Unit:
Τομέας ΚλινικοεργαστηριακόςLibrary of the School of Health Sciences
Dissertation committee:
Κουτσιλιέρης Μ., Καθηγητής, Ιατρική, ΕΚΠΑ
Τζιούφας Α., Καθηγητής, Ιατρική, ΕΚΠΑ
Βλαχογιαννόπουλος Π., Καθηγητής, Ιατρική, ΕΚΠΑ
Αρμακόλας Α., Αναπλ. Καθηγητής, Ιατρική, ΕΚΠΑ
Μαυραγάνη Κ.Π., Αναπλ. Καθηγήτρια. Ιατρική. ΕΚΠΑ
Πρωτογέρου Α., Αναπλ. Καθηγητής, Ιατρική, ΕΚΠΑ
Χατζηγεωργίου Α., Επικ. Καθηγητής, Ιατρική, ΕΚΠΑ
Original Title:
Υποκλινική αθηροσκλήρυνση και διαταραχές οστικού μεταβολισμού σε ασθενείς με ΣΕΛ
Translated title:
Subclinical atherosclerosis and bone metabolis alterations in patients with SLE
Summary:
Heightened rates of both cardiovascular (CV) events and subclinical atherosclerosis, documented by
imaging and vascular function techniques are well established in systemic lupus erythematosus (SLE).
While traditional CV factors such as smoking, dyslipidemia, diabetes mellitus (DM), hypertension, central
obesity and hyperhomocysteinemia have been reported to be prevalent in lupus patients, they do not
fully explain the high rates of ischemic events so far reported, implying that other factors inherent to
disease itself could account for the enhanced risk, including disease duration, activity and chronicity,
psychosocial factors, medications, genetic variants and altered immunological mechanisms. Though the
exact pathogenesis of atherosclerosis in the setting of lupus remains ill defined, an imbalance between
endothelial damage and atheroprotection seems to be a central event. Insults leading to endothelial
damage in the setting of lupus include oxidized low density lipoprotein (oxLDL), autoantibodies against
endothelial cells and phospholipids, type I interferons (IFN) and neutrophil extracellular traps (NETs)
directly or through activation of type I IFN pathway. Increased oxidative stress, reduced levels of the
normally antioxidant high density lipoprotein (HDL), increased levels of proinflammatory HDL (piHDL)
and reduced paraoxonase activity have been related to increased oxLDL levels. On the other hand,
impaired atheroprotective mechanisms in lupus include decreased capacity of endothelial repair-partly
mediated by type I IFN- and dampened production of atheroprotective autoantibodies. In the present
review, traditional and disease related risk factors for CV disease (CVD) in the setting of chronic autoimmune
disorders with special focus on SLE will be discussed.
Main subject category:
Health Sciences
Keywords:
Systemic lupus erythematosus, Subclinical atherosclerosis, Homocysteine. Parathormone, Stress
Number of references:
303
