Pneumocystis carinii pneumonia following a second infusion of infliximab

Tai, Toshihiro

doi:10.1093/rheumatology/41.8.951

Cited by 108 publications

(41 citation statements)

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“…While most of the concepts about the importance of TNF-␣ in antifungal host defense in humans have been extrapolated from animal models of fungal infection, the increasing use of the anti-TNF-␣ MAb infliximab has confirmed the critical role of this inflammatory mediator in antifungal host defense. There are numerous reports of both reactivation and primary fungal infections in rheumatoid arthritis patients being treated with anti-TNF-␣ therapy, including infections due to Histoplasma, Aspergillus, Pneumocystis, and Cryptococcus (24,43,46,49,51). Thus, even though TNF-␣ is a mediator of inflammatory diseases, it is also a critical mediator of protective immunity against fungal infections.…”

Section: Discussionmentioning

confidence: 99%

“…However, an increasingly frequently reported side effect of immunotherapy with a monoclonal antibody (MAb) against tumor necrosis factor alpha (TNF-␣) for rheumatoid arthritis is the subsequent development of fungal infections in these patients (24,43,46,49,51). In animal models, TNF-␣ is required to clear infections by Histoplasma, Blastomyces, Candida, Pneumocystis, Aspergillus, Paracoccidioides, and Cryptococcus species (2,5,6,9,15,19,23,28,29,42).…”

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confidence: 99%

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Transient Neutralization of Tumor Necrosis Factor Alpha Can Produce a Chronic Fungal Infection in an Immunocompetent Host: Potential Role of Immature Dendritic Cells

et al. 2005

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Transient Neutralization of Tumor Necrosis Factor Alpha Can Produce a Chronic Fungal Infection in an Immunocompetent Host: Potential Role of Immature Dendritic Cells

et al. 2005

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“…More recently, PCP has increasingly been reported in immunocompromised patients with connective tissue diseases, patients with malignancies, or in patients after organ transplantation (11,12). The postmarketing surveillance data in Japan and some anecdotal reports of PCP in patients receiving infliximab (13)(14)(15)(16) suggest that patients receiving infliximab comprise a novel high-risk group for development of PCP. A thorough knowledge of the clinical and laboratory characteristics of PCP in patients treated with infliximab is indispensable for prophylaxis, early diagnosis, and proper treatment of this infectious disease.…”

Section: Introductionmentioning

confidence: 99%

Pneumocystis jiroveci pneumonia in patients with rheumatoid arthritis treated with infliximab: A retrospective review and case–control study of 21 patients

Komano¹,

Harigai²,

Koike³

et al. 2009

Arthritis & Rheumatism

148

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Objective. To establish proper management of Pneumocystis jiroveci pneumonia (PCP) in rheumatoid arthritis (RA) patients treated with infliximab. PCP has been observed in 0.4% of patients with RA treated with infliximab in Japan. Methods. Data from patients with RA (n ‫؍‬ 21) who were diagnosed with PCP during infliximab treatment and from 102 patients with RA who did not develop PCP during infliximab therapy were collected from 14 rheumatology referral centers in Japan. A retrospective review of these patients and a case-control study to compare patients with and without PCP were performed. Results. The median length of time from the first infliximab infusion to the development of PCP was 8.5 weeks. At the onset of PCP, the median dosages of prednisolone and methotrexate were 7.5 mg/day and 8 mg/week, respectively. Pneumocystis jiroveci was microscopically identified in only 2 patients, although the polymerase chain reaction test for the organism was positive in 20 patients. The patients with PCP had significantly lower serum albumin levels (P < 0.001) and lower serum IgG levels (P < 0.001) than the patients without PCP. Computed tomography of the chest in all patients with PCP revealed ground-glass opacity either with sharp demarcation by interlobular septa or without interlobular septal boundaries. Sixteen of the 21 patients with PCP developed acute respiratory failure, but all survived. Conclusion. PCP is a serious complication that may occur early in the course of infliximab therapy in patients with RA. For the proper clinical management of this infectious disease, physicians need to be aware of the possibility of PCP developing during infliximab therapy.

