Airway reactivity and lung function in triiodothyronine-induced thyrotoxicosis.
To evaluate the possible relationship between asthma and hyperthyroidism, airway reactivity and lung function were prospectively compared in healthy volunteers before, during, and after liothyronine (triiodothyronine, T3)-induced hyperthyroidism. Base-line evaluation of the 10 subjects included clinical evaluation, thyroid and pulmonary function tests, and airway reactivity assessed by methacholine inhalational challenge (MIC). All studies were normal. During T3-induced hyperthyroidism, no subject developed respiratory symptoms or changes in pulmonary function or airway reactivity. The mean percent change in forced expiratory volume at 1 s from base line (delta FEV1) of -2.4 +/- 3.0 after MIC was not significantly different from that obtained before T3 administration (-1.4 +/- 1.5, P greater than 0.2). When all serum T3 concentrations and delta FEV1 values before, during and after T3-induced hyperthyroidism were compared, there was no significant correlation. We conclude that T3-induced hyperthyroidism of 3-wk duration has no effect on airway reactivity or lung function in normal volunteers.
D000328:Adult; D000403:Airway Resistance; D001249:Asthma / Q000209:etiology; D001980:Bronchi / Q000503:physiopathology*; D001985:Bronchial Provocation Tests; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D006980:Hyperthyroidism / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D008168:Lung / Q000503:physiopathology*; D008297:Male; D016210:Methacholine Chloride; D008688:Methacholine Compounds; D014284:Triiodothyronine / Q000633:toxicity*
D008688:Methacholine Compounds; D014284:Triiodothyronine; D016210:Methacholine Chloride