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Original Research: Chest Infections |

Pneumocystis Pneumonia in Patients Treated With RituximabPneumocystis Following Rituximab Treatment

Isabel Martin-Garrido, MD; Eva M. Carmona, MD, PhD; Ulrich Specks, MD; Andrew H. Limper, MD, FCCP
Author and Funding Information

From the Division of Pulmonary and Critical Care Medicine (Drs Martin-Garrido, Carmona, Specks, and Limper), Mayo Clinic College of Medicine, Rochester, MN; and Servicio de Medicina Interna (Dr Martin-Garrido), Hospital Universitario Virgen del Rocío, Seville, Spain.

Correspondence to: Andrew H. Limper, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, 8-24 Stabile Bldg, 200 First St, Rochester, MN 55905; e-mail: limper.andrew@mayo.edu


Funding/Support: These studies were funded in part by the National Institutes of Health [R01 HL62150] to Dr Limper.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;144(1):258-265. doi:10.1378/chest.12-0477
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Background:  Pneumocystis pneumonia (PcP) is an opportunistic fungal infection. Although T-cell immunity is classically related to Pneumocystis defense, recent data support roles for B lymphocytes in the development of PcP in animals, and we have observed several cases of PcP in patients receiving rituximab. These observations prompted a systematic review of our experience to define the spectrum of clinical presentations in which PcP has occurred in the setting of rituximab therapy.

Methods:  Using a computer-based search, we reviewed the records of patients who received rituximab and developed PcP at Mayo Clinic Rochester over the years 1998 to 2011 to establish the underlying conditions, clinical course, possible risk factors, and potential association between this drug and the development of PcP.

Results:  Over this period, 30 patients developed PcP during treatment with rituximab. The underlying diseases included hematologic malignancies in 90% of cases. Glucocorticoids were used in 73% of these patients, under different chemotherapeutic regimens. Three patients (10%) developed PcP in the setting of rituximab without concomitant chemotherapy or significant glucocorticoid exposure. Of these 30 patients, 88% developed acute hypoxemic respiratory failure and 53% required ICU admission. The clinical course was fatal in 30%.

Conclusion:  PcP can occur in association with rituximab, with the majority of cases having also received cytotoxic chemotherapy or significant doses of glucocorticoids. The clinical course of cases of PcP in patients treated with rituximab can be quite fulminant, with significant mortality. Primary prophylaxis should be considered in patients at risk, and secondary prophylaxis provided unless immune reconstitution is well assured.

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