Sulfasalazine
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Drug induced hypersensitivity syndrome: case report A 67-year-old man developed drug induced hypersensitivity syndrome (DIHS) during treatment with sulfasalazine for rheumatism (RA). The man, with a past history of RA, hypertension and subarachnoid haemorrhage, presented with right hemiparalysis and aphasia. Subsequently, he was diagnosed with left embolic cerebral infarction during trial for RA. On day 1 of hospitalisation, an external decompression was performed. On day 2, he started receiving levetiracetam to prevent convulsions. On day 7, he started receiving oral sulfasalazine [salazosulfapyridine] 500 mg/day. On day 14, the dose was increased to 1000 mg/day. A CT revealed no increase in haemorrhagic infarction. On day 37, dabigatran was initiated to prevent the recurrence of cerebral infarction. On day 41, he developed fever. On the next day, he developed oedema and erythema appeared on his face, while erythema and rash appeared on his trunk and extremities. Because of the gradual onset of erythroderma, diphenhydramine and fexofenadine [fexofenadine hydrochloride] were started. On day 43, a CT scan revealed inflammatory findings in the ileocecal area and a mild nodule shadow at the lower right lung. A drug eruption due to dabigatran was suspected. Thus, therapy with dabigatran was stopped. On day 45, he developed diarrhoea and was started on clostridium butyricum. On day 50, his respiratory function deteriorated (saturation of percutaneous oxygen, SpO2 90%) and oxygen was provided. A drug lymphocyte stimulation test was performed for levetiracetam and dabigatran on day 51, which showed negative results for both. On day 53, his respiratory function further deteriorated (saturation of percutaneous oxygen, SpO2 80%). The man’s therapy with sulfasalazine was discontinued. He received steroid pulse of methylprednisolone to prevent exacerbation of the interstitial pneumonia (IP). After this, the dose of methylprednisolone was reduced. Due to possibility of steroidogenic glucose tolerance abnormality, he received concurrent insulin therapy in combination with methylprednisolone. On day 55, cardiac ultrasound revealed a pericardial effusion with normal wall motion. On day 59, CT showed worsened IP and pericardial effusion. Although, his inflammatory findings in the ileocecal area had decreased. Because of malaise caused by hyponatraemia on day 60, fluids were restricted on suspicion of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) caused due to IP. His hyponatraemia was then gradually managed. Subsequently, he developed stomatitis for which he received dexamethasone ointment. On day 66, the fever, erythema and rash recurred. The CT revealed no pericardial effusion. On day 67, he received increased dose of prednisolone. On day 72, a suspected diagnosis of DIHS induced by sulfasalazine was made [time to reaction onset not stated]. His quantification tests for human herpes virus (HHV)-6 DNA and HHV-7 DNA were found to be negative. An Epstein-Barr (EB) anti-viral capsid antigen (VCA) IgG was incr
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