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[A case of isoniazid (INH)-induced pneumonitis]
1Department of Pulmonary Medicine, Jichi Medical School, Tochigi, Japan.
Insights
Tuberculosis patients can develop drug-induced pneumonitis from isoniazid (INH). This rare condition requires prompt diagnosis and treatment with corticosteroids and alternative anti-TB drugs.
Area of Science:
- Pulmonology
- Infectious Diseases
- Pharmacology
Background:
- Pulmonary tuberculosis (TB) diagnosis and standard treatment regimens.
- Initial presentation of a solitary lung nodule with cavitation.
Observation:
- A 58-year-old male developed acute respiratory distress, fever, and widespread infiltrates after 16 days of anti-TB treatment.
- Diagnostic workup revealed bilateral pleural effusions and interstitial changes on biopsy.
- Drug-induced lymphocyte stimulation test was positive exclusively for isoniazid (INH).
Findings:
- The patient was diagnosed with isoniazid-induced pneumonitis, a rare adverse drug reaction.
- Corticosteroid therapy led to rapid clinical and radiological improvement.
- Successful completion of TB treatment with an alternative regimen (streptomycin, ethambutol, rifampicin).
Implications:
- Highlights the importance of considering drug-induced pneumonitis in TB patients presenting with new respiratory symptoms.
- Emphasizes the utility of drug lymphocyte stimulation testing for diagnosing hypersensitivity reactions.
- Suggests a potential therapeutic strategy involving corticosteroids and alternative anti-TB agents for INH-induced pneumonitis.
Abstract:
A 58-year-old man was referred for the evaluation of a lung nodule on chest X-ray. On admission, chest X-ray showed a solitary nodule with cavitation in the left lung field. Histological examination revealed epithelioid cell granulomas and the diagnosis of pulmonary tuberculosis was made. He was treated with INH, ethambutol (EB), and rifampicin (RFP). On the 16th day of treatment, he developed dry cough and high fever. On the 20th day, dyspnea developed and PaO2 was decreased to 38.2 Torr. Chest X-ray showed new widespread infiltrates in both lung fields and bilateral pleural effusions. The size of the cavitary lesion was decreased. Transbronchial biopsy specimen showed slight interstitial thickening, lymphocyte infiltration, and multiple granulomas. Drug lymphocyte stimulation test was positive only with INH (230%). INH-induced pneumonitis was highly suspected. All drugs was discontinued and hydrocortisone 2400 mg daily was started. He soon became afebrile, and dyspnea and dry cough resolved. Chest X-ray film showed resolution of infiltrative shadows. He was subsequently successfully treated with streptomycin, EB, and RFP without any adverse effects. To our knowledge, this is the sixth reported case of INH-induced pneumonitis.