Jean-Marcel Guillon, MD; Pascal Joly, MD; Brigitte Autran, MD, PhD; Michel Denis, MD; Georges Akoun, MD; Patrice Debré, MD, PhD; Charles Mayaud, MD
Guillon J, Joly P, Autran B, Denis M, Akoun G, Debré P, et al. Minocycline-induced Cell-mediated Hypersensitivity Pneumonitis. Ann Intern Med. 1992;117:476-481. doi: 10.7326/0003-4819-117-6-476
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Published: Ann Intern Med. 1992;117(6):476-481.
▪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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Interstitial Lung Disease, Pulmonary/Critical Care.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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