Diabetes mellitus is a group of metabolic disorders of carbohydrate metabolism in which glucose is both underutilized as an energy source and overproduced due to inappropriate gluconeogenesis and glycogenolysis, resulting in hyperglycaemia1. About 537 million people are living with diabetes. This number is predicted to rise to 643 million by 2030 and 783 million by 20452. In India, there are estimated 77 million people above the age of 18 years who are suffering from type 2 diabetes mellitus3. In Kashmir valley, Rice (Oryza sativa; carbohydrate diet) is a staple food. Rapid urbanization and sedentary lifestyle of people are believed to be risk factors leading to the pathogenesis of T2DM in this region with prevalence of 6.1%4,5,6. Poorly controlled diabetes leads to various microvascular complications and oxidative stress causing oxidative damage to tissues and cells7,8. In addition, increasing evidence suggests that T2Dm is associated with significant alteration in hematological parameters9. Patients with type 2 diabetes mellitus are twice more likely to be prone to anemia than patients without T2DM10. Simple hematological indices obtained from routine blood counts, including neutrophil-to-lymphocyte ratio (NLR)and platelet indices, have emerged as potential low-cost markers of inflammation and disease severity in diabetes11. Despite growing interest in the clinical utility of hematological parameters in diabetes management, data from the Kashmir region remain limited. The unique dietary habits, lifestyle factors, and geographic characteristics of this population may influence both glycemic control and inflammatory responses. Therefore, the present study was undertaken to evaluate the hematological profile of patients with type 2 diabetes mellitus and to assess its correlation with glycemic control as measured by HbA1c.

Study Design and setting- This cross-sectional observational study included 234 patients with type 2 diabetes mellitus aged >35 years, enrolled from March 2022 to February 2024 from the outpatient department of General Medicine, Government Medical College, Srinagar, after informed consent. Ethical approval was obtained from the Institutional Ethics Committee. Patients were categorized into two groups based on glycemic control: good glycemic control (HbA1c ≤7%) and poor glycemic control (HbA1c >7%). Inclusion Criteria • Patients aged >35 years • Diagnosed cases of type 2 diabetes mellitus as per American diabetes association standards of care 2022 • Any duration of type 2 diabetes mellitus. Exclusion Criteria • Type 1 diabetes mellitus • Gestational diabetes • Known hematological malignancies • Chronic liver disease • Chronic kidney disease • Active infection or inflammatory conditions • Malignancy • Patients on drugs affecting hematological parameters like chemotherapeutic drugs. Clinical and Laboratory Assessment: Detailed demographic and clinical data were recorded, including age, sex, duration of diabetes, and body mass index (BMI). The Quetelet index formula was used to calculate BMI. Venous blood samples were collected after an overnight fast. Glycemic control was assessed using glycated hemoglobin (HbA1c), measured by ARCHITECT4000 SYSTEM. Complete blood counts including hemoglobin, total leukocyte count, differential count, platelet count, and platelet indices were analysed using fully automated SYSMEX 6-part analyser (XN-550, XN-1000). Statistical Analysis: Collected data were tabulated in Microsoft Excel and arranged for analysis. Quantitative data were expressed as mean ± SD, and qualitative data as percentages. For the comparison of quantitative and qualitative data, the t-test and Chi-squared test were used, respectively. The Pearson correlation coefficient was used to determine correlations between variables. A p-value of <0.05 was considered significant

