed individual NKRs and this expression occurred at single levels of intensity. This pattern of expression was specific for lymphoproliferative disorders as these resticted NKR repertoires were not found either in healthy donors (n = 9) or in patients with viral or autoimmune disease (n = 5). We conclude that NKRs are clonally expressed in lymphoproliferative disorders of NK or T-cell origin. NKR repertoires may represent a novel tool in diagnosing clonal disorders of NK and T-cell type.

CD3 Complex↗

PubMed1996

Human herpesvirus 6 in human immunodeficiency virus-infected individuals: association with early histologic phases of lymphadenopathy syndrome but not with malignant lymphoproliferative disorders.

Preliminary evidence suggested that human herpesvirus-6 (HHV-6) may act as a cofactor in acquired immunodeficiency syndrome (AIDS) and may contribute to the pathogenesis of lymphoproliferative disorders occurring in individuals infected with the human immunodeficiency virus (HIV). To understand better the biological and clinical significance of HHV-6 infection in the context of HIV-related immunosuppression, the polymerase chain reaction was used to study the frequency and variant distribution of HHV-6 in peripheral blood mononucleated cells (PBMCs) from HIV-seropositive individuals, either asymptomatic or with lymphadenopathy syndrome (LAS) or with overt AIDS. Non-neoplastic and malignant lymphoproliferative disorders from both HIV-infected and HIV-seronegative patients were also investigated using the same series of samples for the presence of Epstein-Barr virus (EBV). When compared with healthy blood donors (12/42, 29%), HHV-6 prevalence in PBMCs showed a progressive decline in HIV-seropositive individuals with asymptomatic HIV infection (3/26, 11%) and in patients with LAS (1/13, 8%) and a significant reduction in patients with overt AIDS (1/20, 20%; P = 0.02). The decrease correlated with the number of CD4+ cells at the time of examination. In addition, HHV-6 DNA sequences were significantly more prevalent in LAS biopsies (13/20, 65%) than in HIV-unrelated reactive lymphadenopathies (2/10, 20%; P = 0.02) and the presence of HHV-6 sequences correlated closely with a histologic pattern of follicular hyperplasia (13/16, 81%; P = 0.003). Strikingly, HHV-6 prevalence decreased in PBMCs of LAS patients, suggesting that the likelihood of interactions between HHV-6 and HIV varies in different body districts. In particular, the demonstration that all HHV-6-carrying LAS samples were also positive for HIV infection suggests that LAS lymph nodes constitute one of the sites where biologically relevant interactions between the two viruses might occur. Also, the prevalence of EBV was higher in LAS (14/20, 70%) than in non-neoplastic lymph nodes from HIV-seronegative individuals (4/10, 40%), although the difference was not statistically significant. EBV was associated strongly with HIV-related malignant lymphoproliferative disorders, being detected in 100% of patients with Hodgkin's disease (HD) and 53% of B-cell non-Hodgkin's lymphomas (NHL). In contrast, the prevalence of HHV-6 DNA in HD and B-cell NHL arisen in HIV-infected patients (30% and 6% respectively) was remarkably lower and similar to that observed in lymphoproliferative disorders from HIV-seronegative patients. Finally, as observed in healthy individuals, HHV-6 variant B was more prevalent than variant A in benign and malignant lymphoproliferative disorders from bot HIV-infected and HIV-seronegative patients. These results suggest that the interactions between HHV-6 and HIV could be different in the various phases of HIV disease and in different districts; HHV-6 has probably no direct role in the pathogenesis of HIV-associated B-cell NHL and HD cases, and behave differently from EBV; and HIV-related immunosuppression does not alter the distribution of HHV-6 variants in these tissues, as observed in the case of EBV.

AIDS-Related Complex↗

PubMed1998

Lymphoproliferative disorders after lung transplantation: imaging features.