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“…In many instances, however, these treatments have been associated with side effects such as impaired host defenses against bacterial and fungal infections [19][20][21][22], autoimmune exacerbations leading to lupus [23] and demyelinating syndromes [24,25], worsening of congestive heart failure [26] and increased occurrence of lymphomas [27][28][29]. Notably, anti-TNF treatments in clinical trials for MS had to be discontinued due to immune exacerbations and worsened disease outcomes [30].…”

Section: Introductionmentioning

confidence: 99%

Transmembrane TNF protects mutant mice against intracellular bacterial infections, chronic inflammation and autoimmunity

et al. 2006

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Using targeted mutagenesis in mice, we have blocked shedding of endogenous murine TNF by deleting its cleavage site. Mutant mice produce physiologically regulated levels of transmembrane TNF (tmTNF), which suffice to support thymocyte proliferation but cannot substitute for the hepatotoxic activities of wild-type TNF following LPS/Dgalactosamine challenge in vivo and are not sufficient to support secondary lymphoid organ structure and function. Notably, however, tmTNF is capable of exerting antiListerial host defenses while remaining inadequate to mediate arthritogenic functions, as tested in the tristetraprolin-deficient model of TNF-dependent arthritis. Most interestingly, in the EAE model of autoimmune demyelination, tmTNF suppresses disease onset and progression and retains the autoimmune suppressive properties of wild-type TNF. Together, these results indicate that tmTNF preserves a subset of the beneficial activities of TNF while lacking detrimental effects. These data support the hypothesis that selective targeting of soluble TNF may offer several advantages over complete blockade of TNF in the treatment of chronic inflammation and autoimmunity.Supporting information for this article is available at: http://www.wiley-vch.de/contents/jc_2040/2006/35921_s.pdf IntroductionOriginally identified as an endotoxin-induced serum factor that causes necrosis of tumors [1] and/or cachexia [2], TNF is currently known to mediate a wide array of biological activities [3, 4]. TNF is produced in response to bacterial toxins, inflammatory products and other stimuli mainly by cells of the myeloid lineage, with additional producers including B and T lymphocytes, NK cells, microglia, astrocytes and adipocytes [3]. TNF is bioactive both as a transmembrane protein and as a homotrimeric secreted molecule [5] and mediates its effects through two distinct TNF receptors, p55TNFR (TNFRI) and p75TNFR (TNFRII) [6]. Transmembrane TNF (tmTNF) appears superior to soluble TNF in activating the p75TNFR, while at physiological concentrations soluble TNF primarily activates the p55TNFR [7]. The two types of TNF receptors share structural homology in the extracellular TNF-binding domains, but they induce separate cytoplasmic signaling pathways following receptor-ligand interaction [8]. Apoptosis and activation of NF-jB are initiated by p55TNFR, whereas p75TNFR appears to play a direct role in only a limited number of TNF responses [6,9]. Several functionally diverse proteins, such as growth factors and cytokines and including TNF, are initially synthesized as biologically active membrane-anchored molecules that are subsequently released from the cell by proteolysis [10]. Thus, surface localization may serve to restrict activity to specific microenvironments, whereas release may lead to distal effects. TNF is synthesized as a 26 kDa type II transmembrane molecule, which can be processed by a TNF-alpha converting enzyme (TACE or ADAM17), to generate secreted 17 kDa monomers that form biologically active homotrimers [11,12]. Indications for a r...

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Pneumocystis carinii pneumonia following a second infusion of infliximab

Cited by 108 publications

References 2 publications

Transient Neutralization of Tumor Necrosis Factor Alpha Can Produce a Chronic Fungal Infection in an Immunocompetent Host: Potential Role of Immature Dendritic Cells

Transient Neutralization of Tumor Necrosis Factor Alpha Can Produce a Chronic Fungal Infection in an Immunocompetent Host: Potential Role of Immature Dendritic Cells

Pneumocystis jiroveci pneumonia in patients with rheumatoid arthritis treated with infliximab: A retrospective review and case–control study of 21 patients

Transmembrane TNF protects mutant mice against intracellular bacterial infections, chronic inflammation and autoimmunity

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