The baseline demographic and clinical characteristics of the study population are shown in Table 1. A total of 234 patients with T2DM were included in the study. The mean age was 54.5 ± 10.4 years, with 150 (64.1%) females and 84 (35.9%) males. Poor glycemic control (HbA1c >7%) was observed in 204 (87.2%) patients, while 30 (12.8%) patients had HbA1c ≤7%. Table 1: Baseline demographic and clinical characteristics of study participants (n=234) Variables Category Value Age in Years (mean + SD) mean ± SD 54.5 ± 10.4 Gender Male n(%) 84 (35.9) Female n(%) 150 (64.1) Duration of diabetes (years) mean ± SD 7.6 ± 4.2 Body mass index (kg/m²) mean ± SD 26.1 ± 3.4 HbA1c Levels <7% n(%) 30 (12.8) >7% n(%) 204 (87.2) The distribution of hematological parameters among the study participants is shown in Table 2. The mean hemoglobin level was 12.38 ± 2.08 g/dL, with a mean total leukocyte count of 7.84 ± 2.31 ×10⁹/L. Platelet parameters revealed a mean platelet count of 185.2 ± 6.38 ×10⁹/L, mean platelet volume of 13.08 ± 2.06 fL, and platelet large cell ratio of 43.95 ± 3.48%. Inflammatory markers showed an elevated mean erythrocyte sedimentation rate of 38.95 ± 2.99 mm/hr. Table 2: Distribution of hematological parameters among patients with type 2 diabetes mellitus (n = 234) Parameter Mean ± SD Hemoglobin (g/dL) 12.38 ± 2.08 Total leukocyte count (×10⁹/L) 7.84 ± 2.31 Neutrophils (%) 63.5 ± 9.4 Lymphocytes (%) 28.1 ± 7.2 Platelet count (×10⁹/L) 185.2 ± 6.38 Mean platelet volume (fL) 13.08 ± 2.06 Platelet distribution width (%) 16.40 ± 1.98 Platelet large cell ratio (%) 43.95 ± 3.48 Red cell distribution width (%) 14.6 ± 1.9 ESR (mm/hr) 38.95 ± 2.99 The comparison of hematological parameters between male and female patients with type 2 diabetes mellitus is presented in Table 3. Male patients had significantly higher hemoglobin levels compared to females (11.67 ± 2.89 g/dL vs 10.66 ± 1.17 g/dL; p = 0.0002). Plateletcrit was also significantly higher among females (p = 0.03). No statistically significant gender-based differences were observed in total leukocyte count, differential counts, red cell indices, platelet count, platelet indices, erythrocyte sedimentation rate. Table 3: Comparison of hematological parameters between male and female patients with type 2 diabetes mellitus Hematological parameter Males (Mean ± SD) Females (Mean ± SD) p-value Hemoglobin (g/dL) 11.67 ± 2.89 10.66 ± 1.17 0.0002 Total leukocyte count (×10⁹/L) 7.48 ± 1.97 8.07 ± 2.07 0.262 Neutrophils (%) 62.75 ± 10.76 62.33 ± 10.20 0.870 Lymphocytes (%) 28.68 ± 18.94 27.76 ± 10.14 0.810 Mean corpuscular volume (fL) 84.39 ± 11.37 83.86 ± 6.45 0.820 Mean corpuscular hemoglobin (pg) 29.41 ± 2.89 27.76 ± 2.91 0.061 Mean corpuscular hemoglobin concentration (g/dL) 32.52 ± 2.51 31.84 ± 2.40 0.280 Red cell distribution width (%) 14.20 ± 1.56 15.33 ± 3.63 0.120 Platelet count (×10⁹/L) 186.4 ± 71.84 187.71 ± 64.34 0.960 Platelet distribution width (%) 16.21 ± 3.13 16.51 ± 3.75 0.730 Mean platelet volume (fL) 12.79 ± 1.71 13.26 ± 2.13 0.340 Platelet large cell ratio (%) 42.80 ± 9.55 44.59 ± 9.57 0.470 Plateletcrit (%) 0.25 ± 0.08 0.30 ± 0.10 0.030 Hematocrit (%) 38.29 ± 2.06 34.12 ± 1.75 0.080 Erythrocyte sedimentation rate (mm/hr) 35.12 ± 13.81 41.11 ± 19.44 0.170 Comparison of hematological parameters based on glycemic control is shown in Table 4. Patients with poor glycemic control (HbA1c >7%) had significantly lower hemoglobin levels and higher total leukocyte counts compared to those with HbA1c ≤7%. Neutrophil percentage, platelet count, platelet distribution width, platelet large cell ratio, and mean platelet volume were significantly higher in patients with HbA1c >7%. Inflammatory markers, including erythrocyte sedimentation rate, were also significantly elevated in the poor glycemic control group. No statistically significant differences were observed in hematocrit, mean corpuscular hemoglobin concentration, red cell distribution width. Table 4: Comparison of hematological parameters between patients with HbA1c ≤7% and HbA1c >7% Hematological parameter HbA1c ≤7% (n=30) Mean ± SD HbA1c >7% (n=204) Mean ± SD p-value Hemoglobin (g/dL) 12.5 ± 2.0 11.1 ± 