| Central TSH suppression has been postulated to occur in patients with acute critical illnesses due to endogenous glucocorticoid elevations and caloric deprivation (1-3). T4 and reverse T3 production rates are within the normal range even in the low total T4 state of critical nonthyroidal illness and free T4 values are normal or elevated by direct equilibrium dialysis in the majority of patients without concurrent hypothalamic-pituitary-thyroid disease (1-5). However, elucidation of the pituitary-thyroid axis in nonthyroidal disorders requires simultaneous assessment of bioactive TSH and free T4 by a method which provides credible values in sick sera. |
