A 30-year-old woman presented to the hospital with a morbilliform and pruritic generalized rash [], along with high-grade fever, fatigue, and malaise for 4 days. Physical examination and blood tests revealed enlarged cervical and inguinal nodes, leukocytosis (up to 66,800 white blood cell/mm3), and elevated levels of hepatic transaminases, lactate dehydrogenase, ß-2 microglobulin, and erythrocyte sedimentation rate. Serology results for hepatitis, syphilis, typhoid fever, and brucella were negative. The whole body computed tomography showed multiple neck, chest, and abdominal lymphadenopathy with splenomegaly suggestive of lymphoma []. A skin biopsy specimen revealed epidermotropism of atypical lymphoid cells, with CD30 positive staining as well as a dense perivascular and perifollicular lymphoid infiltrate []. An excisional biopsy of a 1.0 cm cervical node showed diffuse polymorphic lymphoid hyperplasia with effacement of the normal architecture with strong and diffuse staining for CD30 on immunohistochemistry, positive anti-leukocyte common antigen, and high proliferation index (Ki67 80%). All findings were consistent with lymphoma. However, osteomedullary biopsy showed no evidence of lymphoproliferative disorder, was absent for immunomarkers and high eosinophils proliferation rate. T-cell receptor rearrangement studies on the skin, lymph node, and bone marrow biopsies, failed to detect monoclonality. A detailed review of her past medical history revealed that she was started on lamotrigine 50 mg/day for somatization disorder 40 days prior to the onset of symptoms. Blood samples were positive for human herpesvirus 6 DNA. The diagnosis of DIHS/DRESS was made; lamotrigine was discontinued and treatment with oral corticosteroids (prednisolone, 60 mg/day) was started with rapid tapering. The patient made a full recovery with no organ deficit on follow-up visits at 1, 2, 4, and 6 months.
A 16-year-old female student presented with absence seizures for 2 years of age and no significant past or family history of epilepsy or allergic disorder. The computerized tomography (CT) head and magnetic resonance imaging (MRI) of the brain were found to be normal; electroencephalography (EEG) was abnormal with diffuse cerebral dysfunction. She had been treated with clobazam 10 mg/day OD, for 1.5 years, but was still experiencing seizures about one to two in a day; therefore, LTG was added, starting with 25 mg a day, with weekly escalation, up to a dose of 100 mg/day. After 2 weeks of adding LTG, she developed fever, headaches, chills, and rash all over the body; the patient presented to the dermatology outpatient department (OPD) after 1 week of onset of the symptoms.\nOn examination, maculopapular lesions involving the genitals associated with itching were seen, which then spread to the trunk and then extremities in the next 3 days []. They became tender, and the erythematous, partially blanchable lesions took on a dusky hue over the trunk, upper limb, lower limb, and progressed to involve the face and lips (crusted plaques). No involvement of the oral cavity was noted nor were there any vesicular lesions. On the basis of history and clinical examination, a diagnosis of TEN was made and LTG was discontinued immediately and admitted under the dermatology department. LTG was stopped, and she was started on levetiracetam 500 mg twice a day, continued on clobazam 10 mg/day, intravenous steroids, fluids, and antibiotics. With medications and supportive care, the patient improved without any further complications.