Influence of thyroid function on the in vivo cortisol in equilibrium cortisone equilibrium in man.

To evaluate the effect of thyroid function on the in vivo cortisol in equilibrium cortisone (F in equilibrium E) equilibrium, double-labeled cortisol tracer techniques were used to measure separately the rates of the F leads to E and E leads to F reactions in 4 euthyroid, 2 hypothyroid, and 2 hyperthyroid subjects. The rate of the F leads to E reaction was calculated from the appearance rate of 3H in body water after the i.v. injection of [11 alpha-3H]-cortisol; the rate of the E leads to F reaction was calculated from the difference in the plasma turn-over rates of [11 alpha-3H]-cortisol, and [4-14C]-cortisol after simultaneous i.v. injection of both tracers; the F in equilibrium E set-point was calculated by dividing the F leads to E rate by the E leads to F rate. In euthyroid subjects the F leads to E reaction rate averaged 1.6%/min, the E leads to F reaction rate averaged 1.0%/min, and the F in equilibrium E set-point averaged 1.6. In hyperthyroid subjects the two reaction rates were supranormal: the F leads to E rate averaged greater than or equal to 3.9%/min and the E leads to F rate averaged 1.54%/min; since the increase in the F leads to E rate was proportionally greater, the F in equilibrium E set-point (average greater than or equal to 2.6) was displaced towards cortisone. In hypothyroid subjects both reaction rates were equally slowed, to an average of 1.0%/min (F leads to E) and 0.68%/min (E leads to F); the F in equilibrium E set-point averaged 1.65, the same as in euthyroid subjects. Displacement of the F in equilibrium E equilibrium towards cortisone in hyperthyroid subjects appears to account for their elevated urinary THE/THF ratios, but the normal F in equilibrium E set-point in hypothyroid subjects makes it necessary to invoke a different mechanism for their depressed THE/THF ratio; it is suggested that increased conversion of THE to cortoic acids may be the responsible factor.