Association of Low Free T3 with Disease Presence and Activity in Ankylosing Spondylitis.

Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by axial skeletal involvement and systemic metabolic changes. While inflammation is central to its pathophysiology, the potential role of thyroid hormones, particularly free triiodothyronine (FT3), in disease risk and activity remains underexplored. The objective of this study is to evaluate the relationship between serum FT3 levels and both the presence and clinical activity of AS, while also examining other endocrine-metabolic parameters. In this cross-sectional study, 120 AS patients and 117 healthy controls were assessed. Demographic, anthropometric, hematologic, and biochemical parameters were recorded. Disease activity was determined using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), with BASDAI ≥ 4 indicating active disease. Logistic regression models adjusting for age, sex, BMI, and other relevant covariates were applied to identify independent predictors. FT3 levels were significantly lower in AS patients compared to controls (3.25 [3.01-3.58] vs. 3.44 [3.16-3.69] pg/mL, = 0.037) and in patients with BASDAI ≥ 4 versus BASDAI < 4 (3.20 [2.94-3.48] vs. 3.44 [3.19-3.83] pg/mL, = 0.004). The reduction was more evident in women, where it reflected disease presence, whereas in men it was associated with high disease activity. Low FT3 independently predicted both AS (OR 0.50, 95% CI 0.28-0.92, = 0.026) and active disease (OR 0.48, 95% CI 0.24-0.99, = 0.047). Lower HDL-C, BMI, and creatinine, and higher leukocyte counts were also associated with AS, but not with disease activity. Low-normal FT3 is independently associated with both the presence and activity of AS, reflecting disease presence in women and disease activity in men. This is the first study to demonstrate this sex-specific association after adjusting for metabolic parameters and multiple covariates, highlighting FT3's potential as a marker of inflammation-driven metabolic dysregulation.