Platelet Counts and Platelet Activation Markers in Obese Subjects

Abstract

Objective. In this work we studied the correlation between platelet count, platelet activation, and systemic inflammation in overweight, obese, and morbidly obese individuals. Methods and subjects. A total of 6319 individuals participated in the study. Complete blood counts, high sensitivity C-reactive protein (hs-CRP) serum levels, and body mass index (BMI) were measured during routine checkups. Platelet activation markers were studied among 30 obese (BMI = 41 ± 8 kg/m2) and 35 nonobese (BMI = 24 ± 3 kg/m2) individuals. Platelet activation status was evaluated by flow cytometry using specific antibodies against the activated platelet membrane glycoprotein IIb/IIIa, p-selectin (CD-62 p), and binding of Annexin-V to platelet anionic phospholipids. Results. Overweight, obese, and morbidly obese females had significantly elevated platelet counts ( P < .0001) compared with normal-weight females. No significant elevation of platelet counts was observed in the male subgroups. A significant age adjusted correlation between BMI and platelet counts ( P < .0001) was found among females. This correlation was attenuated (P = .001) after adjustment for hs-CRP concentrations. The flow cytometry analysis of platelets showed no significant differences in activation marker expression between nonobese and obese individuals. Discussion. Obesity may be associated with elevated platelet counts in females with chronic inflammation. Obesity is not associated with increased platelet activation.

Association Between Obesity, White Blood Cell and Platelet Count

“…Studies have found that, there is some sort of association between the increased number of immune cells and obesity as a result of a chronic inflammatory condition which is created by an increase in the production of cytokines by adipose tissue. It has also been show that obesity is associated with low-grade subclinical and smoldering inflammation [18,19]. The health effects of low-grade systemic inflammation in healthy adults have shown an increased risk of cardiovascular disease and diabetes mellitus [20].…”

Causes of Variation in The Neutrophil–Lymphocyte and Platelet–Lymphocyte Ratios: a Twin-Family Study

“…Positive associations between BMI and NLR were observed in two nonpatient populations [8,9], but a third study did not find BMI to be related to NLR nor to PLR [19]. With respect to their subcomponents, larger waist circumference has been related to higher levels of lymphocytes, neutrophils and platelets [20], and these cell counts were also increased in obese women compared with nonobese women [21,22]. Smoking has also been related to increased NLR in two studies in the general population [8,23] and to increased neutrophil [23] and lymphocyte counts [24].…”

Expression of plasma membrane receptor genes during megakaryocyte development

“…receptors; megakaryocytopoiesis; thrombocytopoiesis; hematopoiesis; microarray MEGAKARYOCYTOPOIESIS INVOLVES the proliferation and differentiation of hematopoietic stem cells to form megakaryocyte (MK) progenitors that undergo a maturation process that culminates in a release of ϳ10 11 platelets per day into the blood circulation (31). This process is tightly regulated by a number of factors, which include extracellular cues such as cytokines, cell-to-cell interactions, and cell-to-extracellular matrix interactions.…”

“…Among cytokines that are known to act as important extracellular regulators of megakaryocytopoiesis is the main physiological stimulator of this specific cell-lineage commitment, thrombopoietin (TPO) (17). Additionally, interleukin 3 (IL3), interleukin 6 (IL6), interleukin 11 (IL11), stem cell factor (SCF), and fms-like tyrosine kinase 3 ligand act as positive regulators of MK development (17,31). There are also several cytokines such as transforming growth factor-beta (TGF-␤), platelet factor 4, and interleukin 4 (IL4) that are documented as negative regulators of MK development (31).…”