AIDS-related lymphoproliferative disease

Blood ◽  
2006 ◽  
Vol 107 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Willis H. Navarro ◽  
Lawrence D. Kaplan

Abstract Not long after the recognition of HIV as the causative agent of AIDS, it was evident that individuals infected with HIV developed lymphoma at a greater rate than the population at large. Approximately two thirds of AIDS-related lymphoma (ARL) cases are categorized as diffuse large B-cell type, with Burkitt lymphomas comprising 25% and other histologies a much smaller proportion. Typically, these individuals have presented with advanced extranodal disease and CD4+ lymphocyte counts of less than 200/mm3. Recent clinical trials have demonstrated a better outcome with chemotherapy for ARL since the introduction of combination antiretroviral treatment, termed highly active antiretroviral therapy (HAART). For patients with relapses, solid evidence points to the safety and utility of hematopoietic-cell transplantation as a salvage modality. Coinfection with other viruses such as Epstein-Barr virus and Kaposi sarcoma-associated herpesvirus have led to the genesis of previously rare or unrecognized lymphoma subtypes such as plasmablastic and primary effusion lymphomas. The immunosuppressive impact of treatment for patients with ARL receiving chemotherapy with HAART appears transient and opportunistic infections have become less problematic than prior to HAART. Significant progress has been made in the understanding and management of ARL but outcomes still remain inferior compared to those achieved in HIV- individuals.

2006 ◽  
Vol 8 (5) ◽  
pp. 1301-1307 ◽  
Author(s):  
Tsunekazu Hishima ◽  
Naoki Oyaizu ◽  
Takeshi Fujii ◽  
Natsuo Tachikawa ◽  
Atsushi Ajisawa ◽  
...  

Blood ◽  
2010 ◽  
Vol 116 (18) ◽  
pp. 3398-3408 ◽  
Author(s):  
Alexandra H. Filipovich ◽  
Kejian Zhang ◽  
Andrew L. Snow ◽  
Rebecca A. Marsh

AbstractX-linked lymphoproliferative disease (XLP1), described in the mid-1970s and molecularly defined in 1998, and XLP2, reported in 2006, are prematurely lethal genetic immunodeficiencies that share susceptibility to overwhelming inflammatory responses to certain infectious triggers. Signaling lymphocytic activation molecule-associated protein (SAP; encoded by SH2D1A) is mutated in XLP1, and X-linked inhibitor of apoptosis (XIAP; encoded by BIRC4) is mutated in XLP2. XLP1 is a disease with multiple and variable clinical consequences, including fatal hemophagocytic lymphohistiocytosis (HLH) triggered predominantly by Epstein-Barr virus, lymphomas, antibody deficiency, and rarer consequences of immune dysregulation. To date, XLP2 has been found to cause HLH with and without exposure to Epstein-Barr virus, and HLH is commonly recurrent in these patients. For both forms of XLP, the only curative therapy at present is allogeneic hematopoietic cell transplantation. Beyond their common X-linked locus and their requirement for normal immune responses to certain viral infections, SAP and XIAP demonstrate no obvious structural or functional similarity, are not coordinately regulated with respect to their expression, and do not appear to directly interact. In this review, we describe the genetic, clinical, and immunopathologic features of these 2 disorders and discuss current diagnostic and therapeutic strategies.


2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Kabir Abdullahi ◽  
Yahaya Mohammed ◽  
Saddiku A. Sahabi ◽  
Mahmood M. Dalhat

Introduction: There have been numerous reported opportunistic infections among HIV/AIDS patients. However, coexistence of Kaposi sarcoma and Molluscum contagiosum on the same site is a rare finding.Case presentation: A 37-year-old man poorly adherent to antiretroviral therapy presented with Molluscum contagiosum and Kaposi sarcoma occurring simultaneously on numerous skin lesions around mid-2017 at Usmanu Danfodiyo University Teaching Hospital, Sokoto State, Nigeria.Management and outcome: The patient was counselled and re-initiated on a second-line highly active antiretroviral therapy regimen. The patient’s lesions resolved three months later.Discussion: The case is presented to improve the index of suspicion among clinicians and pathologists on such rare occurrences.


AIDS ◽  
2002 ◽  
Vol 16 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Elisabetta Righetti ◽  
Gianna Ballon ◽  
Lucia Ometto ◽  
Anna Maria Cattelan ◽  
Chiara Menin ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Bibianna Purgina ◽  
Uma N. M. Rao ◽  
Markku Miettinen ◽  
Liron Pantanowitz

The number of reported cases of smooth muscle tumor (SMT) arising in patients with AIDS has been increasing since the mid-1990s. The aim of this study is to characterize the epidemiology, clinical manifestations, pathologic features, prognosis and, management of Epstein-Barr virus-related SMT (EBV-SMT) in patients with AIDS. An English language literature search identified 53 articles including 64 reported cases of EBV-SMT. The majority of these reports involved patients who were young, severely immunosuppressed, and had multifocal tumors. The central nervous system was the most common site to be involved. Histologically, tumors had smooth muscle features and were immunoreactive for muscle markers and all but two tumors demonstrated the presence of EBV by either immunohistochemistry, in situ hybridization, and/or PCR. While mitoses and/or necrosis were used to separate leiomyoma from leiomyosarcoma, these features did not correlate with clinical outcome. Treatment included primarily resection, and less often radiotherapy, chemotherapy and highly active antiretroviral therapy (HAART). Overall, EBV-SMTs appear to have variable aggressiveness and clinical outcome and may exhibit a more favorable prognosis compared to conventional leiomyosarcoma. Tumor-related death from EBV-SMT occurred in only 4 of 51 patients.


2020 ◽  
Vol 35 (2) ◽  
pp. 336-345 ◽  
Author(s):  
Dominique Bertrand ◽  
Nathalie Chavarot ◽  
Philippe Gatault ◽  
Cyril Garrouste ◽  
Nicolas Bouvier ◽  
...  

Abstract Background Belatacept (bela) rescue therapy seems to be a valuable option for calcineurin inhibitor chronic toxicity in kidney transplantation. Nevertheless, the risk of infection associated with bela is not well reported. Methods We report the rate of opportunistic infections (OPI) after a switch to bela in a multicentric cohort of 280 kidney transplant patients. Results Forty-two OPI occurred in 34 patients (12.1%), on average 10.8 ± 11.3 months after the switch. With a cumulative exposure of 5128 months of bela treatment, we found an incidence of 0.008 OPI/month of exposure, and 9.8 OPI/100 person-years. The most common OPI was cytomegalovirus (CMV) disease in 18/42 OPI (42.9%) and pneumocystis pneumonia in 12/42 OPI (28.6%). Two patients presented a progressive multifocal leucoencephalopathy and two patients developed a cerebral Epstein–Barr virus-induced post-transplant lymphoproliferative disease. OPI led to death in 9/34 patients (26.5%) and graft failure in 4/34 patients (11.8%). In multivariate analysis, estimated glomerular filtration rate <25/mL/min/1.73 m2 on the day of the switch and the use of immunosuppressive agents before transplantation were associated with the occurrence of OPI. We found a higher rate of infection-related hospitalization (24.1 versus 12.3/100 person-years, P = 0.0007) and also a higher rate of OPI (13.2 versus 6.7/100 person-years, P = 0.005) in the early conversion group (within 6 months). Conclusions The risk of OPI is significant post-conversion to bela and may require additional monitoring and prophylactic therapy, particularly regarding pneumocystis pneumonia and CMV disease. These data need to be confirmed in a larger case–control study.


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