Why the study?
Does treatment of hyper- and hypothyroidism alter plasma ANP concentrations?
Does treatment of hyper- and hypothyroidism alter plasma ANP concentrations?
Abnormalities in ANP dynamics in thyroid disorders are likely caused by concomitant hemodynamic changes rather than direct effects of thyroid hormone on cardiomyocytes.
ANP changes may reflect thyroid-related hemodynamics; leaves open any role in monitoring or management.
To examine a possible role of atrial natriuretic peptide (ANP) in water and electrolyte disturbances associated with thyroid disorders, plasma ANP levels were studied in patients with hyper- and hypothyroidism. In 5 of the 21 hyperthyroid patients, including two patients with atrial fibrillation and two patients with mild cardiomegaly, the plasma ANP concentration was increased when compared to normal subjects. After treatment with methimazole or propylthiouracil, the plasma ANP concentration fell to normal in 4 patients, while it remained high in one patient who had persistent atrial fibrillation. No significant correlation was found between plasma ANP and the heart rate in untreated hyperthyroid patients. Plasma ANP was within the normal range in all 8 patients with hypothyroidism. During treatment with T4, the plasma ANP concentration increased in 6 of the 7 patients. Chest X-ray films and ultrasonic echocardiography demonstrated pericardial effusion in 4 of these patients before therapy. A weak but significant correlation was found between the plasma ANP and T4 concentration, and between plasma ANP and free T4 in hyper- and hypothyroid patients before and after treatment. These results indicate that abnormalities in ANP dynamics in thyroid disorders may probably be caused by hemodynamic changes resulting from a thyroid hormone excess or deficiency.
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YAMAJI et al. (1988) studied this question.
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