Ibuprofen/paracetamol

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Stevens-Johnson syndrome: case report A 2-year-and-8-month old girl developed Stevens-Johnson syndrome (SJS) during treatment with ibuprofen and paracetamol. The girl with a history of allergy, presented with a 3-day history of general malaise, fever and upper respiratory tract symptoms; she had received paracetamol [acetaminophen] and ibuprofen [routes, dosages and indication not stated]. On day 4 of ibuprofen and paracetamol administration, she developed erythematous violaceous macules on the face and extremities, which disappeared on finger pressure. Additionally, bullous lesions on the face and forearms were noted. She was hospitalised with a suspected diagnosis of DRESS syndrome or SJS. Her examinations upon admission showed the following: haematocrit 43.9%, haemoglobin 15.2 g/dL, neutrophils 30.6%, lymphocytes 62.5%, eosinophils 0.7%, platelets 177 000 cells/mm3, leucocytes 9 890 cells/mm3, CRP 0.18 mg/L, ALT 662 IU/L, AST 386 IU/L, total bilirubin 0.48 mg/dL, direct bilirubin 0.43 mg/dL and ALP 507 IU/L. Her abdominal ultrasound revealed a liver with increased echogenicity. The girl was treated with antihistamine, unspecified systemic steroids and paracetamol to control the fever. On day 2 of hospitalisation, her lesions became generalised; some were palpable and did not disappear on finger pressure. The blister on her face had sloughed and she developed ulcers on the oral mucosa. She did not show eosinophilia or atypical lymphocyte and less than 10% extension of epidermolysis. Hence, based on the presentation, she was diagnosed with SJS with potential triggers from paracetamol and ibuprofen (algorithm for drug causality in epidermal necrolysis: ALDEN scores of 0 and 2, respectively). Her paracetamol was discontinued and she was managed on systemic steroids. Subsequent tests showed the following data: ALT 727 IU/L, AST 409 IU/L, lipase 383 IU/L, GGT 201 IU/L, prothrombin time of 13.2 seconds, INR of 1, partial thromboplastin time of 18 seconds, albumin of 3.2 g/dL, creatinine of 0.3 mg/dL, C3 of 85 mg/dL, C4 of 103 mg/dL and CPK of 30. Her chest X-ray showed pulmonary interstitial infiltrates. Viral infections were ruled out following testing. Her symptoms persisted and she was transferred to a special care unit for management. Her treatment was changed to unspecified γ-globulins and aetylcysteine for hepatic protection. As her γ-globulins treatment was completed, her condition improved with closure of ulcerated lesions of the oral mucosa. She showed signs of remission with a decrease in liver and pancreatic enzymes. Her skin report showed toxicoderma without signs of vasculitis. She was discharged after 10 days of hospitalisation with skin protection, hydration care and restrictions on use of NSAIDs. A patch test was performed on an outpatient basis, with ibuprofen, paracetamol, naproxen, dipyrone, diclofenac, ketoprofen and aspirin. All the results were negative. Further tests were planned to establish antipyretic alternatives due to NSAIDs restriction. Subsequent tests showed negative results to oral

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