| Abstract: | Although it has been experimentally proved that thyroid hormones stimulate beta 2 receptor activity and tissue responsiveness to catecholamines, previous studies have established that asthma and nonspecific bronchial reactivity (NSBR) can worsen if complicated by hyperthyroidism. Our study is an effort toward the analysis of this contradiction. In 20 congenitally hypothyroid children, substitutive opotherapy was completely withdrawn for 1 month, resumed in the original dosage for 2 months, and then increased by 20% from day 91 to day 110. Mean NSBR, expressed in carbachol-related PD20-FEV1 and PD25-V25, was significantly increased by day 30, remained significantly elevated by day 90, and returned to initial values by day 110. These results suggest that thyroid hormones per se in nonasthmatic subjects decrease bronchial reactivity. This observation should be taken into consideration when attempting to explain the worsening condition of asthmatics who became affected with hypothyroidism. Bronchial reactivity appears to be under the control of many factors (including thyroid hormone levels). Once it is altered, a period of time seems necessary to restore the original bronchomotor tone (2 months in our study). |
