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Dr. Villeneuve, et al reply To the Editor: We thank Dr. Roos and colleagues for their comments about our case report of infliximab-induced pneumonitis1. As they mentioned, there are indeed some differences regarding our case and the ones they have reported, but this may highlight the different types of interstitial lung disease (ILD) that can be associated with infliximab therapy. Ostor, et al2 have reported 5 cases of infliximab-induced ILD, 4 of them with usual interstitial pneumonia (UIP) confirmed by pathology or high resolution chest tomography. We agree that, unlike those patients, our patient did not develop an accelerated form of UIP. As they have highlighted, our patient had no history of lung disease and no increased number of mast cells on bronchoalveolar lavage (BAL) that could be suggestive of UIP. But those findings are also true for the 6 other cases that have been reported, where infliximab seemed to have precipitated MTX-induced pneumonitis3,4. Indeed, the lymphocytosis found on the BAL and the reversal of symptoms with corticosteroid treatment and the withdrawal of infliximab are more suggestive of a drug-induced acute interstitial pneumonitis than a UIP. Those different presentations could be because infliximab may induce an accelerated form of UIP with poor prognosis in RA patients with preexisting ILD, or induce a more reversible form of drug-induced pneumonitis or of bronchiolitis obliterans organizing pneumonia (BOOP), similar to the fifth case reported by Roos, et al. Our case also differs in that aspergillus was isolated on the BAL. But as we stated, after discussion with the microbiologist and the pulmonologist, it was considered to be a colonizing organism because it was found in only half the samples and the aspergillus antigen detection assay was negative. In fact, the patient did not improve with caspofungin therapy and only started to improve when he was treated with high-dose corticosteroids. Itraconazole was administered as a prophylaxis with the goal of preventing aspergillus reactivation while the patient was immunosuppressed with the high-dose corticosteroids. With the growing number of infliximab-induced ILD, we are able to better appreciate this rare but severe complication of TNF-a antagonist therapy. Infliximab seems to be able to induce different types of ILD ranging from BOOP to an accelerated form of UIP. Patients with preexisting lung disease seem to have a much worse prognosis and they should be informed about the risk of ILD before they receive infliximab therapy. This could also be true for other anti-TNF-a agents, but there is insufficient evidence for this at the moment. EDITH VILLENEUVE, MD; ANNE ST-PIERRE, MD; BOULOS HARAOUI, MD, Department of Rheumatology, Centre Hospitalier de l'Université de Montréal, Montreal, Quebec, Canada. Address reprint requests to Dr. E. Villeneuve, CHUM, Department of Rheumatology, Pavillon Mailloux, 4th floor, 1560 Sherbrooke est, Montreal, QC H2L 4M1. E-mail: villeed@hotmail.com 2. Ostor AJK, Chilvers ER, Somerville MF, et al. Pulmonary complications of infliximab therapy in patients with rheumatoid arthritis. J Rheumatol 2006;33:622-8. 3. Kramer N, Chuzhin Y, Kaufman L, Ritter J, Rosenstein ED. Methotrexate pneumonitis after initiation of infliximab therapy for rheumatoid arthritis. Arthritis Rheum 2002;47:670-1. 4. Courtney PA, Alderdice J, Whitehead EM. Comment on methotrexate pneumonitis after initiation of infliximab therapy for rheumatoid arthritis [letter]. Arthritis Rheum 2003;49:617; author reply 617-8. |