Comparative systemic inflammatory marker patterns across Hashimoto’s thyroiditis, Graves’ disease, and non-autoimmune goiter

Abstract

Introduction: Autoimmune thyroid diseases (AITDs), including Hashimoto’s thyroiditis (HT) and Graves’ disease (GD), are characterized by immune-mediated thyroid dysfunction. However, whether systemic inflammatory burden differs among thyroid disease phenotypes remains unclear.Methods: In this cross-sectional study, 100 adult patients (HT n=60, GD n=11, goiter n=29) were evaluated. Serum C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), neutrophil-to-lymphocyte ratio (NLR), and procalcitonin levels were compared among groups using the Kruskal–Wallis test with Bonferroni-adjusted post-hoc analyses. General linear models adjusted for age, sex, and disease duration were applied. Associations between inflammatory markers and thyroid parameters were assessed using Spearman correlation analysis.Results: CRP (p=0.638), ESR (p=0.135), and NLR (p=0.466) did not differ significantly among the three thyroid phenotypes. Although statistically significant differences in procalcitonin levels were observed between groups (p=0.031), lower measurable values were observed in the Graves’ disease group, and this difference remained significant after adjustment for confounders (adjusted p=0.041). Correlation analyses demonstrated generally weak associations between inflammatory markers and thyroid autoantibodies, with only a modest correlation between procalcitonin and TRAb reaching statistical significance (r=0.22, p=0.048).Conclusions: Routine systemic inflammatory markers do not meaningfully distinguish autoimmune from non-autoimmune thyroid disease phenotypes. Although procalcitonin demonstrated a phenotype-related difference, its clinical relevance remains uncertain. These findings support the concept that autoimmune thyroid diseases predominantly reflect localized rather than systemic inflammatory activation.