TY - JOUR
T1 - Radiological features and therapeutic responses of pulmonary nontuberculous mycobacterial disease in rheumatoid arthritis patients receiving biological agents
T2 - A retrospective multicenter study in Japan
AU - Mori, Shunsuke
AU - Tokuda, Hitoshi
AU - Sakai, Fumikazu
AU - Johkoh, Takeshi
AU - Mimori, Akio
AU - Nishimoto, Norihiro
AU - Tasaka, Sadatomo
AU - Hatta, Kazuhiro
AU - Matsushima, Hidekazu
AU - Kaise, Shunji
AU - Kaneko, Atsushi
AU - Makino, Shigeki
AU - Minota, Seiji
AU - Yamada, Takashi
AU - Akagawa, Shinobu
AU - Kurashima, Atsuyuki
N1 - Funding Information:
Conflict of interest T. J. has received consultant fees and travel fees from Chugai Pharmaceutical Co., Ltd. N. N. has received consultant fees from Chugai Pharmaceutical Co., Ltd. and F. Hoffmann-La Roche, Ltd.; lecture fees from Chugai Pharmaceutical Co., Ltd.; and research grants from Chugai Pharmaceutical Co., Ltd., Bristol-Myers Squibb Japan, and Pfizer Japan, Inc. S. M. has received licensing fees and subsidies from Chugai Pharmaceutical Co. and subsidies from Mitsubishi-Tanabe Pharmaceutical Co.
PY - 2012/9
Y1 - 2012/9
N2 - Objective This study was performed to evaluate the radiological features of and therapeutic responses to pulmonary disease caused by nontuberculous mycobacteria (NTM) in the setting of biological therapy for rheumatoid arthritis (RA). Methods We conducted a retrospective chart review of 13 patients from multiple centers who had developed pulmonary NTM disease during biological therapy for RA, including infliximab, etanercept, adalimumab, and tocilizumab. Results Most cases were asymptomatic or resulted in only common-cold-like symptoms. Abnormalities in computed tomography (CT) imaging were protean and frequently overlapped. The most predominant pattern was nodular/ bronchiectatic disease (six cases), followed by alveolar infiltrate (three cases), cavitary disease (two cases), and pulmonary nodules (two cases). In most cases, pulmonary NTM disease had spread from a preexisting lesion; in particular, bronchial/bronchiolar abnormalities. In three cases, one or more nodular lesions with or without calcification were a focus of disease. Following the discontinuation of biological agents, most patients responded to anti-NTM therapy. Two patients showed no exacerbation in the absence of any anti-NTM therapy. In one patient, restarting tocilizumab therapy while continuing to receive adequate anti-NTM therapy produced a favorable outcome. In two other patients with a previous history of pulmonary NTM disease, introducing biological therapy led to recurrence, but anti-NTM therapy was effective in these patients. Conclusion CT abnormalities of pulmonary NTM disease in RA patients receiving biological therapy were variable, but were not unique to this clinical setting. NTM disease can spread from preexisting structural abnormalities, even if they are minute. Contrary to our expectations, the therapeutic outcomes of pulmonary NTM disease were favorable in these patients.
AB - Objective This study was performed to evaluate the radiological features of and therapeutic responses to pulmonary disease caused by nontuberculous mycobacteria (NTM) in the setting of biological therapy for rheumatoid arthritis (RA). Methods We conducted a retrospective chart review of 13 patients from multiple centers who had developed pulmonary NTM disease during biological therapy for RA, including infliximab, etanercept, adalimumab, and tocilizumab. Results Most cases were asymptomatic or resulted in only common-cold-like symptoms. Abnormalities in computed tomography (CT) imaging were protean and frequently overlapped. The most predominant pattern was nodular/ bronchiectatic disease (six cases), followed by alveolar infiltrate (three cases), cavitary disease (two cases), and pulmonary nodules (two cases). In most cases, pulmonary NTM disease had spread from a preexisting lesion; in particular, bronchial/bronchiolar abnormalities. In three cases, one or more nodular lesions with or without calcification were a focus of disease. Following the discontinuation of biological agents, most patients responded to anti-NTM therapy. Two patients showed no exacerbation in the absence of any anti-NTM therapy. In one patient, restarting tocilizumab therapy while continuing to receive adequate anti-NTM therapy produced a favorable outcome. In two other patients with a previous history of pulmonary NTM disease, introducing biological therapy led to recurrence, but anti-NTM therapy was effective in these patients. Conclusion CT abnormalities of pulmonary NTM disease in RA patients receiving biological therapy were variable, but were not unique to this clinical setting. NTM disease can spread from preexisting structural abnormalities, even if they are minute. Contrary to our expectations, the therapeutic outcomes of pulmonary NTM disease were favorable in these patients.
KW - Biological therapy
KW - Computed tomography
KW - Nontuberculous mycobacteria
KW - Pulmonary disease
KW - Rheumatoid arthritis
UR - http://www.scopus.com/inward/record.url?scp=84870355639&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84870355639&partnerID=8YFLogxK
U2 - 10.1007/s10165-011-0577-6
DO - 10.1007/s10165-011-0577-6
M3 - Article
C2 - 22207481
AN - SCOPUS:84870355639
SN - 1439-7595
VL - 22
SP - 727
EP - 737
JO - Modern rheumatology
JF - Modern rheumatology
IS - 5
ER -