Peer-reviewed article

SAT-104 Unraveling the Connection Between Cortisol and Pediatric Idiopathic Intracranial Hypertension

Hoyos-Martinez A, Horne V, Wood A, Shah V · 8 May 2020

Summary

Written by AI, not yet AICS's view · claude-haiku-4-5-20251001

This is a medical research paper describing a retrospective study of 64 children with idiopathic intracranial hypertension (IIH), examining the prevalence of adrenal insufficiency in this population. The study found that 75% of children had insufficient or at-risk cortisol levels, and most had been exposed to topical, nasal or inhaled corticosteroids. The authors conclude that steroid exposure and adrenal insufficiency should be considered in IIH development and that all children presenting with IIH should be evaluated for steroid exposure and adrenal function.

Key points

75% of children with IIH had insufficient or at-risk cortisol levels
70-80% of those with low cortisol had been exposed to topical, nasal or inhaled (not systemic) corticosteroids
Only 60% and 12% of those with insufficient or at-risk cortisol underwent confirmatory stimulation testing
Children with adrenal insufficiency were more likely to have a history of asthma (53% vs 12-18% in other groups)
Adrenal function did not differ significantly by age, race/ethnicity, BMI, or prolonged steroid exposure

Limitations

This is a retrospective chart review with no control group, making it impossible to determine causation or whether the observed cortisol levels are specific to IIH. The study cannot establish whether treating adrenal insufficiency actually resolves IIH or improves outcomes in these children.

Abstract

Abstract Background: Idiopathic intracranial hypertension (IIH) is a condition of elevated intracranial pressure without identifiable secondary causes. The childhood incidence is 0.7 per 100,000 and increases with age, obesity, and female gender. Few case reports in the literature, and our own experience, suggest there may be an association between IIH and adrenal insufficiency (AI) but the real extent is unknown. Aim: To describe the prevalence of AI in children presenting with IIH to a large pediatric referral center. Methods: Retrospective chart review identified all children who presented with IHH and had cortisol measured between January 2010 and September 2019. Based on morning, random or 1 mcg ACTH stimulated cortisol levels, adrenal functioning was classified as: (1) deficient (peak cortisol <16 μg/dl, AM cortisol <5 μg/dl), (2) at risk (peak cortisol 16 - 20 μg/dl, AM cortisol 5 - 13 μg/dl or random < 13 μg/dl), or (3) sufficient (peak cortisol >20 μg/dl, AM or random cortisol >13 μg/dl). Descriptive data present mean (+/- standard deviation), and chi-squared (χ 2) tests of differences are used to examine differences between the adrenal functioning groups. Results: Participants (N=64) were 40.6% male, of mixed ancestry (61% non-Hispanic white; 19% African-American, 16% Hispanic White and 5% Asian), with a mean age of 10.8 (4.8) years. Cortisol levels were obtained at an average of 0.6 (1.9) years after diagnosis of IIH; 23% and 52% of patients had insufficient or at risk cortisol levels. The majority of those in the insufficient (70%) or at risk (80%) groups were exposed to topical, nasal or inhaled corticosteroids, but not systemic. Only 60% and 12 % of those with IIH and insufficient or at risk cortisol testing, respectively, underwent definitive testing with a stimulation test. Adrenal function did not differ by age, race/ethnicity, zBMI, nor prolong exposure to steroids (> 2 weeks), time between IIH diagnosis and cortisol testing (all P>.05). Those in the deficient group were less likely to be female (33%) than those in the at risk (61%; χ 2=3.07, df=1, P=.001) or sufficient (81%; χ 2=7.30, df=1, P<.001) groups. Those with AI were more likely to have history of asthma (53%; vs: 18% at risk and 12% normal; both P>.05) Conclusions: Steroid use and AI are common in IIH and need consideration as a cause of IIH development. Appropriate diagnosis and treatment of AI in children who present with IIH may lead to its resolution, significantly impacting clinical outcomes of these children. In our cohort, the majority had AI or at risk cortisol levels, and many did not undergo further testing. All young children who present with IIH should be evaluated for steroid exposure, including non-systemic steroids, and undergo evaluation for AI. Caution should be utilized in pediatric providers prescribing these medications. More prospective studies are required to evaluate the effects of steroid use in relation to IIH development.