Fatal Late-Onset Pneumocystis Pneumonia After Rituximab: Administration for Posttransplantation Recurrence of Focal Segmental Glomerulosclerosis—Case Report

Dęborska−Materkowska, Dominika; Kozińska-Przybył, Olga; Mikaszewska-Sokolewicz, Małgorzata; Durlik, M.

doi:10.1016/j.transproceed.2014.09.010

Cited by 14 publications

(11 citation statements)

References 31 publications

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“…Rituximab and alemtuzumab are reported to cause interstitial pneumonia development [32]. Prospectively, after rituximab treatment, neutropenia with pneumonia and other infectious complications may develop in up to 17% [33,34]. There are reports about development of male infertility due to either gonadal dysfunction or antisperm autoantibodies production [35].…”

Section: Rituximabmentioning

confidence: 99%

Plasmapheresis in Treatment of Myasthenia Gravis

Voinov¹

2019

Selected Topics in Myasthenia Gravis

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Treatment of myasthenia gravis is still a rather difficult task, since there is no single tactic to use different drugs (corticosteroids, rituximab, immunoglobulins), especially since it is associated with a number of side effects. They are not able to remove the accumulating autoantibodies and immune complexes, the large size of which does not allow them to be excreted by the kidneys as well. Special problems of treatment arise when myasthenic crises develop associated with respiratory failure requiring artificial lungs ventilation. Plasmapheresis can help to solve this for it is possible to remove antibodies and other pathological metabolites. In addition, regular plasmapheresis is able not only to prevent exacerbations but also to reduce doses of the maintenance therapy with less risk of their side effects, which is confirmed by our own experience.

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Section: Rituximabmentioning

confidence: 99%

Plasmapheresis in Treatment of Myasthenia Gravis

Voinov¹

2019

Selected Topics in Myasthenia Gravis

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“…1 In solid organ transplant (SOT) recipients, pneumocystis pneumonia (PJP) is associated with a significant morbidity and allograft loss. [5][6][7][8][9][10] SOT recipients appear to remain susceptible to develop PJP in case of exposure to P. jirovecii regardless of the interval since transplantation. 4 However, several studies reported clusters of patients with post-transplant PJP who received complete course of prophylaxis.…”

Section: Introductionmentioning

confidence: 99%

“…4 However, several studies reported clusters of patients with post-transplant PJP who received complete course of prophylaxis. [5][6][7][8][9][10] SOT recipients appear to remain susceptible to develop PJP in case of exposure to P. jirovecii regardless of the interval since transplantation. Post-transplant PJP is associated with allograft failure and death.…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus infection and graft rejection as risk factors for pneumocystis pneumonia in solid organ transplant recipients: A systematic review and meta‐analysis

Hosseini-Moghaddam

Krishnan

Guo

et al. 2018

Clinical Transplantation

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A growing number of publications have reported the outbreaks of post-transplant pneumocystis pneumonia (PJP). In most studies, the onset of PJP was beyond 6-12 months of prophylaxis. Cytomegalovirus (CMV) infection and allograft rejection have been repeatedly reported as probable risk factors for post-transplant PJP. In this systematic review and meta-analysis, we determined the pooled effect estimates of these 2 variables as risk factors. Data sources included PUBMED, MEDLINE-OVID, EMBASE-OVID, Cochrane Library, Networked Digital Library of Theses and Dissertations, World Health Organization, and Web of Science. We excluded publications related to hematopoietic stem cell transplantation (HSCT) or Human Immunodeficiency Virus (HIV) patients. Eventually, 15 studies remained for the final stage of screening. Cytomegalovirus infection (OR: 3.30, CI 95%: 2.07-5.26, I : 57%, P = 0.006) and allograft rejection (OR:2.36, CI95%: 1.54-3.62, I2: 45.5%, P = 0.05) significantly increased the risk of post-transplant PJP. Extended prophylaxis targeting recipients with allograft rejection or CMV infection may reduce the risk of PJP.

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“…There is no known ligand for CD20; however, it is believed to play a role in B-cell development and differentiation into plasma cells and in T-cell-independent antibody (Ab) responses (3). With the increased use of anti-CD20 as a treatment, there have been several recent reports of patients receiving anti-CD20 and subsequently developing infection with the opportunistic pathogen Pneumocystis jirovecii, which may develop into a fatal pneumonia even with antibiotic therapy (4). However, there is debate about the precise role of anti-CD20 in conferring risk, as many of these patients are also on concomitant immunosuppressive drugs, thus complicating any analyses of clinical studies (5)(6)(7).…”

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confidence: 99%

Anti-CD20 Antibody Therapy and Susceptibility to Pneumocystis Pneumonia

et al. 2015

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b Anti-CD20 antibody therapy has been a useful medication for managing non-Hodgkin's lymphoma as well as autoimmune diseases characterized by autoantibody generation. CD20 is expressed during most developmental stages of B lymphocytes; thus, CD20 depletion leads to B-lymphocyte deficiency. As the drug has become more widely used, there has been an increase in the number of case reports of patients developing Pneumocystis pneumonia. The role of anti-CD20 in Pneumocystis jirovecii infection is under debate due to the fact that most patients receiving it are on a regimen of multiple immunosuppressive medications. To address the specific role of CD20 depletion in host immunity against Pneumocystis, we examined a murine anti-CD20 depleting antibody. We demonstrated that anti-CD20 alone is permissive for Pneumocystis infection and that anti-CD20 impairs components of type II immunity, such as production of interleukin-4 (IL-4), IL-5, and IL-13 by whole-lung cells, in response to Pneumocystis murina. We also demonstrated that CD4 ؉ T cells from mice treated with anti-CD20 during Pneumocystis infection are incapable of mounting a protective immune response when transferred into Rag1 ؊/؊ mice. Thus, CD20 ؉ cells are critical for generating protective CD4؉ T-cell immune responses against this organism.

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Fatal Late-Onset Pneumocystis Pneumonia After Rituximab: Administration for Posttransplantation Recurrence of Focal Segmental Glomerulosclerosis—Case Report

Cited by 14 publications

References 31 publications

Plasmapheresis in Treatment of Myasthenia Gravis

Plasmapheresis in Treatment of Myasthenia Gravis

Cytomegalovirus infection and graft rejection as risk factors for pneumocystis pneumonia in solid organ transplant recipients: A systematic review and meta‐analysis

Anti-CD20 Antibody Therapy and Susceptibility to Pneumocystis Pneumonia

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