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Is Dopamine an Iatrogenic Disruptor of Thyroid and Cortisol Function in the Extremely Premature Infant?

DOI: 10.1155/2014/973184

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Abstract:

Background. Dopamine is frequently used as an inotropic and vasoactive agent in neonatal intensive care units. Recent studies have reported that treatment with dopamine is associated with hypothyroxinaemia of prematurity. Objectives. The aim of this study was to determine if dopamine treatment in extremely premature infants altered thyroid and cortisol function. Methods. We prospectively measured plasma cortisol, TSH, free T4, total T4, and free triiodothyronine concentrations in babies born below 28 weeks’ gestation within 5 days of birth, who were either treated with dopamine (D+) or who did not receive any dopamine (D?) within 12 hours of birth. Clinical Risk Index for Babies scores, lowest mean arterial pressure and highest plasma lactate concentrations in the first 12 hours, were recorded. Results. There were 78 babies included in the study (43 males). Mean gestational age was 25 weeks and 3 days (SD 1.3 weeks). Univariate analyses showed significant differences in cortisol and thyroid function between D+ and D?. Multivariable analyses showed that dopamine, gestation, and CRIB were independent factors affecting FT4 concentrations. No independent factors were shown to affect cortisol or TSH concentrations. Conclusion. Dopamine administration appeared to affect FT4 concentrations but not cortisol concentrations. The mechanisms are unclear but the effect does not appear to be related to hypotension or tissue underperfusion. 1. Introduction Derangement of thyroid function in extreme prematurity has been commonly described [1, 2]. Preterm infants are also frequently hypotensive within the first 24 hours of birth. Dopamine, which is a natural catecholamine, is often used as a first line inotropic and vasoactive agent in neonatal intensive care. Dopamine has been reported in human studies to cause suppression of anterior pituitary hormone secretion [3, 4] and animal experiments have reported that basal secretion of TSH from pituitary thyrotrophs was significantly inhibited by dopamine in a dose-dependent manner in adult species, although no work has been done on embryonic or fetal animals [5, 6]. Infants with severe thyroidal disruption are at an increased risk of abnormal neurodevelopment [7, 8] and dopamine has been associated with hypothyroxinaemia of prematurity [4, 9, 10]. In a randomised controlled trial of dopamine versus dobutamine, dopamine administration was associated with reduced serum concentrations of growth hormone, TSH, T4, and prolactin after 12 hours of administration in very low birth weight infants [3]. The apparent effect of dopamine

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