# Association Between Systemic Immune‐Inflammation Index and Thyroid Function: A Cross‐Sectional Population‐Based Study

## TL;DR

This study found that higher levels of a blood inflammation marker are linked to changes in thyroid hormone levels in U.S. adults.

## Contribution

The study is the first to show a relationship between systemic inflammation and thyroid function in a large population.

## Key findings

- Higher lgSII levels were linked to lower free triiodothyronine and thyroid-stimulating hormone.
- Total thyroxine levels increased with higher lgSII after adjusting for other factors.
- An L-shaped relationship was observed between lgSII and free triiodothyronine and TSH.

## Abstract

The systemic immune‐inflammation index (SII), an emerging inflammatory biomarker, has been associated with various diseases, but its relationship with thyroid function remains unclear. Our study aimed to investigate the potential connections between SII and thyroid function in the U.S. population.

We conducted a cross‐sectional study using the National Health and Nutrition Examination Survey (NHANES) 2007–2012 data to evaluate the association between SII and thyroid function, including free triiodothyronine (FT3), free thyroxine (FT4), total triiodothyronine (TT3), total thyroxine (TT4), and thyroid‐stimulating hormone (TSH). Furthermore, the correlation was evaluated using multiple linear regression, smooth curve fitting, and threshold effect analysis.

After multivariable linear regression, higher lgSII levels were independently associated with lower FT3 (β = −0.17, p < 0.0001), TT3 (β = −3.06, p = 0.0149), and TSH (β = −0.38, p = 0.0204), whereas TT4 levels were positively associated with lgSII after full adjustment (β = 0.27, p = 0.0016). Smooth curve fitting revealed an L‐shaped relationship between lgSII and FT3 and TSH. Threshold effect analysis identified an inflection point at lgSII = 2.29 (log‐likelihood ratio, P < 0.001).

In U.S. adults, lgSII was negatively associated with FT3 and TSH and positively associated with TT4. These findings highlight a potential link between systemic inflammation and thyroid function, warranting further prospective studies to investigate causal relationships.