enfermeria


lnflammalion-Induced Thrombosis

sis, inflammation, and transfer of malignancies and infections [77-
82]. As MPs engulf cytoplasm during their formation, they acquire proteins and RNA that originate from the cytosol of the parent cell. Therefore, they may also serve as vectors for information transfer and may function as a transport and delivery system for bioactive molecules [83].C-REACTIVE PROTEIN AND THROMBOSIS
C-reactive protein (CRP) may be accepted as the prototype acute phase protein, whieh inereases dramatically following tissue injury or intlarnmation [84]. Additionally, the level of CRP eleva­ tion generally reflects the severity of systemic inflarnmation and disease activity. CRP faeilitates immune defense against variouspathogens. CRP acts as an opsonin for various pathogens, binds to Fe receptors, and activates the complement cascade [84, 85]. CRP also plays a role in the clearance of apoptotic and necrotie cells, which is very important to prevent autoirnmunity [86).
Plasma CRP levels generally positively correlate with the dura­ tion and intensity of systemie inflammation (87). However, there are sorneexceptional inflammatory diseases including SLE, Sjogren syndrome, systemic sclerosis and inflammatory myositis, where plasma CRP levels may not reflect the amount of inflamma­ tion [87].
Inflarnmation plays a pivotal role in the pathogenesis of athero­ sclerosis, and high CRP and serum amyloid A (SAA) levels may potentiate prothrombotic and proinflammatory events in acutecoro­ nary syndromes [88]. CRP may activate thrombosis formation by different mechanisms involved in primary and secondary hemosta­ sis. CRP activates primary hemostasis by increasing the count, adhesiveness and aggregability of the platelets. CRP also signifi­ cantly decreases PGI2 release from human endothelial cells [84]. On the other hand, CRP activates secondaryhemostasis by increas­ ing TF [89], vWF and tPA, as weJl as by decreasing TFPI [90]. Taken together, CRP may exert several prothrombotic activities, including activation of blood coagulation, impairment of the en­ dogenous fibrinolytic capacity, and stimulation ofplatelets [84].
From an epidemiological point ofview, elevated CRP levels are c1early associated with increasedrisk ofVTE [91]. However, since genetically elevated CRP levels do not associate with increased VTE risk, this may not necessarily be a causal association. Accord­ ing to Lippi, increased CRP concentrations might be an epiphe­ nomenon rather than a cause ofvenous thrombosis [84].

INFECTIOUS AGENTS AND THROMBOSIS
Environmental factors including infectious agents may alsocause a tendency to inflarnmation-induced thrombosis development, besides genetic factors. Although Chlamydia pneumoniae (C. pneumoniae) has been suggested to contribute to inflarnmation­ induced thrombosis, this could not be confirmed in a previous study [92-94]. Other than C. pneumoniae, oral bacteria such as Porphy­ romonas gingivalis (p. gingivalis), were implicated in the patho­genesis ofTAO in the context of poor oral hygiene [22, 95]. It was reported that lipopolysaccharides of P. gingivalis could activate endothelial cells, promote platelet aggregation, and degrade endo­ thelial TM, leading to vascular inflammation and thrombosis. Be­ sides, Streptococci are weJl known to contribute to both impaired oral health and pathogenesis in BD [96, 97].AUTOANTIBODIES AND THROMBOSIS
The prototype autoantibodies causing thrombosis are antiphos­ pholipid (aPL) antibodies [98], which will be discussed later in the context of antiphospholipid syndrome (APS). Antiendothelial cell antibodies may also playa role in the pathogenesis of TAO [99]. On the other hand, ANCA has previously been speculated to playa role in thrombotic tendency seen...