PURPOSE: To define the imaging features of lymphoproliferative disorders that occur after lung transplantation. MATERIALS AND METHODS: In a retrospective review of the cases of 246 patients who had undergone lung transplantation (62 single- and 184 double-lung transplants) between 1987 and 1997, the authors found nine patients (seven men and two women, aged 16-59 years [mean, 42.2 years]) with posttransplantation lymphoproliferative disorders. All imaging, clinical, and pathologic findings pertaining to these disorders were reviewed. RESULTS: Eight of the nine patients had isolated intrathoracic disease. The most common abnormality (six patients) was the presence of multiple, well-defined pulmonary nodules. These nodules, when multiple, had basilar and peripheral predominance. Other abnormal features included hilar or mediastinal adenopathy (two patients), a consolidated upper lobe (one patient), a pleural mass (one patient), and bulky abdominal lymphadenopathy (one patient with pathologically proved Hodgkin lymphoma). Three patients had nodules with a surrounding area of ground-glass opacity (halo sign), and one patient had multiple ill-defined areas of centrilobular opacity. Air bronchograms were not often seen, and pleural effusions were absent. CONCLUSION: The presence of well-defined pulmonary nodules in a patient who has undergone lung transplantation should raise concern about the possibility of posttransplantation lymphoproliferative disorder. In such cases, performance of pathologic studies should be expedited.

Adult↗

PubMed1994

In situ hybridization for the Y chromosome reveals a donor origin for a posttransplant lymphoproliferative disorder in a sex-mismatched hepatic allograft.

We report a case of posttransplant lymphoproliferative disorder diagnosed within 4 weeks of orthotopic liver transplantation from a male donor to a female recipient. To determine whether the posttransplant lymphoproliferative disorder was of donor or recipient origin, nonisotopic in situ hybridization for the human Y chromosome was performed on formalin-fixed, paraffin-embedded sections of the donor liver using a digoxigenin-labeled probe. The lymphoid cells hybridized with the Y chromosome probe, indicative of a male genotype consistent with posttransplant lymphoproliferative disorder of donor origin. This case illustrates that nonisotopic in situ hybridization for the Y chromosome can discriminate between donor and recipient cells in sex-mismatched organ transplants.

Female↗

PubMed2005

Angiogenesis in lymphoproliferative disorders: a therapeutic target?

PURPOSE OF REVIEW: Several recent studies have focused on the role of angiogenesis in hematologic malignancies. This review specifically discusses angiogenesis in lymphoproliferative disorders, with a special emphasis on the most recent publications. The novel therapeutic strategies arising from advances in this field are reviewed, and the potential pitfalls of these therapies are also discussed. RECENT FINDINGS: Recent publications confirm that angiogenesis and angiogenic factors are increased in lymphoproliferative disorders. In addition, several studies have demonstrated that angiogenesis is directly involved in the pathogenesis of these disorders. SUMMARY: Knowledge of angiogenesis in lymphoproliferative disorders has increased substantially in the past few years. Angiogenic factors such as vascular endothelial growth factor have been shown to be important in the progression or maintenance of lymphoproliferative disorders. Targeting of these factors is therefore a promising new therapeutic approach. Hematopoietic angiogenesis is a nascent field, however, and its concepts are still evolving. A systematic approach to understanding and characterizing the angiogenic phenotype is required for the design of efficacious antiangiogenic therapeutic regimens.

Angiogenesis Inhibitors↗

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↗

PubMed2003

EBV-induced polymorphic lymphoproliferative disorder of the iris after heart transplantation.

