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Table of Contents
Vol. 93, No. 2, 2011
Issue release date: March 2011
Section title: Original Paper
Neuroendocrinology 2011;93:126–132
(DOI:10.1159/000324097)

Beta-Cell Dysfunction and Insulin Resistance after Subarachnoid Haemorrhage

Kruyt N.D.a, f · Musters A.a · Biessels G.J.g · DeVries J.H.b · Coert B.A.c · Vergouwen M.D.I.d · Horn J.e · Roos Y.B.a
Departments of aNeurology, bInternal Medicine, cNeurosurgery, dExperimental Vascular Medicine and eIntensive Care, Academic Medical Centre, University of Amsterdam, fDepartment of Neurology, Slotervaartziekenhuis Amsterdam, Amsterdam, and gDepartment of Neurology, Rudolf Magnus Institute of Neuroscience, University Medical Centre Utrecht, Utrecht, The Netherlands

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: November 03, 2010
Accepted: February 01, 2011
Published online: February 04, 2011
Issue release date: March 2011

Number of Print Pages: 7
Number of Figures: 1
Number of Tables: 2

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN

Abstract

Background: Hyperglycaemia is a common finding and an independent risk factor for increased morbidity and mortality in aneurysmal subarachnoid haemorrhage (SAH). Although in these patients hyperglycaemia is commonly ascribed to insulin resistance, there is little understanding of underlying mechanisms. Aims: To prospectively study temporal disturbances of glucose metabolism after aneurysmal SAH in patients without known abnormalities of glucose metabolism and to explore possible correlations with markers of stress. Methods: In consecutive aneurysmal SAH patients not subjected to insulin therapy, in-hospital and follow-up oral glucose tolerance tests (OGTTs) and assessments of insulin resistance, pancreatic β-cell function, free fatty acids (FFA) and cortisol were performed and compared with reference values. Results: We included 13 patients. In the first 2 weeks of admission, median fasting glucose and FFA levels were elevated while insulin levels were not. OGTTs were indicative of glucose intolerance in all patients at days 3 and 7, while on follow-up 1 patient had glucose intolerance and all patients had normal fasting glucose levels. Pancreatic β-cell function was impaired throughout the first week and insulin resistance from day 4 to 10. Levels of cortisol correlated with higher fasting glucose and increased FFA. FFA in turn correlated with pancreatic β-cell dysfunction. Conclusions: Aneurysmal SAH patients have transient abnormalities of glucose metabolism. During the first week, it appears to result predominantly from transient pancreatic β-cell dysfunction, in combination with insulin resistance.

© 2011 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: November 03, 2010
Accepted: February 01, 2011
Published online: February 04, 2011
Issue release date: March 2011

Number of Print Pages: 7
Number of Figures: 1
Number of Tables: 2

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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