Rheumatology 2002; 41: 231
© 2002 British Society for Rheumatology
Letters to the Editor |
Miliary tuberculosis after biological therapy for rheumatoid arthritis
Clinical Immunology and Rheumatology Unit, Department of Internal Medicine, San Raffaele University Hospital, Via Olgettina 60, 20132 Milano, Italy
SIR, Inhibition of tumour necrosis factor 
(TNF-) in rheumatoid arthritis (RA) patients has yielded benefits with few side-effects [1–2]. In particular, although TNF- is well known to play a crucial and possibly non-redundant role in the response to mycobacteria [3], severe infectious complications after its blockade are seldom important and no opportunistic infections have so far been described. This may be due to the exclusion of patients with known infections, whether chronic, recurrent or active [4]. We report a case of military tuberculosis after treatment with infliximab in a patient with a family and personal history negative for tuberculosis. The patient, a 63-yr-old woman, had had RA and Sjögren's syndrome for 10 yr. A thoracic radiograph taken before the initiation of the therapy showed normal findings. She was treated initially by intravenous infusion of 3 mg/kg of infliximab and again 2 and 6 weeks later, in association with methotrexate (7.5 mg per week) and prednisone (7.5 mg per day). Two weeks after the last administration of infliximab she developed intermittent fever (maximum 39.2°C) and entered another hospital, where therapy was discontinued. Blood and bronchoalveolar lavage cultures and microbiological investigations, including bacterioscopic assessment of aerobic and anaerobic bacteria, fungi and mycobacteria, were negative. Thoracic radiography, ultrasonographic examination of the abdomen, pelvis and heart, computed tomography (CT) of the chest and abdomen and scintigraphy with radiolabelled leucocytes were negative. Bronchoalveolar lavage samples were cultured for mycobacteria. The fever was interpreted as being due to a flare of RA and the patient was treated with methylprednisolone, tapered to a maintenance dose of 24 mg per day. Six weeks later, bronchoalveolar lavage cultures were positive for Mycobacterium tuberculosis. The patient entered our infectious disease clinic, where a CT scan revealed multiple nodular lesions in the lungs, liver and spleen; miliary tuberculosis was diagnosed. Treatment with ethambutol, isoniazid, pyrazinamide and rifampicin only partially succeeded and the RA worsened. In conclusion, the risk of infections during biological therapy and, in particular, of atypical presentation of tuberculosis in patients without any previous known contact with M. tuberculosis, should not be underestimated.
Notes
Correspondence to: P. R. Querini, San Raffaele Scientific Institute, DIBIT 3A1, Via Olgettina 58, 20132 Milano, Italy. 
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