BACKGROUND: Posttransplantation lymphoproliferative disorder (PTLD) of the iris is a rare entity with only ten cases having been published as yet. Its clinical aspect is typical. Therapy is multimodal and affords an interdisciplinary approach. METHODS: A 7-year-old boy developed a lymphoproliferative mass of the iris with uveitis 4 years after heart transplantation and immunosuppression. A progressive, flesh-colored thickening of the iris with secondary angle closure glaucoma necessitated a diagnostic and therapeutic iridectomy. Morphological investigation of the iris specimen disclosed a polymorphic posttransplantation lymphoproliferative disorder (PTLD) and the presence of Epstein-Barr virus (EBV) within the tissue. The EBV load in peripheral blood monocytes was massively elevated, thus indicating a chronic EBV infection. After conservative treatment and radiation therapy, the iris mass quickly resolved. There was no evidence of systemic PTLD. CONCLUSIONS: PTLD is a well-known, EBV-induced entity that rarely affects the eye. EBV is principally detectable in specimens of iris PTLD. If conservative, antiviral treatment fails, the iris lesions can be treated by local radiation therapy with very good success. In the near future, patients with PTLD of the eye may benefit from immunologic treatment with ex vivo generation of virus-specific T-lymphocytes.

Antiviral Agents↗

PubMed2002

B-cell lymphoproliferative disorders.

The differential diagnosis of the B-cell lymphoproliferative disorders can sometimes by tricky. When the morphology and flow cytometric studies are classic, the case should not present a diagnostic challenge. However, when the lesion does not read the book, one must take into consideration the morphology/cytology, flow cytometry, and clinical history. Integrating all three of these will often lead to the correct diagnosis; however, there will be occasional cases where the best that a pathologist can say is "B-cell lymphoproliferative disorder". In those instances, one should not overcall something, but rather should state what the problems are, and what are most likely to be the diagnostic possibilities.

B-Lymphocytes↗

PubMed2000

Regression of Epstein-Barr virus-associated lymphoproliferative disorders in patients with acquired immunodeficiency syndrome during therapy with foscarnet.

Epstein-Barr virus (EBV)-associated lymphoproliferative disorders frequently develop in patients with acquired immunodeficiency syndrome (AIDS). The lymphoproliferative disorders are usually treated with a combination of cytotoxic drugs, and virustatic medication is thought to be ineffective. However, we report about two AIDS patients with EBV-associated lymphoproliferative disorders not responding to a standard chemotherapy, who achieved complete tumour regression after virustatic therapy with foscarnet.

Acquired Immunodeficiency Syndrome↗

PubMed1998

Hodgkin's disease-like lymphoproliferative disorders in patients with different underlying immunodeficiency states.

Epstein-Barr virus (EBV)-associated lymphoproliferative diseases are a frequent occurrence in immunodeficient patients. Most commonly seen are polymorphic B-cell lymphoproliferative disorders and malignant B-cell lymphomas. Classical Hodgkin's disease (HD), however, is rare in these patients. In the present study, we attempted to characterize cases resembling HD in patients with a variety of underlying immunodeficiency states using clinical aspects, immunohistochemistry, in situ hybridization, and polymerase chain reaction. All of the six cases that we investigated presented clinically with B symptoms and a short, devastating course. Histologically, they showed a lymphocytic depletion and multiple cells that resembled HD and Reed-Sternberg cells. Many of those were atypical blast cells that stained positively for B-cell surface antigens, such as CD20 and CD79a, whereas others were of the typical HD and Reed-Sternberg phenotype. Another frequent finding, especially in the extranodal sites, was a perivascular arrangement of large blast cells intermingled with small lymphoid cells. All of the cases were EBV-associated (proved latent membrane protein-1 immunohistochemical analysis, EBV-encoded RNA in situ hybridization, and polymerase chain reaction for subtypes A and B), with a frequent coinfection of type A and B. This was in contrast to ordinary HD, which is characterized by single infection of only one strain, i.e., the subtype A in Western countries. Three cases showed clonal B-cell populations, at least at terminal stages of the disease. We describe a lymphoproliferative disorder in immunodeficient patients with features of HD that, in some respects, resembles an EBV-driven lymphoproliferative disorder seen in cases of fatal infectious mononucleosis. We conclude that clinical and pathologic features of these disorders might cause some problems for histologic differential diagnosis and might represent a separate entity of their own in immunodeficient patients.

Adult↗

PubMed1997

2-Chlorodeoxyadenosine in cutaneous T-cell lymphoproliferative disorders.

