Inflammation of Disconnection: Exploring the Link Between Continuity of Care and Systemic Immune-Inflammation Index (SII) in Rural Primary Care

Busra Bilik Sezer, Solmaz Alkan, Emel Ucarer

Keywords: Continuity of Care (CoC), Systemic Immune-Inflammation Index (SII), Family Medicine, Dyslipidemia, Inflammation

Background:

Continuity of Care (CoC) is a fundamental determinant of health outcomes; fragmented care may induce psychosocial stress and low-grade systemic inflammation. In dyslipidemic patients, persistent inflammation despite achieving LDL targets represents a significant "residual risk." This pilot study investigated whether the Systemic Immune-Inflammation Index (SII)-an accessible hemogram-derived parameter-could serve as a biological reflection of CoC and an indicator of persistent inflammatory risk.

Research questions:

1)Can SII serve as a biological indicator of CoC in primary care populations?
2)Does SII predict residual inflammatory risk in dyslipidemic patients achieving LDL targets?
3)How do interactions between age, CoC, and SII influence long-term cardiovascular outcomes in family medicine?

Method:

This retrospective cross-sectional study included 198 patients (97 screening, 101 follow-up) from a rural primary care unit in Türkiye. Participants were registered for 1 year and screened or treated for dyslipidemia. CoC levels (High/Low) were categorized via the Bice Index over 12 months. SII was calculated as (neutrophils x platelets) / lymphocytes.

Results:

The follow-up group had significantly higher mean primary care visit (9.3 ± 4.38) and hospital admission frequencies (9.6 ± 6.25) than the screening group (p < 0.05). A positive correlation was observed between age and SII (r = 0.171, p = 0.016). Mean SII was higher in the high-CoC group (500.5 ± 246.8) compared to the low-CoC group (438.7 ± 186.9), though the difference was not statistically significant (p = 0.317). The predictive value of SII for cardiovascular risk was limited (AUC: 0.505, p = 0.91), while age remained the strongest independent predictor (OR: 1.073, p < 0.001).

Conclusions:

SII may reflect age-related inflammatory burden as an accessible “biological mirror.” The absence of a significant CoC–SII relationship may relate to the small low-CoC subgroup. Persistent SII elevation despite LDL control supports integrating inflammatory markers as potential “early warning systems” in cardiovascular risk monitoring.

Points for discussion:

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