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 54-year-old housewife, known case of bipolar disorder with anxiety, presented to the neurology OPD. She was on valproate, fluoxetine, and olanzapine but for the past 3–4 months had worsened despite being on these three medications. Mirtazapine and LTG drugs were added by the psychiatrist, 15 days after which she complained of fever, pain in both ears, and presented to the dermatology OPD with rashes. On examination multiple discrete papules which were erythematous to hyper pigmented were seen all over the body;also seen were mucosal congestion and conjunctival involvement (matted eye lashes with crusting). There was also necrosis in nasal, oral (hemorrhagic crusting on lips), and genital (moist gray-white slough on the vaginal mucosa) areas []. There was no past or family history of any allergies. On the basis of clinical evaluation, the patient was diagnosed with SJS. LTG was stopped immediately and appropriate treatment was initiated. Patient's general condition improved, and on discharge, she was given antibiotic, steroid, and antihistaminic medications.