Systemic immune-inflammation index in fibromyalgia and rheumatoid arthritis patients and relationship with disease activity

Aim: Rheumatoid arthritis (RA) is an chronic inflammatory rheumatic disease. Although the etiology of fibromyalgia syndrome (FMS) is not known exactly, there are studies showing that inflammatory processes are effective. The systemic immune inflammation index (SII) is a biomarker that has been shown to be an effective prognostic factor in diseases with inflammation-related etiology. In our study, we examined the change of SII in FMS and RA patients, its status compared to the healthy group, and its relationship with disease activity. Materials and methods: Ages between 18-65, 40 FMS patients, 36 RA patients, and 39 healthy individuals as the control group were included in the study. Demographic information of all participants was obtained. The pain of the patients was determined by the visual pain score (VAS). The Fibromyalgia Impact Questionnaire (FIQ) was completed to determine disease activity in FMS patients. Disease Activity Score (DAS28-ESR) was calculated to determine disease activity in RA patients. RA and FMS groups were divided into groups according to their disease activity. Blood samples were taken for complete blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) tests from all participants. Platelet distribution width (PDW), red cell distribution width (RDW), neutrophil lymphocyte ratio (NLR), platelet lymphocyte ratio (PLR) and systemic immune inflammation index (SII) were calculated from the complete blood count. CRP, ESR, SII, PDW, RDW, NLR, PLR were compared between the patient and control groups. The correlation of these indices with DAS28-ESR in the RA group and with the FIQ score in the FMS group was analyzed. Findings: CRP was found to be significantly higher in FMS group compared to the control group (p<0.001), but no correlation was found with disease severity (p=0.455). There was no significant difference between FMS and RA in terms of CRP values. Statistically significant relationship was found between FIQ score and SII (p<0.001). The cut-off value was calculated to distinguish the group with high disease activity according to the FIQ score. The cut-off value is 517.81 with 68% sensitivity and 80% specificity. CRP in RA was found to be significantly higher than the control group (p<0.001) and positively correlated with disease activity (p=0.018). In RA group, it was shown that inflammatory markers (SII, NLR, PLR) were suppressed in patients using anti-TNF drugs compared to non-users (SII p=0.024, NLR p= 0.038, PLR p=0.026). In the comparison of the patients who did not use anti-TNF and the control group, SII, NLR, PLR were found to be significantly higher in the patient group. (SII p=0.006, NLR p=0.025, PLR=0.019). The median values of SII were 586.79 in the RA group, 517.81 in the FMS group, and 450.97 in the control group. Although the median values of SII in RA and FMS were higher than the control group, no significant difference was found between the groups (p=0.165). The RDW in RA was found to be significantly higher than in the FMS and control groups (p=0.019), and no correlation was found between RDW and disease severity (p=0.936) Conclusion: The increase in SII with disease activity in FMS supports the role of inflammatory processes in the etiopathogenesis. SII can be used as a new biomarker in FMS, as a cheap and easily available parameter in demonstrating and monitoring disease activity. The fact that SII is higher in RA patients who do not use anti-TNF drugs compared to those who use anti-TNF drugs indicates that anti-TNF drug therapy suppresses SII. Key words: Systemic immune inflammation index, rheumatoid arthritis, fibromyalgia syndrome