Serum albumin as a determinant of cortisol release in patients with acute ischemic stroke. 
Animal studies demonstrated that protein malnutrition increases pituitary-adrenorcortical activity and leads to excessive cortisol release.  The aim of our study was to determine the association between serum albumin and cortisol level in patients with acute ischemic stroke.  Fifty-nine patients with first-ever ischemic stroke were included.  Serum albumin level was measured within 36 h after stroke symptoms onset.  Serum cortisol was measured between 36 and 72 h after stroke onset at 6 a.m., 10 a.m., 6 p.m. and 10 p.m. The patients in upper tertile of serum albumin had significantly lower cortisol level measured at 6 a.m. (median with interquartiles: 549.0 [430.4-667.7] nmol/L vs 590.4 [482.8-918.7] nmol/L, P=0.047) and 10 a.m. (402.8 [344.9-510.4] nmol/L vs 634.6 [482.8-827.7] nmol/L, P<0.01) than patients in lower and middle tertiles.  On logistic regression analysis adjusted for age and stroke severity, patients in lower and middle tertile of serum albumin had about 7-times higher risk of hypercortisolemia than patients in upper tertile (P<0.01).  Low serum albumin level in patients with ischemic stroke is associated with higher serum cortisol level and predisposes to hypercortisolemia.