Inflammation-mediated changes in haemostatic variables of pulmonary tuberculosis infected subjects in the course of treatment.

Abstract Background Tuberculosis (TB) is a chronic infectious disease usually marked by a high level of inflammatory response. Haemostasis and inflammation are closely linked both in health and disease in such a way that inflammation leads to activation of the haemostatic system that in turn influences inflammatory activity. This prospective follow-up study was designed to assess inflammation-mediated changes in haemostatic variables of pulmonary tuberculosis infected subjects in the course of therapy. Method A total of 60 TB-infected individuals, aged 18-65 years participated in the study. The individuals were recruited before commencement of therapy and followed up to 6 month into therapy. Tuberculosis was diagnosed using Ziehl Neelsen acid-fast bacilli test and GeneXpert MTB/RIF assay. Pro-inflammatory cytokines: tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-2 (IL-2), anti-inflammatory cytokines: interleukin-10 (IL-10), transforming growth factor-beta (TGF-β) and haemostatic variables: thrombopoietin (TPO) P-selectin (P-SEL), platelet activating factor (PAF), platelet factor-4 (PF-4) and GP IIb/IIIa complex were measured by ELISA methods. These parameters were measured at pre-treatment, 2 month and 6 month into therapy. Data were analyzed using SPSS version 22. Results The results showed that TNF-α, IL-6, IL-2 (pro-inflammatory cytokines) and P-selectin, GP IIb/IIIa, thrombopoietin (haemostatic variables) were significantly increased at 2 month into therapy compared to pre-treatment values (p= <0.001, <0.001, <0.001, 0.015, 0.035 and 0.017 respectively) and decreased at 6 month into therapy. Also at 6 month into therapy in comparison to 2-month into therapy, there were significant increase in IL-10 and TGF-β (anti-inflammatory cytokines) (p=0.020 and 0.001 respectively) as well as a significant decline in PF-4 (p=0.030). There were significant positive correlations between GP IIb/IIIa and TNF-α (r=0.372; p=0.031), IL-6 and PSEL (r=0.413; p=0.027), IL-6 and TPO (r=0.335; p=0.046), PF4 and TGF-β (r=0.463; P=0.006), while PAF correlated negatively with TGF-β (r=-0.368; p=0.032). Conclusion The changes in the pro- inflammatory cytokines (TNF-α, IL-6, IL-2) aligned with changes in the levels of P-selectin, GP IIb/IIIa, and TPO in the course of TB therapy. This suggests that inflammation modulates the levels of these haemostatic variables in TB individuals.