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Idiopathic intracranial hypertension, hormones, and 11ß-hydroxysteroid dehydrogenases

Authors Markey KA, Uldall M, Botfield H, Cato L, Miah M, Hassan-Smith G, Jensen R, Gonzalez AM, Sinclair AJ

Received 15 September 2015

Accepted for publication 29 December 2015

Published 19 April 2016 Volume 2016:9 Pages 223—232

DOI https://doi.org/10.2147/JPR.S80824

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Kerui Gong

Peer reviewer comments 3

Editor who approved publication: Dr Michael Schatman


Keira A Markey,1 Maria Uldall,2 Hannah Botfield,1 Liam D Cato,1 Mohammed A L Miah,1 Ghaniah Hassan-Smith,1 Rigmor H Jensen,2 Ana M Gonzalez,1 Alexandra J Sinclair1

1Neurometabolism, Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK; 2Danish Headache Center, Clinic of Neurology, Rigshospitalet-Glostrup, University of Copenhagen, Glostrup, Denmark

Abstract: Idiopathic intracranial hypertension (IIH) results in raised intracranial pressure (ICP) leading to papilledema, visual dysfunction, and headaches. Obese females of reproductive age are predominantly affected, but the underlying pathological mechanisms behind IIH remain unknown. This review provides an overview of pathogenic factors that could result in IIH with particular focus on hormones and the impact of obesity, including its role in neuroendocrine signaling and driving inflammation. Despite occurring almost exclusively in obese women, there have been a few studies evaluating the mechanisms by which hormones and adipokines exert their effects on ICP regulation in IIH. Research involving 11ß-hydroxysteroid dehydrogenase type 1, a modulator of glucocorticoids, suggests a potential role in IIH. Improved understanding of the complex interplay between adipose signaling factors such as adipokines, steroid hormones, and ICP regulation may be key to the understanding and future management of IIH.

Keywords: 11beta-hydroxysteroid dehydrogenase type 1, steroid and adipokines, obesity, leptin

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