284 The Korean Journal of Internal Medicine Vol. 24, No. 3, September 2009 Figure 1. Rash on the back of the patient. Diffuse erythematous papular lesions are noted. Figure 2. Microscopic view of the skin biopsy specimen (H-E stain, ×400). Leukocytoclastic vasculitis is noted. tebral tenderness, but this disappeared later. Her laboratory findings were a white blood cell count of 2,340/µL (lymphocytes 10%, stab neutrophils 78%, neutrophils 8%, monocytes 1%, eosinophils/basophils 0%, myelocytes 3%), a hemoglobin level of 8.0 g/dL and a platelet count of 177,000/µL. The erythrocyte sedimentation rate (ESR) was 57 mm/hours (reference, 0-20 mm/hours) and the C- reactive protein was 11.1 mg/dL (reference, 0-0.6 mg/dL). The hepatic transaminase levels were elevated (AST 128 IU/L and ALT 41 IU/L). The renal function tests were normal and neither sediments nor protein were found on spot urine analysis. Three days after admission the WBC and platelet counts fell to 1,240/µL and 70,000/µL, respectively, and antinuclear antibody tests revealed an 1:1280 homogenous pattern with the presence of extractable nuclear antigens (ENA) like anti-Ro (3+), La (1+), RNP (3+), nucleosomes (3+), Sm (+/-) and histone (-), according to the immunoblot method. Her anti-ds- DNA titer was 73 IU/mL (reference, 0-5.3 IU/mL) and the complement levels were C3: 34.7/C4: 13.6 mg/dL (reference, 88-201/ 16-47 mg/dL). Hypergammaglobulinemia was also noted. Interestingly, the IgE levels was elevated (1,364 IU/mL [reference, 0-20 IU/mL]), but radioallergosorbent tests (RAST) for honeybee, yellow hornet and common wasp allergens were negative (class 0). Other autoantibodies like rheumatoid factor, ANCA, and anti-phospholipid antibodies were not detected. Her chest X-ray showed infiltrations in the right lower lung region suggestive of bronchitis, but she did not produce sputum. Abdominal sonograms revealed only a mild to moderate fatty liver, without splenomegaly. Pathologic examination of the skin lesions revealed leukocytoclastic vasculitis (Fig. 2). With the findings of facial rash, pancytopenia and the presence of ANA and specific autoantibodies, the diagnosis of a new onset lupus was made, which seemed to be triggered by the bee venom therapy, and she was treated with intravenous pulse steroids (methylpred- nisolone 1 g for 1 day) and subsequent high dose oral steroids (prednisolone 1 mg/kg) with hydroxychloroquine (400 mg/day). Empirical antibiotics, with oral fluconazole for her oral candidiasis, were maintained during the treatment period. Prompt defeversence was noted and the rash subsided within a few days. She did suffer a compli- cation of delirium during the treatment period, which was probably due to the high doses of steroids. However the pancytopenia along with her clinical state improved, and she was discharged 10 days after admission, relatively symptom-free. The chest radiographs improved during the treatment period. She was found to have complete cutaneous resolution at the first visit one week later, but she was lost to further follow-up. DISCUSSION The idea of using bee venom as a treatment for arthritic symptoms is not a new one, and it is thought to have originated during ancient times [3]. Bee venom is effective in murine arthritic models [4,5] and it has also shown effectiveness in human trials [2]. Its effectiveness is thought to be mediated through inhibition of macrophages and lymphocytes, which leads to decreased IL-1/IL-2 pro- duction and inhibition of NF-κb [3]. In addition, bee