Suzuki K, Tanaka H, Fujishima T, Teramoto S, Kaneko S, Saikai T, Suzuki A, Takahashi Y, Honma H, Sugaya F, Abe S
Third Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, 060-8543, Japan.
Nihon Kokyuki Gakkai Zasshi. 2001 Sep;39(9):699-704.
A 46-year-old woman had been treated with 1,600-2,000 micrograms/day of beclomethasone dipropionate (BDP) and oral theophylline on the basis of a diagnosis of bronchial asthma in 1993. Eosinophilic pneumonia was diagnosed in June 1999, and she was then treated with 40 mg/day of oral prednisolone (PSL), which was gradually tapered off, and then stopped in October 1999. She was referred to our hospital because acid-fast bacilli were found in the sputum on January 18, 2000. Her chest radiographs and CT scans showed partial atelectasis of the right upper lobe, and fiberoptic bronchoscopy revealed bronchial inflammatory changes and whitish mucosal nodular lesions in the walls of the lower trachea, the right main bronchus and the orifice of the right upper lobe bronchus. She was found to have endobronchial tuberculosis. Anti-tuberculosis treatment with isoniazid, rifampicin, streptomycin and pyrazinamide was started. Serum levels of interferon-gamma were markedly elevated on admission. Asthma symptoms improved for a period of one month after the beginning of anti-tuberculosis treatment, despite the termination of inhaled corticosteroid. However, as the tuberculosis improved, the frequency and severity of the asthma increased and so corticosteroid inhalation was started again. Four months after administration of the anti-tuberculosis drug, fiberoptic bronchoscopy revealed that the endobronchial lesions had improved without any stenosis or constrictive changes. It was speculated that high doses of inhaled corticosteroid may have the potential to cause endobronchial tuberculosis whilst, ironically, at the same time preventing bronchial stenosis by endobronchial tuberculosis. This is an interesting case in which the asthma symptoms first decreased during the acute phase of endobronchial tuberculosis and then increased again after the tuberculosis improved.
一名46岁女性于1993年被诊断为支气管哮喘，一直接受每日1600 - 2000微克丙酸倍氯米松（BDP）和口服茶碱治疗。1999年6月诊断为嗜酸性粒细胞性肺炎，随后接受每日40毫克口服泼尼松龙（PSL）治疗，剂量逐渐减少，于1999年10月停药。2000年1月18日因痰中发现抗酸杆菌而被转诊至我院。她的胸部X线片和CT扫描显示右上叶部分肺不张，纤维支气管镜检查发现气管下段、右主支气管及右上叶支气管开口处有支气管炎症改变及白色黏膜结节性病变。她被诊断为支气管内结核。开始使用异烟肼、利福平、链霉素和吡嗪酰胺进行抗结核治疗。入院时血清γ-干扰素水平显著升高。抗结核治疗开始后，尽管停用了吸入性糖皮质激素，但哮喘症状在一个月内有所改善。然而，随着结核病病情好转，哮喘的发作频率和严重程度增加，于是再次开始吸入糖皮质激素治疗。抗结核药物治疗四个月后，纤维支气管镜检查显示支气管内病变有所改善，无任何狭窄或缩窄性改变。据推测，高剂量吸入性糖皮质激素可能有导致支气管内结核的潜在风险，而具有讽刺意味的是，与此同时它又能预防支气管内结核引起的支气管狭窄。这是一个有趣的病例，哮喘症状在支气管内结核急性期首先减轻，然后在结核病病情好转后又再次加重。
