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.