8°C), and dyspnea. On admission,

the patient was conscious and reported chills, coughs, and rhinorrhea of two days’ duration. She had developed rash on her face six days after starting epilepsy treatment, with the condition progressing rapidly to her trunk, limbs, neck, and chest over the next four days. The facial rash subsequently evolved into pustules. On examination, there were multiple erosions over the mouth and vulva, and the conjunctiva was inflamed. Nikolsky’s sign Inhibitors,research,lifescience,medical was positive. The total extent of the erythematous rash was 55% of the BSA. Histological investigation of the injured skin revealed an aspect for drug eruption (extensive epidermal necrosis, focal subepidermal necrotic blisters, melanin incontinence, and moderate perivascular lymphocytic infiltrate in the absence of eosinophils, neutrophils, and viral inclusions). Immunofluorescence

Inhibitors,research,lifescience,medical markers showed negative staining. The diagnosis of SJS-TEN caused by antiepileptic drugs was established. On the other hand, laboratory testing Inhibitors,research,lifescience,medical revealed anemia, eosinophilia, increased inflammatory markers, and white blood cell count of 10×109 /µL. Chest X-ray demonstrated multifocal patch consolidations with ground-glass opacity in both lungs. No bacterial pathogen was isolated in the respiratory tract, urine, and blood. Viral serology (HIV and hepatitis B and C) was negative. Real Time Polymerase Chain Reaction (RT-PCR) (R-gène® Kits) of bronchoalveolar lavage (BAL) revealed that the cause of the respiratory symptom was cytomegalovirus (CMV); the finding was thereafter confirmed Inhibitors,research,lifescience,medical by cell culture on MRC-5 cells. Prior serology data showed that our patient had already sustained a primary CMV infection at 6 years old, which was in favour of the current reactivation. As was expected, RT-PCR in blood showed fulminant viremia

with 459 copies/ml (threshold: Inhibitors,research,lifescience,medical 350). The antiepileptic drugs were withdrawn and anticoagulant therapy, parenteral analgesia, eye drops, and mouth antiseptic therapy were initiated. Intravenous Ganciclovir (10 mg/kg/day) was started. Oxygen therapy was initiated with parenteral nutrition and adequate hydration. Serial BAL assays were negative six days after the commencement of antiviral therapy, and the skin lesions began to heal without the need to introduce corticosteroids. The patient’s condition Dipeptidyl peptidase improved, and she was transferred to the general ward with a prescription of Ganciclovir for a further two weeks. Tacedinaline manufacturer Discussion TEN and SJS are severe adverse cutaneous drug reactions.4,5 Treatment with corticosteroids is recommended but not necessarily effective.5-7 Several drugs are at “high” risk of inducing TEN-SJS.1 Mycoplasma pneumoniae and herpesvirus infections are well-documented causes. In some rare cases, however, the etiology remains unknown.