Mean platelet volume in patients with rheumatoid arthritis: the effect of anti-TNF-alpha therapy

Abstract

A number of mediators are involved in the inflammatory processes that affect joints and vascular wall of patients with rheumatoid arthritis (RA). Tumour necrosis factor alpha (TNFa) is one such mediator, and it is widely regarded as an important target for anti-rheumatic treatment. Most recent studies show that anti-TNFa medication suppresses inflammation and reduces overall activity of RA. The aim of the current study was to investigate changes of mean platelet volume (MPV) in response to the 3-month anti-TNFa therapy in RA. Twenty-one RA patients without established cardiovascular disease were recruited for anti-TNFa therapy and underwent thorough clinical and laboratory evaluation at baseline, 2 weeks, and 12 weeks. Anti-TNFa therapy resulted in a significant (p = 0.01) increase in MPV over the duration of the study (7.7 +/- 0.9, 7.8 +/- 1.1, and 8.4 +/- 1.1 fL at baseline, 2 weeks, and 12 weeks, respectively). The results of the study expand perspectives of the use of MPV in conditions associated with high-grade inflammation, particularly RA, for monitoring anti-inflammatory treatment. More prospective studies with large numbers of patients are warranted to ascertain associations of high and low values of MPV with diverse markers of inflammation and vascular pathology.

Mean platelet volume in acute appendicitis: A gender difference

“…Gasparyan et al [16] suggested two possible mechanisms of decreased MPV in high-grade inflammatory conditions. First is the overproduction of pro-inflammatory cytokines and acutephase reactants interfering with megakaryopoiesis which in turn results in subsequent release of small size platelets from the bone marrow.…”

Mean platelet volume in Korean patients with hepatic diseases

“…MPV has been studied in various disease groups other than hematologic disease such as cardiovascular and rheumatic diseases [2][3][4][5]. It has been also investigated in several hepatic diseases and showed significant differences in these disease entities [1,[6][7][8][9][10].…”

“…Thrombopoietin (TPO), which is synthesized in the liver, could play a relevant role to increase MPV in hepatic diseases. Moreover, in addition to TPO, several cytokines, inflammatory mediators, and growth factors may affect MPV, with subsequent production of larger and more reactive platelets [2][3][4][5]. These mechanisms could be involved in several hepatic diseases, such as CHB and HCC.…”

Whether or not the association of MPV with coronary collateral development is independent of hs-CRP level?

“…In addition, recently, some studies have suggested that MPV can be used as marker of inflammation and disease activity [10,11]. Interestingly, it has been noted by Gasparyan et al [11] that the intensity of systemic inflammation determines the size of circulating platelet size.…”