| 저자(한글) |
Ishii, Junko,Yamamoto, Shiro,Yoshimura, Hajime,Todo, Kenichi,Kawamoto, Michi,Kohara, Nobuo |
| 초록 |
An 82-year-old woman with a history of asthma was admitted to our hospital because of dyspnea. On admission, laboratory testing showed a white blood cell count of 17,700/μl with hypereosinophilia of 9,204/μl (52% of all white blood cells). Various examinations, including a bone marrow biopsy for the cause of eosinophilia, were unremarkable. The patient was diagnosed with hypereosinophilic syndrome (HES). Treatment with intravenous methylprednisolone was initiated. The patient #039;s eosinophil count normalized within 1 day. On the 6th day, she developed left-sided hemiparesis. Magnetic resonance imaging (MRI) of the brain showed acute multiple infarcts in arterial border zones of bilateral cerebral and cerebellar hemispheres, and in bilateral basal ganglia and the thalamus. Magnetic resonance angiography was normal. Coagulation factors were normal, except for an elevated D-dimer level (12.9?μg/ml). A transthoracic echocardiogram showed thickening of the left ventricular endocardium with immobile thrombus, compatible with L?ffler endocarditis. Treatment with oral prednisolone was started at 30?mg/day and then tapered to a maintenance dose of 5?mg/day. Anticoagulation was concurrently started for prevention of stroke. Ten months later, an echocardiogram showed that the thrombus had decreased in size, and MRI revealed no new cerebral infarctions. The cause of cerebral infarction in patients with hypereosinophilia is thought to be thromboembolism or cerebrovascular endothelial toxicity of eosinophils. In this patient, the cerebral infarcts may have been the result of embolism from the left ventricular thrombus. Because HES with L?ffler endocarditis is frequently associated with a poor prognosis, cardiovascular problems should be evaluated and treatment started as soon as possible. |
