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Journal Article

Citation

Westling S, Ahren B, Träskman-Bendz L, Brundin L. Acta Psychiatr. Scand. 2011; 124(4): 301-306.

Affiliation

Department of Clinical Sciences, Section for Psychiatry, Lund University, Lund Department of Clinical Sciences, Medicine, BMC, Lund University Hospital, Lund Department of Clinical Sciences, Section for Psychiatry, Psychoimmunology Unit, Lund University, Lund, Sweden.

Copyright

(Copyright © 2011, John Wiley and Sons)

DOI

10.1111/j.1600-0447.2011.01734.x

PMID

21762115

Abstract

Westling S, Ahrén B, Träskman-Bendz L, Brundin L. Increased IL-1β reactivity upon a glucose challenge in patients with deliberate self-harm. Objective:  A disturbed glucose metabolism has been observed in patients with aggressive behaviour. Interleukin (IL)-1β is a pro-inflammatory cytokine that can induce hypoglycaemia, but has also been suggested to be involved in the generation of hostility and aggression. Our group has previously shown an altered glucose metabolism in patients with self-inflicted aggressive behaviour. We investigated the hypothesis that the levels of IL-1β would be increased in these patients, because this might explain the aberrant glucose metabolism and add further knowledge to the aetiology of self-inflicted aggressive behaviour. Method:  We investigated plasma cytokine changes in 13 patients with borderline personality disorder and 13 healthy controls during a 5-h glucose challenge. Plasma samples were analysed for cytokines IL-1β, TNF-α and IL-6 using high-sensitivity multiplex ELISA. Psychiatric symptoms were rated using the Aggression Questionnaire Revised Swedish Version. Results:  Basal plasma levels of the three cytokines did not differ between patients and controls. All three cytokines reacted significantly upon the glucose challenge. The increase in IL-1β levels in response to glucose was significantly greater in patients than in controls. Furthermore, IL-1β reactivity was associated with symptoms of hostility. Conclusion:  An increased reactivity of IL-1β might be part of a pathogenetic mechanism in patients with deliberate self-harm.


Language: en

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