Objectives: The adverse effects of smoking in various pathologies are mediated by its effects on the inflammatory system. The monocyte to high-density lipoprotein cholesterol (HDL-C) ratio (MHR) has recently emerged as an indicator of inflammation. We aimed to investigate the relationship between MHR and cigarette smoking. Patients and Methods: Three hundred and ninety seven consecutive participants who smoke and 515 healthy subjects with no history of smoking enrolled in the study. Complete blood count parameters and lipid profile were analyzed in all study participants. Smoking habits were calculated as pack.years and number of cigarettes smoked per day. Results: MHR levels were significantly higher in smokers compared to non-smokers (respectively, 15.71 (12.02–20.00) and 11.17 (8.50–14.16), p < 0.0001)). Pearson’s correlation analysis revealed a weak but positive correlation between pack.year and MHR in the smokers group, and there was a moderate positive correlation between the number of cigarettes smoked daily and MHR in the group. In receiver operating characteristics (ROC) analyses, it was determined that a MHR value >13.00 measured in smoker participants at application had a predictive specificity of 66.6% and sensitivity of 70.0% for smoking (area under the curve [AUC] 0.729, 95% CI 0.696, 0.762; p < 0.0001). Conclusions: Elevated MHR is associated with cigarette smoking and may be a useful indicator of a systemic inflammatory response in smokers. Smoker participants who have high MHR levels can easily be identified during routine complete blood count (CBC) analysis and could possibly benefit from preventive treatment.

Our study demonstrated that MPV and NLR levels are increased despite similar hsCRP levels in patients with PCOS. However, we failed to demonstrate these differences in obese PCOS patients. Further studies with larger sample size are required to determine the significance of BMI in the inflammation of PCOS patients.

Objective Smoking has been proven to increase systemic inflammation in previous studies using different biomarkers. The eosinophil-to-lymphocyte ratio (ELR), neutrophil-to-lymphocyte ratio (NLR), and lymphocyte-to-monocyte ratio (LMR) are new indicators of systemic inflammation that are used as predictors of systemic inflammation, morbidity, and mortality associated with many diseases. We investigated the effects of smoking on these inflammatory indicators. Methods In total, 616 consecutive smoking healthy subjects and 387 age-matched nonsmoking healthy subjects were enrolled. White blood cell counts (neutrophils, lymphocytes, basophils, eosinophils, and monocytes) were determined by electrical impedance with an automatic blood cell counting device. The ELR, LMR, and NLR were calculated based on these cell counts. Smoking habits of participants were calculated as pack/year. Results The NLR and ELR were significantly higher and the LMR was significantly lower in smokers than nonsmokers. The pack-years were positively correlated with the NLR and ELR and negatively correlated with the LMR. Conclusion A high NLR and ELR and low LMR are associated with cigarette smoking and may be useful indicators of systemic inflammation activity, even in healthy smokers. Smokers with a high NLR and ELR and low LMR can easily be identified during routine blood analysis and might benefit from preventive treatment.

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ObjectiveTo determine whether neutrophil/lymphocyte ratio (NLR) differed between patients with isolated coronary artery disease (CAD), isolated coronary artery ectasia (CAE), coronary slow flow and normal coronary anatomy.MethodsPatients who underwent coronary angiography were consecutively enrolled into one of four groups: CAD, coronary slow flow, CAE and normal coronary anatomy.ResultsThe CAD (n = 40), coronary slow flow (n = 40), and CAE (n = 40) groups had similar NLRs (2.51 ± 0.7, 2.40 ± 0.8, 2.6 ± 0.6, respectively) that were significantly higher than patients with normal coronary anatomy (n = 40; NLR, 1.73 ± 0.7). Receiver operating characteristics demonstrated that with NLR > 2.12, specificity in predicting isolated CAD was 85% and sensitivity was 75%, with NLR > 2.22 specificity in predicting isolated CAE was 86% and sensitivity was 75%. With NLR > 1.92, specificity in predicting coronary slow flow was 89% and sensitivity was 75%. Multivariate logistic regression analyses identified NLR as an independent predictor of isolated CAE (β = −0.499, 95% CI −0.502, −0.178; P <  0.001), CAD (β = −0.426, 95% CI −1.321, −0.408; P <  0.001), and coronary slow flow (β = −0.430, 95% CI −0.811, −0.240; P = 0.001 Table 2).ConclusionsNLR was higher in patients with CAD, coronary slow flow and CAE versus normal coronary anatomy. NLR may be an indicator of CAD, CAE and coronary slow flow.