[Severe peripheral neuropathy, cardiac hypofunction, and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Churg-Strauss syndrome].

A 64-year-old Japanese male was admitted to Kotoh General Hospital because of fever and cough on July, 14, 1997. Laboratory data showed hypereosinophilia (11,500/microliter) and high titer of anti-myeloperoxidase antineutrophil cytoplasmic antibody (319 EU). A physical examination revealed progressive peripheral neuropathy. He had been diagnosed as having bronchial asthma since November, 1996. Therefore, he was diagnosed as having Churg-Strauss syndrome (CSS). He was treated with methylprednisolone pulse therapy (500 mg/day for 3 days) and oral prednisolone (PSL, 60 mg/day). However, peripheral neuropathy was rapidly progressive, and echocardiogram revealed cardiac hypofunction (ejection fraction (EF); 39%). He was refereed to Akita University Hospital for further examination. On admission, laboratory data showed hyponatremia (125 mEq/l) with inappropriate secretion of antidiuretic hormone (ADH, 13.0 pg/ml). Atrial natriuretic peptide was normal (26 pg/ml). Urinary osmorality was 488 mOsm/l, and urinary sodium excretion was 86 mEq/l. Renal, adrenal, and thyroid functions were normal. From these data, his hyponatremia was caused by syndrome of inappropriate secretion of ADH (SIADH). After cyclophosphamide-pulse therapy (500 mg) and oral administration of cyclophosphamide (50 mg/day) and PSL (50 mg/day), peripheral neuropathy improved gradually, and his serum sodium returned to normal, but cardiac hypofunction continued. A possible relationship between SIADH and CSS is discussed.