Akademik Veri Yönetim Sistemi
ENDOCRINE, sa.3, ss.513-516, 2006 (SCI-Expanded)
A 53-yr-old previously healthy man was admitted to our hospital for thyrotoxicosis without ophthalmopathy. Initial therapy with propylthiouracil caused an acute elevation of liver enzymes. Then, he received a first course of I-131 therapy (20 mCi). At the end of 6-mo follow-up after I-131, he was still thyrotoxic and developed moderately severe ophthalmopathy. The patient refused thyroid surgery and decided to undergo second course of I-131 therapy (30 mCi). Concomitantly with the I-131, we opted to give high-dose pulse glucocorticoid therapy (PGT) to prevent further deterioration of on intravenous methylprednisolone pulse therapy 1 g daily in a cycle (one cycle every 2 wk,. each cycle comprising two infusions on alternate days). After the end of the second day of PGT administration, he suddenly developed onset of acute pulmonary edema and hypertension. There was no previous history of cardiac disorder or conditions predisposing to cardiac failure other than thyrotoxicosis. A presumptive diagnosis of fluid overload and/or hypertension-induced acute heart failure was made. After prompt investigations excluding cardiogenic causes, we thought that this condition was triggered by PGT that was superimposed on thyrotoxicosis-related hemodynamic instability. Graves' patients with uncontrolled thyrotoxicosis should be under careful surveillance when PGT is planned. To our knowledge, this is the first reported case of life-threatening acute pulmonary edema caused by PGT in GO.