The efficacy and toxicity of 2-chlorodeoxyadenosine (2-CdA) in cutaneous T-cell lymphoproliferative disorders was examined. Between February 1991 and April 1996, 25 patients with relapsed or refractory cutaneous T-cell lymphoproliferative disorders (24 mycosis fungoides or Sezary syndrome, one Ki-1+ anaplastic large cell lymphoma) were treated with 2-CdA initially administered by continuous intravenous infusion at a dose of 0.1 mg/kg/d for 7 days (13 patients). The infusion duration was subsequently reduced to 5 days (9 patients) because of prohibitive hematologic toxicity. Three patients were treated at the same daily dose by bolus injection over two hours for 5 days. Cycles were administered at 28 day intervals. Seventeen patients received more than one cycle. An overall response rate of 24% was achieved. Three patients (12%) had a complete response with a median duration of 4.5 months (range, 2.5 to 16). Three (12%) had a partial response with a median duration of 2 months (range, 2 to 4). Nineteen patients (76%) had no response. The most significant toxicities encountered were myelosuppression (64%) and infectious complications (64%). 2-CdA has activity as a single agent in patients with previously treated relapsed T-cell lymphoproliferative disorders.

Adult↗

PubMed2002

The clinical value of rearrangement of IgH gene and bcl-2/J(H) fuse gene in the diagnosis of orbital lymphoproliferative disorders.

OBJECTIVE: To determine whether polymerase chain reaction (PCR) for the assay of B-cell gene rearrangement in patients with orbital lymphoproliferative disorders could be useful in the diagnosis of lymphoma, especially in differentiating a benign lesion from a malignant one. METHODS: In addition to clinical, pathological and immunohistochemical evaluations, 48 cases of orbital lymphoproliferative disorders were examined for immunoglobulin heavy chain (IgH) gene rearrangement and bcl-2/J(H) fuse gene rearrangement by means of PCR to amplify the third frame work region (FR3) and bcl-2/J(H) fuse gene with formalin-fixed and paraffin-embedded tissues. RESULTS: The PCR using primer FR3A showed that 22 cases had discrete single products, which were within the molecular weight range of 100 to 120 bp, and were therefore interpreted as monoclonal. The positive rates of FR3 region of IgH gene rearrangement in patients with malignant lymphoma, benign reactive lymphoid hyperplasia and lymphocytic inflammatory pseudotumor were 75.0% (15/20), 40.0% (4/10) and 16.7% (3/18) respectively. The four patients with simultaneously bilateral ocular adnexal lymphoid neoplasm exhibited identical clonal IgH gene rearrangement patterns. A faint smear pattern or no band at all was demonstrated in the remaining 26 cases, representing polyclonal populations of lymphoid cells. The PCR using bcl-2 primer showed that 6 cases had discrete single products that were within the molecular weight range of 100 to 300 bp, and were interpreted as having bcl-2/J(H) fuse gene. They were 2 cases of follicular B-cell lymphomas, 1 case of diffuse mixed large and small cell B-lymphoma and 3 cases of diffuse small cell B-lymphoma. A faint smear pattern or no band at all was demonstrated in the remaining 17 cases of lymphomas, lymphocytic inflammatory pseudotumor and benign reactive lymphoid hyperplasia. The positive rates of bcl-2/J(H) fuse gene rearrangement in patients with malignant lymphoma, benign reactive lymphoid hyperplasia and lymphocytic inflammatory pseudotumor were 30.0% (6/20), 0% (0/10), and 0% (0/18), respectively. CONCLUSIONS: Molecular genetic analysis by PCR using the FR3A primer is helpful in the diagnosis of orbital lymphoproliferative disorders, especially those in which the diagnosis can not be made by routine histopathological finding and immunohistochemistry evaluation. However, the rate of bcl-2/J(H) fuse gene rearrangement is too low to be suitable for clinical diagnosis of orbital lymphoproliferative disorders.

Gene Rearrangement↗

PubMed1998

B-lymphoproliferative disorders in patients with hepatitis C virus infection.