2.2 0.049 Total leukocyte count (×10⁹/L) 7.8 ± 1.7 8.1 ± 2.0 0.006 Neutrophils (%) 63.3 ± 7.7 71.3 ± 10.7 0.020 Lymphocytes (%) 29.3 ± 7.7 27.7 ± 26.7 0.041 Platelet count (×10⁹/L) 150.6 ± 40.1 191.1 ± 68.6 0.002 Platelet distribution width (%) 14.3 ± 2.7 16.5 ± 3.6 0.040 Platelet large cell ratio (%) 43.6 ± 7.1 46.0 ± 9.8 0.021 Plateletcrit (%) 0.3 ± 0.1 0.2 ± 0.1 0.070 Mean platelet volume (fL) 11.0 ± 2.0 14.0 ± 1.9 0.030 Hematocrit (%) 35.5 ± 2.6 35.6 ± 2.7 0.860 Mean corpuscular volume (fL) 84.0 ± 8.1 90.1 ± 8.6 0.030 Mean corpuscular hemoglobin (pg) 28.1 ± 2.6 30.7 ± 3.1 0.040 Mean corpuscular hemoglobin concentration (g/dL) 31.9 ± 2.6 32.1 ± 2.4 0.650 Red cell distribution width (%) 14.8 ± 1.2 14.9 ± 3.3 0.770 Erythrocyte sedimentation rate (mm/hr) 37.9 ± 15.1 46.0 ± 18.0 0.020 The association between glycemic control and inflammatory indices is shown in Table 5. Patients with poor glycemic control (HbA1c >7%) had significantly higher absolute neutrophil counts and lower absolute lymphocyte counts compared to those with HbA1c ≤7%. The neutrophil–lymphocyte ratio was also higher in patients with poor glycemic control, reaching borderline statistical significance. Table 5: Association of glycemic control with neutrophil–lymphocyte ratio (NLR) in Parameter HbA1c ≤7% (Mean ± SD) HbA1c >7% (Mean ± SD) p-value Absolute neutrophil count (×10⁹/L) 4.5 ± 2.7 7.3 ± 2.5 0.002 Absolute lymphocyte count (×10⁹/L) 2.2 ± 1.2 2.0 ± 0.9 0.040 Neutrophil–lymphocyte ratio (NLR) 2.04 ± 0.40 3.65 ± 1.30 0.050 Pearson correlation analysis showed a significant negative correlation between HbA1c and hemoglobin levels. HbA1c demonstrated significant positive correlations with platelet count, mean platelet volume, platelet distribution width, platelet large cell ratio, total leukocyte count, neutrophil percentage, neutrophil–lymphocyte ratio, and erythrocyte sedimentation rate (Table 6) (p < 0.05). Table 6: Pearson correlation analysis between HbA1c and selected hematological and inflammatory parameters (n = 234) Parameter Pearson correlation coefficient (r) p-value Hemoglobin (g/dL) −0.28 0.001 Platelet count (×10⁹/L) +0.31 <0.001 Mean platelet volume (fL) +0.39 <0.001 Platelet distribution width (%) +0.30 0.002 Platelet large cell ratio (%) +0.27 0.004 Total leukocyte count (×10⁹/L) +0.29 0.001 Neutrophil percentage (%) +0.35 <0.001 Neutrophil–lymphocyte ratio +0.43 <0.001 Erythrocyte sedimentation rate (mm/hr) +0.37 <0.001

Persistent hyperglycemia triggers a cascade of interconnected alterations that contribute to endothelial dysfunction and the development of vascular complications in diabetes. Elevated glucose promotes the formation of advanced glycation end products, activates protein kinase C, and disrupts the polyol pathway- mechanisms that together drive the progression of diabetic vascular disease.12. Individuals with type 2 diabetes mellitus (T2DM) exhibit a heightened predisposition to coagulation abnormalities and thromboembolic complications. This increased risk has been attributed to enhanced platelet activation, augmented adhesion, and excessive aggregation, processes driven by underlying metabolic derangements, insulin resistance, persistent hyperglycemia, and dyslipidemia13. Multiple factors contribute to sustained platelet activation and enhanced secretion of pro thrombotic mediators in type 2 diabetes mellitus (T2DM). These include systemic inflammatory processes, disturbances in calcium homeostasis, diminished nitric oxide bioavailability, and aberrant phosphorylation and glycosylation of cellular proteins, all of which collectively promote a pro coagulant state14. Elevated mean platelet volume (MPV) is closely linked with prediabetes, type 2 diabetes, and diabetic vascular complications, reflecting platelet hyperactivity and heightened thrombotic risk15. Furthermore, the literature highlights a significant association between mean platelet volume (MPV) and impaired glucose regulation in individuals with diabetes, suggesting that altered platelet