A 36-year-old woman presented at our institution (Gachon University Gil Hospital) with erythematous confluent maculopatches on her face, trunk, and palms; jaundice; fatigue; pruritus; and aggravation of skin lesions over the previous week. She had been previously diagnosed as having erythema multiforme 2 weeks earlier at a private dermatology clinic and had also been administered dapsone with oral antihistamines (mequitazine and cetirizine) and topical corticosteroid for 8 months.\nOn admission, her vital signs were a blood pressure of 110/70 mm Hg, heart rate of 78 beats/min, respiratory rate of 18 breaths/min, and body temperature of 38.8℃. She reported no night sweats, loss of weight, or arthralgia. A physical examination conducted at presentation revealed bilateral, multiple enlarged lymph nodes on both sides of the neck with splenomegaly. All of the nodes were non-tender, firm, and measured 0.5 cm to 1.0 cm in diameter. Laboratory tests results were as follows: Hb 11.2 g/dL, white blood cell 13,070/mm3 (segmented neutrophils 24%, lymphocytes 66.3%, and eosinophils 0.1%), platelets 245,000/mm3, total bilirubin 5.4 mg/dL, direct bilirubin 3.8 mg/dL, aspartate aminotransferase/alanine aminotransferase (AST/ALT) 233/366 U/L, lactate dehydrogenase 1,610 IU/L (normal range, 200 to 485 IU/L), and an international normalized ratio of 1.25. She was negative for hepatitis B surface antigen, anti-hepatitis C virus Ab, and anti-human immunodeficiency Ab, but positive for hepatitis B surface antibody; and positive for anti-nuclear Ab, but negative for rheumatoid factor, anti-neutrophil cytoplasmic Ab, anti-Ro (SS-A, B) Ab, and anti-smith Ab. Serology tests showed no evidence of active Epstein-Barr virus (EBV) infection and no bacterial growth was found during a blood culture study. There was no hypergammaglobulinemia.\nAn excisional biopsy of a 1.0 cm cervical node showed diffuse polymorphic lymphoid hyperplasia with effacement of the normal architecture and abundant high endothelial venules; the cellular infiltrate was polymorphic, with abundant transformed lymphocytes and plasma cells (). Sinuses were frequently recognizable, but reactive germinal centers were not found.\nImmunohistochemically, the majority of infiltrating atypical lymphocytes were CD3+ T-cells (), and some activated large cells were reactive for CD30 (). Follicular dendritic cell meshworks expressing CD21 were expanded (), and infiltrating atypical T-cells were negative for CD10, BCL-6, and EBV by in situ hybridization. For a definitive diagnosis, a molecular study on the rearrangement of the T-cell receptor (TCR)-gamma gene was performed and showed polyclonality (). An IgH gene rearrangement study also showed polyclonality.\nAn abdomino-pelvic computed tomography (CT) scan revealed splenomegaly (14 cm), an enlarged portocaval lymph node (1.7 cm), and gallbladder wall edema (). No evidence of lymphomatous involvement was found by chest CT or a bone marrow trephine biopsy.\nBecause aggravation of the skin eruption persisted and the liver function test remained abnormal, the possibility of DHS (exfoliative dermatitis, acute hepatitis, and multiple lymphadenopathy) was raised. The findings of a transjugular liver biopsy were compatible with drug-induced hepatitis manifesting as granulomatous inflammation (). No evidence of lymphomatous hepatic involvement was found. In view of her skin lesions, medication history, and age, we concluded that the cervical lymphadenopathy was actually pseudolymphoma. Accordingly, low dose prednisolone (30 mg/day) per os was started after transjugular liver biopsy to relieve the dapsone-induced skin lesions and hepatitis. Gradually, the skin lesions improved and the cervical lymph node enlargement regressed. Her total bilirubin, AST, and ALT values also normalized after 3 weeks of prednisolone, which was then tapered over a month. Follow-up CT scans conducted 3 and 6 months after presentation showed that the size of the cervical lymph nodes and spleen had normalized, and produced no other findings suggestive of lymphoma progression ().
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.