Recent studies on murine models have shown that maturation of platelets takes place, to some extent in the lungs, this raises the possibility that chronic lung diseases could affect platelet maturation or count [4]. Chronic lung disease carries many challenges for the patients and their caregivers, such as having an unpredictable clinical course, absence of a definitive treatment, restriction of activities whether due to the disease or the medications as well as later psychosocial effects [2]. Our study found a significant rise in platelet count in the patients group when compared against the normal control group, this comes in agreement with the study by Maclay et al. [12] which may be attributed to hypoxemia, underlying inflammation, and oxidative stress, although it disagrees with results obtained by Skoczyński et al. [13] both studies however were carried on adult COPD patients.
In agreement with our current study, the number of platelets in the COPD patients was inversely associated with the hemoglobin level [13]. The cause of anemia in COPD is related to certain pro-inflammatory markers, at least a component of the anemia is attributable to inflammation (anemia of chronic disease) [14].
CLD is associated with low-grade systemic inflammation, activation of circulating inflammatory cells, and increased levels of inflammatory cytokines. This is postulated to explain the significant rise in both CRP and ESR among the patients group when compared to the normal control. We also found a significant reduction in the MPV among patients, and when the patients’ group was subdivided into Interstitial lung disease and non-CF bronchiectasis both subgroups still had a significantly lower MPV when compared to the normal control but not when compared to each other. Low levels of MPV are associated with high-grade inflammatory diseases and reverse in the course of anti-inflammatory therapy [15].
Mean platelet volume (MPV) is one of the parameters routinely generated by blood counters; it reflects the platelet production rate and stimulation. An inverse correlation between MPV and disease activity was demonstrated in inflammatory bowel diseases, rheumatoid arthritis, and ankylosing spondylitis [16]. Other studies have demonstrated elevated MPV values in COPD patients [17]. In 2016, Agapakis and coauthors concluded that MPV may be an inflammatory marker and could be a useful tool to detect patients with an increased risk of exacerbation as the mean platelet volume levels were significantly decreased in the exacerbation period in a study carried on adult COPD patients [18].
Proinflammatory cytokines such as CRP, tumor necrosis factor-α, and interleukin-6 are increased in COPD and contribute to the generation of oxidative stress with subsequent platelet activation and also MPV reduction [19]. Moreover, the previous hypothesis is supported by the significantly higher CRP and ESR among the patients’ group compared to the normal control group. In our study, the MPV levels had a significant negative correlation with elevated CRP, as the higher CRP values are associated with lower MPV, this comes in agreement with the findings of Agapakis et al. [18] However, this finding does not agree with the results obtained by Kalemci et al. [20] were they reported a significant increase in MPV with increasing severity of adult COPD yet, in agreement with the current study they reported an increase in platelets count and subsequently PCT with increased severity of adult COPD.
Plateletcrit represents the actual platelet mass as it constitutes the percentage of the volume that platelets occupy in blood, it normally ranges around 0.2% blood volume. For such an important role and variable functions to be concentrated in this small volume, this makes the research of variations in platelets number and volume of big value [8].