1. Cortisol precursors in neonates with vasopressor-resistant hypotension in relationship to demographic characteristics.
- Author
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Khashana A, Ahmed H, Ahmed A, Abdelwahab A, Saarela T, Rämet M, and Hallman M
- Subjects
- 17-alpha-Hydroxypregnenolone blood, Cohort Studies, Dehydroepiandrosterone blood, Drug Resistance, Female, Gestational Age, Humans, Hydrocortisone analogs & derivatives, Hydrocortisone metabolism, Hypotension epidemiology, Infant, Newborn, Infant, Premature blood, Infant, Premature, Diseases blood, Infant, Premature, Diseases drug therapy, Infant, Premature, Diseases epidemiology, Male, Pregnenolone blood, Risk Factors, Treatment Failure, Hydrocortisone blood, Hypotension blood, Hypotension congenital, Hypotension drug therapy, Vasoconstrictor Agents therapeutic use
- Abstract
Objective: To correlate between cortisol precursors in neonates with vasopressor resistant hypotension and demographic characteristics., Methods: We investigated 48 neonates with vasopressor-resistant hypotension. Gestation at birth ranged from 34 to 42 weeks and postnatal age from 4 to 14 days. Cortisol and precursor steroids were measured soon after the onset of volume expansion and inotropes for treatment of shock. Their concentrations were determined using liquid chromatography/mass spectrometry., Results: In neonates with vasopressor-resistant hypotension, the serum levels of cortisol were within normal nonstress range. There was a strong negative linear association between postnatal age and dehydroepiandrosterone level (r = -0.50, p < .01), which decreased with neonatal age. In addition, there was a significant positive association between gestational age at birth and 17-hydroxy-pregnenolone (r = 0.33, p = .02). No further significant associations were evident between the neonatal weight, duration of gestation or gender and of the levels of cortisol or the other steroids (p > .05). The cause of therapy-resistant hypotension did not appear to influence the steroid levels., Conclusions: Cortisol stress response is absent in these severely ill late preterm and term infants. This may be due to inhibition of the distal pathway of cortisol synthesis.
- Published
- 2018
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