Amikacin/cefoxitin/cotrimoxazoleNeutropenia, renal injury and peripheral neuropathy: case report A 36-year-old man developed neutropenia during treatment with cefoxitin, renal injury during treatment with amikacin, cefoxitin and cotrimoxazole, and peripheral neuropathy during treatment cotrimoxazole and cefoxitin for Mycobacterium abscessus infection [routes and dosages not stated; durations of treatment to reactions onsets not stated; not all outcomes stated].The man was hospitalised with fever, pleuritic pain, dyspnoea, productive cough, and 15kg weight loss in April 2014. He had a medical history of pulmonary tuberculosis and pulmonary aspergilloma that required superior lobectomy. His initial examination showed tachycardia, fever and cutaneous fistulas along with mucopurulent discharge at the lobectomy incision site. Subsequent CT scan showed nodules in the right inferior, atelectasis and cylindrical bronchiectasis. Thereafter, he was diagnosed with Mycobacterium abscessus (M. abscessus) on hospitalisation day 14. Therefore, empirical treatment with imipenem, amikacin, moxifloxacin and azithromycin was initiated. On day 28, treatment was adjusted to amikacin, cefoxitin, clarithromycin, and cotrimoxazole [trimethoprim-sulfamethoxazole]. Subsequently, fistula discharge decreased; but, his right pleuritic pain, fever and mild dyspnoea had still persisted. On hospitalisation day 34, he underwent pneumonectomy and pathological investigation of the specimen confirmed the pulmonary M. abscessus. On hospitalisation day 70, he developed mild neutropenia. However, he was found clinically stable; hence, the antibacterial treatment was continued. He was discharged on hospitalisation day 82. Thereafter, his open thoracic window was surgically closed. Subsequently, an increase in the serum creatinine was noted, which was possibly due to renal injury related with amikacin. Thus, amikacin was discontinued, without rechallenge. After the discharge, he developed peripheral neuropathy along with a painful burning sensation in the limbs.The man was treated with pregabalin that resulted into resolution of the neuropathy. He received parenteral cefoxitin for 6 months as an outpatient treatment, and oral clarithromycin and cotrimoxazole were discontinued after 18 months of treatment. During follow-up visits, his serum creatinine remained stable at ≤120 µmol/L with estimated glomerular filtration rate of approximately 80 mL/minute per 1.73m2. At the latest follow-up visit, it was noted that he had resumed normal activity and investigation showed normalisation of inflammatory parameters and body weight of 70kg. It was considered that the neutropenia was secondary to cefoxitin use. His renal injury was due to amikacin, cefoxitin and competition of creatinine tubular secretion with cotrimoxazole. The causality score was 3 on the Naranjo scale, indicating possible relationship between renal injury and cotrimoxazole. The peripheral neuropathy was secondary to prolonged treatment with cotrimoxazole and cefoxitin. The causality score was 4...