Transient Neonatal Hypocortisolism in Neonates with Hypoglycemia – Coexistence or Cause?

Author:

Mondal Sunetra1,Nagendra Lakshmi2,Chowdhury Amarta S.3,Palui Rajan3,Biswas Soumyadeep4,Mukherjee Devdeep5,Khan Krishnendu4,Sengupta Aritra5,Pandey Anupama6

Affiliation:

1. Department of Endocrinology, Healthworld Hospitals, Durgapur, India

2. Department of Endocrinology, JSS Academy of Higher Education and Research, Mysore, India

3. Department of Endocrinology, The Mission Hospital, Durgapur, India

4. Department of Pediatrics, Healthworld Hospitals, Durgapur, India

5. Department of Pediatrics, The Mission Hospital, Durgapur, India

6. Department of Pediatrics, JSS Academy of Higher Education and Research, Mysore, Karnataka, India

Abstract

Abstract Introduction: Infants born preterm, with low birth weight (LBW), or with perinatal stress are at high risk for neonatal hypoglycemia. Low cortisol levels have also been demonstrated in this group of neonates, which is often transient. We report a series of neonates with transient hypocortisolism who had neonatal hypoglycemia. Methods: A descriptive study on clinic-biochemical parameters of a group of five neonates who had persistent neonatal hypoglycemia and had demonstrated low cortisol on critical sample testing. Results: All five neonates had birth weights below normal and four were born preterm. A history of perinatal asphyxia was seen in four cases and neonatal sepsis in two. During critical sample testing (when blood glucose [BG] was <50 mg/dl), hyperinsulinism (Insulin >2 mIU/ml) was seen in three infants whereas insulin was undetectable in two. The median cortisol during critical sample testing was 1.9 mcg/dl (0.88 – 3.7). Critical GH was normal in all, and ACTH ranged from 7.2 pg/ml to 41.3 pg/ml. None of the infants had overt clinical features of panhypopituitarism or primary adrenal insufficiency. USG brain revealed germinal matrix hemorrhage in two infants, which resolved on follow-up. USG adrenals and electrolytes were normal in all. Four of the five babies were started on oral hydrocortisone, to which they responded well with the resolution of hypoglycemia. No adverse events were noted. On follow-up, the median time to recover of serum cortisol to normal was 4 months. Conclusion: The contribution of transient hypocortisolism to hypoglycemia in infants at risk, including preterm, LBW, or those with perinatal stress, in the presence or absence of hyperinsulinism, is not well known. While the non-specific use of glucocorticoids is not advocated, the role of therapeutic glucocorticoids among at-risk neonates with documented hypocortisolism during hypoglycemia should be an area for research. Close follow-up of these neonates for spontaneous recovery of cortisol levels is warranted.

Publisher

Medknow

Reference20 articles.

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2. Williams Textbook of Endocrinology;Badiu;Acta Endocrinol (Buchar),2019

3. Sperling Pediatric Endocrinology E-Book;Sperling;Elsevier Health Sciences;2020

4. Cortisol and growth hormone responses to spontaneous hypoglycaemia in infants and children;Crofton;Arch Dis Child,2004

5. Transient adrenal insufficiency in the premature newborn;Quintos;Curr Opin Endocrinol Diabetes Obes,2010

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