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Title: Relationship between psychiatric disorders, coronary risk factors, and inflammatory mediators among elderly diabetic patients
Author: Moatasem S. Amera, Heba H. Elshahawib, Mohamed Khatera, Randa A. Mabroukc and Maram M. Munira
Abstract:
Immune mechanisms seem to play a key role in the development of many diseases. Among psychiatric disorders, the most studied disorder is depression; immune mechanisms play a major role in the development of this disorder. This is evidenced clinically by an episodic and fluctuating course with partial or complete remission [1] and by lab investigation through an increase in interleukin- 1b (IL-1b) in dysthymic patients and IL-1 in those with major depression, which in turn affects the hypothalamic pituitary adrenal axis [2]. Moreover, an elevated plasma level of inflammatory markers, especially C-reactive protein (CRP), was a significant predictor of type II diabetes, even after the adjustment for BMI, waist circumference, physical activity, and conventional risk factors [3,4]. This triggering of the inflammatory response can lead to the destruction of pancreatic islet cells [5]. Furthermore, inflammation also plays a role in the pathogenesis of atherosclerosis, development of unstable plaques, and the risk for coronary heart disease (CHD) [6]. Depression and or anxiety, diabetes mellitus (DM), and CHD all have almost common immune mechanisms of pathogenesis. Depression through affection of CRP and interleukin-6 can lead to the development of insulin resistance, growth of atherosclerotic plaques, and thrombogenesis [7]. Anxiety disorder can play a role in CHD through the development of hypertension, smoking habit [8,9], and affection of electrical stability of the heart [10], although the relationship between anxiety and inflammatory markers is controversial [11].influence on insulin resistance and secretion [12]. It serves as a link between depression and the development of atherosclerosis [7,13]. IL-1b was studied as its interaction with IL-6 can affect the synthesis of CRP. IL-1b induces proinflammatory mediators such as corticoptropin, platelet factor-4, prostaglandin2, which cause local and systemic inflammation [3].
Journal: Middle East Current Psychiatry 2012, 19:171–178
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