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+In March 2009, a 21-year-old man was admitted to another institution with symptoms of intermittent fever, headache, polyarthralgias, skin rash over the trunk, and petechiae in the fingers and palms.
+The patient was previously healthy, had no history of drug abuse, and took no regular medication.
+He also had no pets and had not traveled recently.
+He had been in his usual state of health until one month before admission, when intermittent high fever developed (maximum axillary temperature, >39 °C).
+In addition, he reported headaches, bilateral and symmetric arthralgia on the wrists and hands (with an inflammatory pattern), petechiae over the palms and fingers, salmon-colored rash on the trunk, nausea, and vomiting.
+An evanescent, salmon-colored rash was observed on his chest and abdomen, and 2-mm petechiae covered the palms and the fingers.
+No signs suggested arthritis, and there was no lymphadenopathy or hepatosplenomegaly.
+Blood testing showed elevated inflammatory markers (Table II).
+The electrocardiographic (ECG) and chest radiographic results were normal.
+Ibuprofen (1,200 mg/d) and acetaminophen (as needed) were begun and provided symptomatic relief.
+An extensive evaluation was performed, including blood cultures, viral and bacterial serologic studies, immunologic screening (rheumatoid factor and antinuclear antibodies), and computed tomographic (CT) studies of the chest, abdomen, pelvis, and cranium.
+No significant changes were found.
+However, a transthoracic echocardiogram (TTE) showed circumferential, mild pericardial effusion (maximal diameter, 8 mm), with no signs of tamponade or other relevant findings.
+A few days later, dyspnea and diffuse chest pain developed.
+The pain was relieved by chest anteflexion and aggravated by deep inspiration and by lying supine.
+The patient was hypotensive, tachycardic, and hyperpneic, and he manifested jugular venous distention.
+The ECG showed sinus tachycardia and diffuse ST-segment elevation (Fig.1), the chest radiograph revealed an enlarged cardiac silhouette (Fig.2), and the inflammatory markers were again elevated (Table II).
+A repeat TTE showed an increase in the pericardial effusion (maximal diameter, 12 mm) (Fig.3) and collapse of the right heart chambers.
+Emergency pericardiocentesis drained 60 mL of serosanguineous fluid.
+When repeated, CT of the chest and abdomen revealed mild right and severe left pleural effusion, as well as mild ascites.
+Thoracocentesis was then performed, during which 350 mL of serosanguineous pleural fluid was drained.
+Both heart and lung fluids were exudates that yielded negative microbiologic examination and were unremarkable upon histologic analysis.
+The diagnosis of AOSD was established, and the patient was medicated with prednisone (0.5 mg/kg/d), with major clinical and laboratory improvement (Table II).
+There was also ST-segment normalization, and the follow-up echocardiogram showed only mild pericardial effusion (2–3 mm), without hemodynamic compromise.
+Screening for autoimmune and infectious disorders was repeated, and no significant changes were found.
+The patient was discharged from the hospital on a regimen of prednisone.
+There was a recurrence of pericardial and pleural effusion 2 months after discharge (after corticosteroid weaning and withdrawal), which was resolved by resuming the prednisone therapy.
+Ten months after discharge, the patient presented at our institution for a follow-up visit.
+He was asymptomatic and was maintained on corticosteroid therapy.
+Follow-up ECG and TTE showed no significant changes (Figs.4 and ​5).