A cohort of 148 consecutive patients with hepatitis C virus infection were studied at the rheumatology out-patient clinic of a tertiary care teaching hospital. The diagnosis of hepatitis C virus infection was supported by detection of HCV RNA in the serum. Cryoglobulin screening was done in all patients and the presence of a monoclonal component was investigated when the cryocrit was higher than 1%. Patients with lymphoproliferative disorders were further investigated. Four patients had a B lymphoproliferative disorder, which represents a prevalence of 2.7% in this cohort of patients with hepatitis C virus infection. Mixed cryoglobulinemia (MC), with cryocrit higher than 1%, was found in 16 of 148 patients (11%). It was type III MC in 13 patients and type II MC in 3. All patients who developed a B lymphoproliferative disorder had mixed cryoglobulinemia, with a monoclonal component (type II MC) in two patients and without a monoclonal component (type III MC) in the other two. The incidence of B-lymphoproliferative disorders among this cohort of patients with hepatitis C virus infection seems to be significantly increased. However, the high frequency of asymptomatic, undiagnosed HCV infection among the apparently healthy general population may decrease the true significance of this association. Systematic screening of cryoglobulin production in patients with hepatitis C virus infection might clarify whether the risk of B lymphoproliferative disorders increases when type II or type III mixed cryoglobulinemia is present.

B-Lymphocytes↗

PubMed2002

Iatrogenic lymphoproliferative disorders in non-transplantation settings.

Over the last decade, it has become clear that iatrogenic immunodeficiency-related lymphoproliferative disorders can occur in non-transplantation settings. These lymphoproliferative disorders occur predominantly in patients with rheumatologic diseases who are treated with immunomodulatory drugs. Like immunodeficiency-related lymphoproliferations in other settings, these represent a spectrum of lymphoid neoplasms and are frequently associated with Epstein-Barr virus. The distribution of histologic types of iatrogenic lymphoproliferations in non-transplantation settings appears to differ from that seen in other immunodeficiency settings with a probable increase in representation of Hodgkin's disease and lymphoproliferations resembling Hodgkin's disease. Recognition of these immunodeficiency-related lymphoproliferative disorders is important for appropriate patient management.

Humans↗

PubMedDate not supplied

[Role of Epstein-Barr Virus in lymphoproliferative disorders].

The EBV plays a major role in the development of lymphoproliferative disorders in immunosuppressed patients. After organ transplantation most of lymphoproliferative disorders associated with EBV are polymorphic, with various expression of clonality. The pattern of EBV latency genes expression is rather the same as in lymphoblastoid cells lines and the EBV infected cells strongly expressed activation and adhesion molecules in most cases. In AIDS-related lymphomas the frequency of EBV as well as the expression of latency genes are related to the localization and to the histological subtypes. While EBV is observed in 30 to 50% of cases of Burkitt's lymphomas occurring the early stage of AIDS, its association in primary brain lymphomas and immunoblastic lymphomas developed in the late stage is observed in nearly all cases as well as in Hodgkin's disease. In primary brain lymphomas, the high expression of LMP-1 protein is correlated to the expression of BCL2 oncoprotein suggesting a transactivation of bcl2 by LMP-1 as it was reported in vitro. In non overt immunosuppressed patients the role of EBV is less clearly established, particularly in Burkitt's lymphoma where EBV is now considered as a cofactor. In B-cell lymphoma EBV is detected in about 5% of cases except in peculiar situations such as in lymphoma occurring in pleural cavity after longstanding pleural chronic inflammation and in Richter's syndrome with Reed-Sternberg-like cells. In peripheral T-cell lymphomas, EBV is observed in about 25% of cases, but its frequency varies with the histology and the localisation. EBV is present in nearly all cases of angio-immunoblastic type and in the nasal lymphoid proliferations developed from the NK cells. Detected in 30 to 80% in the Reed-Sternberg cells of Hodgkin's disease cases, the pathogenic significance of EBV remains to be determined in this disease.

Herpesvirus 4, Human↗