https://orcid.org/0000-0002-0585-1563
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Tina H Dao, Christopher D Jackson, When trimethoprim–sulfamethoxazole goes rogue, Postgraduate Medical Journal, Volume 101, Issue 1195, May 2025, Pages 487–488, https://doi.org/10.1093/postmj/qgae192
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Case description
A 27-year-old female patient with polycystic ovarian syndrome and obesity presented to the emergency department with headache and fever that started 1 day ago. She was recently treated for a urinary tract infection with trimethoprim-sulfamethoxazole (TMP-SMX). On physical exam, she was febrile at 102.9°F with respiratory rate 18 bpm, blood pressure 128/72 mm Hg, tachycardic 162 beats per minutes (bpm), and 100% oxygen saturation on room air. Laboratory test results were notable for white blood cell count of 3400 cells/μl, platelet count of 101,000 platelets/μL, and lactate 4.0 mmol/L. She received empiric antibiotics for suspected sepsis. She subsequently developed distributive shock requiring several vasopressors and was intubated for acute hypoxemic respiratory failure. She improved clinically and was discharged home after finishing the empiric antibiotic therapy. However, no underlying cause of sepsis was identified. Three years later, she presented to the same emergency department with altered mental status, headache, and fever within a few days after receiving TMP-SMX for cellulitis. Her symptoms during the second admission were less severe than those during her first one. Infection causes were deemed unlikely as resolution of sepsis did not correlate with the empiric antibiotic treatment. Pertinent antibody tests were negative, suggesting that autoimmune etiology was also unlikely (Table 1). Immunoglobulin work up was only notable for borderline decreased IgA (Table 1). Lumbar puncture, urine drug screen, blood and urine cultures, and transthoracic echocardiogram did not reveal any cardiac, infectious, or toxic etiologies (Table 1). She was diagnosed with a severe allergy to TMP-SMX, confirmed by similar reactions on re-exposure to skin testing.
