We described a case of a 30-year-old female patient with bipolar disorder who experienced the anticonvulsant hypersensitivity syndrome (AHS) during treatment with lamotrigine and aripiprazole. She developed fever (38.4 degrees C), leukopenia, skin rash, and elevated serum transaminase levels on the 11th day of lamotrigine treatment (20th day of aripiprazole). Hypersensitivity to lamotrigine was suspected; lamotrigine was discontinued and prednisolone (30 mg/day) was administered to the patient. The clinical manifestations and laboratory findings showed improvement. However, on the 11th day of lamotrigine discontinuation (7th day of prednisolone treatment), she developed maculopapular skin rash over the entire body except the mucosa. There were no other symptoms and the laboratory findings were within normal limits. Skin biopsy showed erythema multiforme. After prescribing 55 mg/day of predisolone for additional 8 days, the recovery was uneventful, and it took 4 weeks from the onset of the second skin rash. Lamotrigine induced AHS showed broad spectrum of presentation and some manifestations can be flared up several days after discontinuation as did in this case. If unexplained systemic symptoms or a skin rash of unknown cause develop during the use of lamotrigine, clinicians should discontinue lamotrigine promptly and monitor the patient carefully at least for several weeks.
Adult ; Biopsy ; Bipolar Disorder ; Erythema Multiforme ; Exanthema ; Female ; Fever ; Humans ; Hypersensitivity* ; Leukopenia ; Mucous Membrane ; Prednisolone ; Skin ; Aripiprazole

No abstract available.
Abscess* ; Nocardia*

A l3-year-old boy was admitted to our hospital with severe hypertension, visual blurring, excessive sweating, polyuria and polydipsia. On admission, the blood pressure was persistently elevated at 230/180 mmHg. and an ophthalmologist was consulted, the funduscopic examination showed bilateral grade IV retinopathy. Cardiomegaly with dyspneic on exertion and persistent tachycardia were present. In urine examinations, proteinuria was sustained and glycosuria was traced. B. U. N. was 9.4 mg/dl. Urinary catecholamine was 12480 mic.g./day ; urinary V. M. A. was 20.2 mg./day. Regitine test was positive but histamine test was not performed. Presacral air insufflation with nephrotomography showed egg sized soft tissue mass locating at just above the upper pole of left kidney. He was operated with transabdominal approach. There were bilateral pheochromocytomas on suprarenal areas. Two weeks after operation, he was discharged with good general condition and we report this case with review of literatures.
Blood Pressure ; Cardiomegaly ; Glycosuria ; Histamine ; Humans ; Hypertension ; Insufflation ; Kidney ; Male ; Ovum ; Phentolamine ; Pheochromocytoma* ; Polydipsia ; Polyuria ; Proteinuria ; Sweat ; Sweating ; Tachycardia

No abstract available.

PURPOSE: To evaluate the characteristics of MUC2, MUC5AC expression and the effect of beta-blocker on MUC2, MUC5AC expression in cultured human conjunctival cell. METHODS: Human conjunctival cell was cultured. After obtaining the monoclonality of conjunctival cells, secondary culture was done. Cultured conjunctival cell was treated with 0.2 nM timolol. Specimen was collected in 1, 3, 5, 10 days after the confluence of cultured conjunctival cells. To determine the effect of beta blocker, Periodic acid-Schiff (PAS) staining, immunohistochemistry, RT-PCR, and flowcytometry were performed. RESULTS: Goblet cell was found in cultures of conjunctival cell. MUC5AC was detected in RT-PCR, immunohistochemistry, and flowcytometry, but MUC2 was detected only in flowcytometry. Beta blocker didn't have significant effects on expression of MUC2 and MUC5AC in flowcytometry. CONCLUSIONS: MUC2 and MUC5AC were detected in cultured conjunctival cell. Beta blocker may not affect goblet cell. The other factor will be related to goblet cell suppressing the mucin in long standing antiglaucomatous medication.
Goblet Cells ; Humans* ; Immunohistochemistry ; Mucins ; Timolol