Guillon and colleagues [1] evaluated the mechanism of hypersensitivity pneumonitis after exposure and re-exposure to minocycline in a patient with chronic lung disease. We saw a similar phenomenon in 1986 in a 17-year-old woman without chronic lung disease. She experienced progressively severe pulmonary and extrapulmonary reactions to exposure and inadvertent re-exposures to minocycline.

The patient had taken minocycline, 100 mg/d, for 18 months to control acne vulgaris. In childhood, she had been treated for myasthenia gravis, and the disease had been in remission for 5 years. A nonproductive cough began 4 weeks before evaluation, and a sore throat accompanied by fever began 1 week before the patient's visit. Exertional dyspnea, aching limbs, and intensified cough developed. Findings included nonexudative pharyngitis, a tender forearm and wrist with no signs of synovitis, physical findings of lung consolidation bilaterally, and radiologic evidence of patchy infiltrate with volume loss in the lower lobes and of small pleural effusions. The symptoms cleared, and a clinical lung examination was normal after a 2-week course of erythromycin, during which she took no minocycline.

The illness "relapsed" three times until the relation to minocycline became evident. On each occasion, challenge with a single 100-mg dose of minocycline was followed within 1 to 2 hours by shaking chills, a temperature of up to 40 °C, and, at the final occurrence, hypotension. All symptoms cleared during abstinence from minocycline. The total and differential leukocyte counts remained normal. The alanine aminotransferase level was elevated during relapses, with a maximum of 396 U/L (normal, 0 to 38 U/L). The highest observed -glutamyltransferase level was 71 U/L (normal, 0 to 36 U/L). Cryoglobulin, anti-DNA, anti-SCL70 antibodies, antibodies to extractable nuclear antigens, and rheumatoid factor were absent or normal. The antinuclear antibody titer was 1:640 with a nucleolar fluorescence pattern.

In this case, hypersensitivity developed only after prolonged exposure to minocycline, possibly triggered by a respiratory infection, and was specific to minocycline, not to tetracycline. Liver toxicity was apparent. Except for the absence of eosinophilia, this case is similar to three cases reported in the literature [2, 3]. Previous autoimmune disease suggests that this patient may have been predisposed to this reaction.