Satoh-Kamachi A, Munakata M, Kusaka Y, Amishima M, Furuya K, Takahashi T, Kawakami Y
First Department of Medicine, School of Medicine, Hokkaido University, Sapporo, Japan.
Am J Ind Med. 1998 Apr;33(4):379-83. doi: 10.1002/(sici)1097-0274(199804)33:4<379::aid-ajim8>3.0.co;2-p.
A 23-year-old man who worked at a hard metal factory from 1988 had developed bronchial asthma in 1990. He was diagnosed as having bronchial asthma by inhalation challenge with cobalt. He never developed a severe attack after that by avoiding inhalation of cobalt. In 1993, he developed iridocyclitis, and his chest radiograph showed bilateral hilar lymph node swelling. He was diagnosed as having sarcoidosis with pathological certainty and an increased serum angiotensin-converting enzyme (ACE) level. On second admission, an inhalational challenge with cobalt resulted in no significant decrease of FEV1. Cobalt is well known to cause occupational asthma and other interstitial lung diseases. Although we could not get clear evidence suggesting an association between the sarcoidosis and his history of cobalt exposure, there is a possibility that changes in the immune reaction to cobalt might explain the improvement of asthma followed by sarcoidosis in this case.
一名23岁男性,自1988年起在一家硬质合金工厂工作,1990年患上支气管哮喘。通过钴吸入激发试验,他被诊断为支气管哮喘。此后,通过避免吸入钴,他从未发生过严重发作。1993年,他患上了虹膜睫状体炎,胸部X线片显示双侧肺门淋巴结肿大。他被确诊为结节病,病理诊断明确,血清血管紧张素转换酶(ACE)水平升高。再次入院时,钴吸入激发试验未导致第一秒用力呼气容积(FEV1)显著下降。众所周知,钴可导致职业性哮喘和其他间质性肺病。尽管我们未能获得明确证据表明结节病与他的钴接触史之间存在关联,但在这种情况下,对钴免疫反应的变化可能解释了哮喘改善后继而出现结节病的原因。