indices may serve as markers of metabolic dysregulation and heightened thrombotic risk16. Similar to mean platelet volume (MPV), increased platelet distribution width (PDW) has been reported in association with diabetes and its vascular complications, reflecting heightened platelet heterogeneity and a pro thrombotic tendency in affected individuals17. Studies show conflicting results: some report a positive association between diabetes and platelet count, while others find no significant relationship 18. Elevated total leukocyte count (TLC) is a marker of inflammation, closely linked with hyperglycemia and insulin resistance in diabetes19. Moreover, increased levels of PLR and NLR have been reported in T2DM and diabetes-related nephropathy20. In the present study, 234 patients were enrolled. The majority were between 51 and 60 years of age (35%), consistent with the findings of Mathur et al. (2022), who reported the highest prevalence of impaired fasting glucose and diabetes among individuals aged 50–69 years21. In this study, the gender distribution revealed a higher prevalence among females (64.1%) compared to males (35.9%). This pattern is consistent with the findings of Pradeepa R, Mohan V, et al. (2021), who reported a greater lifetime risk of diabetes in women (64.6%) than in men (35.4%)22. The higher prevalence of diabetes in women may be explained by hormonal changes, greater body fat, gestational diabetes risk, lower physical activity, and limited healthcare access, collectively increasing lifetime risk compared to men23. In this study, 59% of patients were overweight (BMI 25–29.9). Obesity is a well-established risk factor for type 2 diabetes, consistent with the findings of Bray and Bellanger (2006), who emphasized its strong association with metabolic syndrome and increased diabetes risk24. The comparison of blood parameters between those with HBA1C ≤7 and those with HBA1C >7 revealed significant differences, indicating the systemic effects of poor glycemic control. In this study, we found that among white blood cell indices, inflammatory markers such as total WBC count, neutrophil count were significantly higher in patients with poorly controlled T2DM compared to those with good control. The study demonstrated that patients with HbA1c ≤7% had a mean TLC of 7.8 (SD 1.7), whereas those with HbA1c >7% showed a higher mean TLC of 8.1 (SD 2.0), a statistically significant difference (p = 0.006). Neutrophil counts were also significantly elevated in patients with HbA1c >7% (71.3%) compared to those with HbA1c ≤7% (63.3%) (p = 0.02). These findings are consistent with Prakash S et al. (2020), who reported increased TLC in uncontrolled diabetics25, and Kumar VS et al. (2020), who observed higher neutrophil percentages in poorly controlled cases (80%) versus controlled cases (65%) (p < 0.001)26. Differential WBC counts are likely altered in patients with T2DM as a consequence of hyperglycemia. Elevated TLC serves as a key indicator of systemic inflammation, and epidemiological studies have demonstrated a direct correlation between WBC count and the development of T2DM related complications27. Under hyperglycaemic conditions, WBCs are activated via oxidative stress, while the concurrent cytokine-driven inflammatory response contributes to vascular complications in diabetes. Additional inflammatory markers, such as neutrophils are likewise implicated in the pathogenesis of vascular complications in T2DM28. The study also observed lower lymphocyte counts in patients with HbA1c >7% (27.7%) versus those with HbA1c ≤7% (29.3%) (p = 0.041). Our study demonstrated that the neutrophil-to-lymphocyte ratio (NLR) was significantly elevated in patients with HbA1c >7% (3.65 ± 1.3) compared to those with HbA1c ≤7% (2.04 ± 0.4) (p = 0.05). These findings are consistent with prior reports: Hussain et al. (2017) observed higher NLR in poorly controlled diabetics (4.3 ± 2.8, p = 0.001), Varma et al. (2021) documented increased NLR in patients with HbA1c >9% (6.30 ± 2.646, p < 0.001)11,29. Elevated neutrophil-to-lymphocyte ratio (NLR) in patients with poor glycemic control can be explained by the pro-inflammatory milieu of hyperglycemia. High glucose levels promote oxidative stress and stimulate neutrophil activation, while simultaneously suppressing lymphocyte function, thereby shifting the immune balance toward neutrophilia. This imbalance reflects systemic inflammation, which plays a central role in the pathogenesis of vascular complications in type 2 diabetes mellitus (T2DM)30. HbA1c has a direct positive correlation with TLC (r = 0.29, p = 0.001), neutrophils (r = 0.35, p <0.001), NLR (r = 0.43, p <0.001) in our study. Red blood cell indices, like hemoglobin, MCV, and MCH, were significantly lower in the uncontrolled diabetic group compared to the controlled diabetic group (p < 0.05), while ESR was found to be significantly higher in the uncontrolled diabetic group (mean 46.0) compared to the controlled diabetic group (mean 37.9) (p = 0.02). Several studies have demonstrated that patients with diabetes are at increased risk of anemia, primarily due to impaired renal function and diminished erythropoietin production, which ultimately leads to a reduction in red blood cell count31. HbA1c has a direct positive correlation with ESR (r = 0.37, p <0.001), significant negative correlation with hemoglobin (r = −0.28, p = 0.001) A plausible explanation for this difference is that chronic hyperglycemia induces nonenzymatic glycosylation of red blood cell (RBC) membrane proteins, accelerating RBC aging. The marked elevations in hematocrit (HCT) and mean corpuscular volume (MCV) are likely attributable to morphological alterations in RBCs and plasma compositional changes commonly observed in type 2 diabetes mellitus (T2DM)32. Platelet indices including PLT, PDW, MPV, and P-LCR were found to be significantly elevated in the uncontrolled diabetic group compared to the controlled group (p < 0.005). These results align with the observations of Jindal et al. (2011)33, who reported increased platelet indices in diabetics with microvascular complications, and Demirtunc et al. (2009), who associated poor glycemic control with enhanced platelet activation and elevated MPV34. HbA1c demonstrated a positive correlation with platelet count (r = 0.31, p <0.001), MPV (r = 0.39, p <0.001), PDW (r = 0.30, p = 0.002), and P-LCR (r = 0.27, p = 0.004) Platelet indices such as PLT, PDW, MPV, and P-LCR are elevated in uncontrolled diabetes because chronic hyperglycemia induces platelet activation, oxidative stress, and endothelial dysfunction, which together create a prothrombotic state. This leads to larger, more reactive platelets (reflected in higher MPV and PDW) and increased platelet turnover, contributing to vascular complications in type 2 diabetes mellitus (T2DM)35.

The present study demonstrates that poor glycemic control in type 2 diabetes mellitus is associated with significant alterations in hematological and inflammatory parameters. HbA1c showed meaningful associations with markers of systemic inflammation such as neutrophil–lymphocyte ratio, total leukocyte count, and erythrocyte sedimentation rate, as well as with platelet indices including mean platelet volume, platelet distribution width, and platelet large cell ratio, reflecting an increased inflammatory and pro-thrombotic state. These findings suggest that easily available and inexpensive hematological indices can serve as useful adjunctive markers for assessing the severity of glycemic dysregulation and the associated risk of complications in patients with type 2 diabetes mellitus, particularly in resource-limited primary care settings. LIMITATIONS The sample size was limited, and for confirmation of results, we need a larger sample size. It was a single-center, observational, crosssectional study, and if it had been multicentric, we might have had different results due to a different study population

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