4.5 Article

Increased IL-1β reactivity upon a glucose challenge in patients with deliberate self-harm

期刊

ACTA PSYCHIATRICA SCANDINAVICA
卷 124, 期 4, 页码 301-306

出版社

WILEY-BLACKWELL
DOI: 10.1111/j.1600-0447.2011.01734.x

关键词

borderline personality disorder; cytokine; IL-1 beta; aggression, glucose

资金

  1. Swedish Research Council [14548-04-3, K2009-61X-21524-01-1]
  2. National Health Service
  3. Lund University Hospital
  4. Faculty of Medicine, Lund University
  5. Soderstrom-Konigska Foundation
  6. Sjobring Foundation
  7. OM Persson Foundation
  8. Lundbeck Foundation
  9. Swedish Psychiatry Foundation
  10. Region Skane

向作者/读者索取更多资源

Objective: A disturbed glucose metabolism has been observed in patients with aggressive behaviour. Interleukin (IL)-1 beta 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-1 beta 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-1 beta, TNF-alpha 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-1 beta levels in response to glucose was significantly greater in patients than in controls. Furthermore, IL-1 beta reactivity was associated with symptoms of hostility. Conclusion: An increased reactivity of IL-1 beta might be part of a pathogenetic mechanism in patients with deliberate self-harm.

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