Frontiers in pharmacology · 2026
Toxicity-guided dose modification for disseminated Nocardia farcinica brain abscess in a patient with pneumoconiosis: a brief research report.
СтатьяНазвание и аннотация: Перевод в очереди
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Liu Hui Juan, Wang Liang Fen, Li Xiao Yue, Li Ling
Аннотация
BACKGROUND: Optimal antimicrobial strategies for disseminated nocardiosis with central nervous system (CNS) involvement remain poorly defined, particularly regarding trimethoprim-sulfamethoxazole (TMP-SMX) dosing in immunocompromised patients with severe drug intolerance.
METHODS: This observational case study analyzed the clinical course and pharmacological management of a 55-year-old male gold miner with pneumoconiosis and chronic corticosteroid use who developed Nocardia farcinica brain abscess. Diagnosis was established via metagenomic next-generation sequencing (mNGS) and phenotypic culture. An individualized antimicrobial regimen was designed based on toxicity monitoring.
RESULTS: Diagnosis of N. farcinica was confirmed by mNGS within 48 h. The patient initially failed empirical meropenem but responded to combination therapy with imipenem, amikacin, and TMP-SMX. Due to grade III gastrointestinal toxicity (CTCAE v5.0), TMP-SMX was de-escalated from 15 mg·kg-1·d-1-11.25 mg·kg-1·d-1, with maintenance at 7.5 mg·kg-1·d-1. Clinical improvement was observed at Day 120, though durable cure remains unconfirmed.
CONCLUSION: In extreme circumstances of severe dose-limiting toxicity, temporary TMP-SMX dose reduction with intensive monitoring may be feasible as a bridge to complete guideline-concordant therapy, though this approach falls below current recommendations and requires robust therapeutic drug monitoring. Species-directed antimicrobial selection and early molecular diagnosis facilitated initial clinical resolution in this high-risk immunocompromised host.
METHODS: This observational case study analyzed the clinical course and pharmacological management of a 55-year-old male gold miner with pneumoconiosis and chronic corticosteroid use who developed Nocardia farcinica brain abscess. Diagnosis was established via metagenomic next-generation sequencing (mNGS) and phenotypic culture. An individualized antimicrobial regimen was designed based on toxicity monitoring.
RESULTS: Diagnosis of N. farcinica was confirmed by mNGS within 48 h. The patient initially failed empirical meropenem but responded to combination therapy with imipenem, amikacin, and TMP-SMX. Due to grade III gastrointestinal toxicity (CTCAE v5.0), TMP-SMX was de-escalated from 15 mg·kg-1·d-1-11.25 mg·kg-1·d-1, with maintenance at 7.5 mg·kg-1·d-1. Clinical improvement was observed at Day 120, though durable cure remains unconfirmed.
CONCLUSION: In extreme circumstances of severe dose-limiting toxicity, temporary TMP-SMX dose reduction with intensive monitoring may be feasible as a bridge to complete guideline-concordant therapy, though this approach falls below current recommendations and requires robust therapeutic drug monitoring. Species-directed antimicrobial selection and early molecular diagnosis facilitated initial clinical resolution in this high-risk immunocompromised host.