Platelet supersensitivity to thrombin stimulation in depression: a possible mechanism for the association with cardiovascular mortality.

Berk,M and Plein,H 2000, Platelet supersensitivity to thrombin stimulation in depression: a possible mechanism for the association with cardiovascular mortality., Clinical Neuropharmacology, vol. 23, no. 4, pp. 182-185.

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Title Platelet supersensitivity to thrombin stimulation in depression: a possible mechanism for the association with cardiovascular mortality.
Author(s) Berk,MORCID iD for Berk,M orcid.org/0000-0002-5554-6946
Plein,H
Journal name Clinical Neuropharmacology
Volume number 23
Issue number 4
Start page 182
End page 185
Publisher Lippincott, Williams & Wilkins
Place of publication UNITED STATES
Publication date 2000-07
ISSN 0362-5664
Keyword(s) Science & Technology
Life Sciences & Biomedicine
Clinical Neurology
Pharmacology & Pharmacy
Neurosciences & Neurology
depression
mortality
platelet
calcium
cardiovascular system
INTRACELLULAR CALCIUM RESPONSE
ISCHEMIC-HEART-DISEASE
CORONARY-ARTERY DISEASE
MYOCARDIAL-INFARCTION
MAJOR DEPRESSION
PHOBIC ANXIETY
PANIC DISORDER
SEROTONIN
RISK
LEUKOENCEPHALOPATHY
Summary The mortality risk associated with cardiovascular disease is significantly increased in patients with major depression and panic disorder. The mechanism of this phenomenon is unclear. Thrombin is responsible for platelet aggregation and shape change, and it plays a significant role in the development of thromboembolic events. In this study, we examined the platelet second messenger intracellular calcium response to thrombin stimulation in patients with major depression (n = 13), major depression after response to electroconvulsive therapy (ECT; n = 13), subsyndromal depression (n = 16), schizophrenia (n = 15), and control subjects (n = 65). Patients with major depression had significantly higher intracellular calcium responses to thrombin stimulation than control subjects, patients with subsyndromal depression, and patients with schizophrenia (p < 0.05). Electroconvulsive therapy did not significantly change this supersensitivity. This suggests that the platelet response to activation in patients with major depression is supersensitive. This study suggests a possible mechanism for the increased risk of cardiovascular disease that is seen in these two psychiatric disorders. The lack of difference between the control and subsyndromal depression groups appears to validate current diagnostic thresholds in depression. The failure of nonpharmacologic treatment to alter this marker suggests that it may be a trait marker of depression.
Language eng
Field of Research 0 Not Applicable
Socio Economic Objective 0 Not Applicable
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2000, Lippincott, Williams & Wilkins
Persistent URL http://hdl.handle.net/10536/DRO/DU:30071329

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
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