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Minocycline-induced Cell-mediated Hypersensitivity Pneumonitis

Jean-Marcel Guillon, MD; Pascal Joly, MD; Brigitte Autran, MD, PhD; Michel Denis, MD; Georges Akoun, MD; Patrice Debré, MD, PhD; and Charles Mayaud, MD
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Requests for Reprints: Jean-Marcel Guillon, MD, service de Pneumologie, hôpital Tenon, 4, rue de la Chine, 75020, Paris, France.

Current Author Addresses: Drs. Guillon, Denis, Akoun, and Mayard: service de Pneumologie, hôpital Tenon, 4, rue de la Chine, 75020, Paris, France.

Dr. Joly: Service de Dermatologie, Hôpital Charles Nicolle, 1, rue de Germont, 76031, Rouen, France.

Drs. Autran and Debré: Laboratoire d'Immunologie cellulaire, Hôpital Pitié-salpêtrière, 81, Boulevard de l'hôpital, 75013, Paris, France.

Ann Intern Med. 1992;117(6):476-481. doi:10.7326/0003-4819-117-6-476
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Objective: To identify the cause of a hypersensitivity pneumonitis and to determine its pathogenesis.

Design: Case study.

Setting: Intensive care unit of a referral hospital.

Patient: A 51-year-old man with chronic bronchitis who developed a hypersensitivity pneumonitis within 1 month after exposure to minocycline, amoxicillin, and erythromycin.

Intervention: Sequential bronchoalveolar lavages after reexposure to minocycline and amoxicillin.

Measurements: Immunologic analysis of the phenotype and function of alveolar lymphocytes.

Results: Reexposure to minocycline but not to amoxicillin was followed by an interstitial pneumonitis. Sequential bronchoalveolar lavages showed a transient rise of eosinophils and neutrophils and a persistent alveolar lymphocytosis. Alveolar lymphocytes consisted predominantly of CD8+ but also CD4+ cells. Two C08+ lymphocyte subsets were identified: CD8+ D44+ cytotoxic T cells that increased rapidly after the drug was resumed and CD8+ CD57+ suppressor T cells that predominated 11 days after the drug's withdrawal. In-vitro assays showed the presence of a lymphocyte-mediated specific cytotoxicity against minocycline-bearing alveolar macrophages.

Conclusion: These results support the hypothesis of a central role of T lymphocytes in the pathogenesis of drug-related hypersensitivity pneumonitis.





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