
Research view
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].
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Journal: | Middle East Current Psychiatry 2012, 19:171–178 |
Text: | |
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