# Moxifloxacin-Induced Peripheral Neuropathy: A Rare Side Effect of Fluoroquinolone Therapy in Tuberculosis Management

## TL;DR

A 60-year-old man developed peripheral neuropathy after four months of moxifloxacin treatment for tuberculosis, highlighting a rare but important side effect.

## Contribution

This case report identifies a delayed, cumulative neurotoxic effect of moxifloxacin not previously emphasized in clinical guidelines.

## Key findings

- Peripheral neuropathy occurred after 17 weeks of moxifloxacin therapy in a TB patient.
- Symptoms improved after discontinuing moxifloxacin and pyridoxine supplementation.
- The case suggests a need for routine neurological monitoring during long-term moxifloxacin treatment.

## Abstract

Moxifloxacin (MXF) is a cornerstone of the newly recommended four-month 2HPMZ/2HPM regimen for drug-susceptible pulmonary tuberculosis (TB). However, potential side effects such as cumulative neurotoxicity remain poorly characterized in clinical practice. Here, we report a rare case of peripheral neuropathy (PN) occurring after 17 weeks (four months) of MXF treatment in a 60-year-old Vietnamese man treated for drug-sensitive pulmonary TB. Following early isoniazid-induced hepatotoxicity, the patient's regimen was modified to include MXF 400 mg daily, notably without other neurotoxic agents such as linezolid or ethambutol. After 17 weeks of MXF therapy, the patient developed symmetrical stocking-glove PN. Extensive workup, including hemoglobin A1c and folate levels, ruled out common metabolic and nutritional etiologies. Cessation of MXF and pyridoxine supplementation led to gradual symptom improvement with full resolution after four months. While FDA warnings emphasize the often-rapid onset of fluoroquinolone-associated nerve damage within days of initiation, this case illustrates a delayed, cumulative toxicity profile that aligns with recent epidemiological evidence. As global TB guidelines shift toward four-month MXF regimens, this report highlights a critical safety consideration for clinicians and the importance of routine neurological screening throughout the entire treatment course to detect early signs of toxicity and prevent the development of potentially permanent PN.