Plasma aldosterone levels in the 1st week of life in infants of less than 30 weeks gestation.
ABSTRACT Plasma aldosterone levels were measured in 50 infants of less than 30 weeks gestation at 24 h (D1) and 7 days (D7). The relationship between the plasma aldosterone level and a number of clinical and biochemical variables was explored. Plasma aldosterone levels ranged from 1000 to 30000 pmol/l and were inversely correlated with the severity of illness (D1 or D7), serum sodium (D7) and 24 h sodium intake (D1). No correlation with the serum potassium level was noted. Conclusion:Plasma aldosterone levels in this extremely premature cohort were significantly greater than those reported in more mature infants. Important determinants were severity of illness and sodium homeostasis.
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ABSTRACT: Heparin may cause hyperkalemia by blocking aldosterone biosynthesis in the adrenal gland. Dizygotic twin sisters were born by Cesarean section at 25 weeks' gestation. The younger sister developed acute hyperkalemia (7.4 mEq/L) at 10 days of age. At the time of the development of the hyperkalemia, there were no signs of systemic infection, cardiac or renal failure, adrenal insufficiency, or sudden anemia. She was receiving no medication other than heparin to maintain the vascular catheter. Heparin was changed to dalteparin at 12 days of age. The plasma potassium level normalized after 14 days of age. After this change, the urinary potassium concentration and the aldosterone and plasma renin activity increased. The urinary aldosterone levels before and after the changes were 31 and 183 pg/μg creatinine, respectively. When heparin-induced hyperkalemia is suspected, stopping the heparin administration facilitates diagnosis and treatment; if anticoagulant therapy is required; one treatment option is changing from unfractionated heparin to low-molecular-weight heparin.Journal of Clinical Research in Pediatric Endocrinology 06/2014; 6(2):125-128. DOI:10.4274/Jcrpe.1255
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ABSTRACT: Hormonal regulation of adrenal function occurs primarily through activation of GPCRs. GPCRs are central to many of the body's endocrine and neurotransmitter pathways. Recently it was shown that activation of GPR103 by its ligand QRFP induced feeding, locomotor activity and metabolic rate, and QRFP is bioactive in adipose tissue of obese individuals. Given that the adrenal gland is pivotal organ for energy balance and homeostasis we hypothesised that GPR103 and QRFP are involved in steroidogenic responses. Using qRT-PCR and immunohistochemistry we mapped both GPR103 and QRFP in human fetal and adult adrenal gland as well as rat adrenals. Both were primarily localised in the adrenal cortex but not in the medulla. Activation of GPR103 in human adrenocortical H295R cells led to a decrease in forskolin-increased cAMP and increase of intracellular Ca(++) levels. In addition, treatment of H295R cells with QRFP induced aldosterone and cortisol secretion as measured by ELISA. These increases were accompanied by increased expression and activity of StAR, CYB11B1 and CYP11B2 as assessed by qRT-PCR and luciferase-reporter assay respectively. Using specific inhibitors we also demonstrated that the aldosterone induction involves MAPK, PKC and/or T-type Ca(++) channel dependent pathways. These novel data demonstrate that QRFP induces adrenal steroidogenesis in vitro by regulating key steroidogenic enzymes involving MAPK/PKC and Ca(++) signalling pathways.AJP Endocrinology and Metabolism 08/2013; 305(9). DOI:10.1152/ajpendo.00191.2013 · 4.09 Impact Factor
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ABSTRACT: Extremely immature newborns develop a self-limiting normal anion gap metabolic acidosis in early life. This study examined the natural history of this acidosis in a population of infants of gestation less than 26 weeks in the first 14 days of life. The acidosis was maximal on day 4 with a mean base deficit of 10.6 mmol/l and had resolved in 90 % of infants by day 11. Dopamine usage was the only independent predictor of the acidosis. Its use was associated with a greater degree of acidosis. Conclusion: Extremely preterm infants experience a self-limiting normal anion gap metabolic acidosis in the first 2 weeks of life which is consistent with renal tubular immaturity.European Journal of Pediatrics 06/2014; 174(1). DOI:10.1007/s00431-014-2364-9 · 1.98 Impact Factor