Sulfasalazine
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Sulfasalazine-induced hypersensitivity syndrome: case report A 58-year-old woman developed sulfasalazine-induced hypersensitivity syndrome (SIHS) during treatment with sulfasalazine for Crohn’s disease [dosage and route not stated]. The woman was diagnosed with Crohn’s disease during a routine-screening colonoscopy. She started receiving treatment with budesonide and sulfasalazine. Ten days later, she presented to a hospital with emesis and fever. Initially, she was tachycardic and mildly hypotensive, but was responsive to fluid resuscitation with oxygen requirement of 2 L/minute. Laboratory tests revealed elevated erythrocyte sedimentation rate and C-reactive protein with normal liver function tests (LFTs), WBC count, and lactic acid. Her respiratory viral panel was negative. CT scans were without significant abnormalities. She was suspected of sepsis secondary to pneumonia (differential diagnosis) and was initiated on empirical antibiotic therapy including azithromycin and ceftriaxone. Her home medication including budesonide and sulfasalazine were withdrawn. The following day, the woman developed pancytopenia and a diffuse morbilliform rash. Epstein-Barr virus, cytomegalovirus IgM serologies and blood cultures were all negative. Her urine culture showed presence of methicillin sensitive Staphylococcus aureus; however, she had no urinary symptoms. Later, her LFTs rose and she became hypotensive. An abdominal ultrasound showed mild gallbladder wall thickening without gallstones. Her antibiotic treatment regimen were extended to doxycycline, levofloxacin and vancomycin because of concern for worsening sepsis. Over the next 2 days, her laboratory and vital signs were found to be normalised. Even with uncertainty of the diagnosis, she was discharged from the hospital after 5 days on doxycycline to complete a 14 day course of antibiotics. After 16 days, she was advised to restart treatment with sulfasalazine. The woman experienced abrupt-onset chills emesis, and fever within less than 10 hours of restarting sulfasalazine. Upon arrival to an emergency room (ER), her temperature was 39.5°C. She then received treatment with meropenem due to concern for sepsis. Shortly after her admission, she developed distributive shock with blood pressure decreasing into the 70s/40s mmHg and an associated lactic acid level of 4.3 mEq/L. She then received fluid resuscitation with 8L of sodium chloride [saline] and was transferred to an intensive care unit (ICU) for vasopressor therapy. She developed hyperemic skin, pancytopenia, mildly elevated LFTs, and anasarca. Her antibiotics were broadened from meropenem to clindamycin and vancomycin. Her blood cultures throughout the hospitalisation grew no bacteria. At this point, non-infectious aetiologies were also considered and an extensive autoimmune workup was performed. She was found to have non-specific elevations in rheumatoid factor and ferritin levels along with hypocomplementemia. Based on a non-specific autoimmune work-up and no detectable source of infection, SIHS was suspected
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