Etanercept-induced SLE 947 [L] 12 cm Fig. 1. Chest radiography shows pneumonic consolidation and pulmonary edema in both lung fields Fig. 2. Chest CT shows pneumonic consolidation, pulmonary edema, and pleural effusion or possible pulmonary hemorrhage. in the oral cavity. On chest examination, crackles were heard over both lung fields. There was no abnormal finding with- out hepatosplenomegaly in the abdomen. Initial complete blood count revealed hemoglobin of 7.7 g/dL, white cell count of 3,000/ L (65% neutrophil, 26% lymphocyte), and platelet of 40,000/ L. Peripheral blood smear showed no abnormal hematologic cells. Erythrocyte sedimentation rate was 11 mm/ hr and C-reactive protein was positive at 0.6 mg/dL (normal <0.3). Blood chemistry values revealed a total protein of 6.6 g/dL, albumin of 2.4 g/dL, BUN 17 mg/dL, creatinine 0.6 mg/dL, AST 447 IU/L, and ALT 113 IU/L. Creatine kinase was elevated to 253 IU/L. Urinalysis revealed one positive for protein. ANA was positive at a titer of 1:640, staining speck- led pattern, and rheumatoid factor was positive at 2,180 IU/ mL (normal <15 IU/mL). Anti-dsDNA was positive at 14.2 IU/mL (normal <10 IU/mL). Antibodies against ribonucle- oprotein and Ro/SS-A were positive, but La/SS-B and Smith were negative. C3 was 19.2 mg/dL, C4 was 9.9 mg/dL. Sym- metrically narrowed joint spaces, bony erosion, and osteope- nia were shown in hand radiography suggesting chronic RA with destructive change. Chest radiography revealed pneu- monia and pulmonary edema in both lung field (Fig. 1). Chest CT showed pneumonia, pulmonary edema, and pleural effu- sion with pulmonary hemorrhage suggestive of lupus pneu- monitis (Fig. 2). Bone marrow examination was normal except for increased megakaryocyte without evidence of hematologic malignancies. A diagnosis of SLE with major organ involvement with pneumonitis and thrombocytopenia was made. Etanercept was discontinued and high dose corticosteroid was started. Lupus pneumonitis complicated with pulmonary hemorrhage was improved with corticosteroids treatment. However, resi- dual lung infiltration remained. Bronchoscopic cell culture and PCR of sputum revealed coexistent adenoviral infection, and acyclovir was instituted. Two month later, her general condition markedly improved. However, she was complicated by unilateral pleural effusion, which showed positive for acid- fast bacilli PCR. Anti-tuberculous therapy of isoniazid, etham- butol, rifampin, and pyrazinamide was started. She is main- tained on prednisolone 20 mg/day, hydroxychloroquine 300 mg/day, and nabumetone 1 g/day with minimal symptoms upon 12 months of follow up. However, she still had high titers of ANA and anti-dsDNA antibodies. DISCUSSION TNF is an important pro-inflammatory cytokine that can cause inflammation and bony erosion in RA. TNF inhibi- tors, such as infliximab, etanercept, and adalimumab were shown to be very effective in reducing synovial inflammation and retarding structural damage in RA patients. Anti-TNF therapy has opened a new era in treatment of RA, and is being used more and more in current rheumatologic practice. Al- though TNF inhibitors are effective therapy for RA, the con- cerns for serious side effects have been also raised. Adverse events that can potentially occur in anti-TNF treated patients include tuberculosis, bacterial sepsis, heart failure, hemato- logic malignancy, and systemic autoimmune disease such as SLE and systemic sclerosis (15). Autoantibody formation was reported at high frequency in anti-TNF treated patients. In RA patients treated with