Background Moderate-to-severe plaque psoriasis frequently coexists with metabolic comorbidities, yet the impact of interleukin-17 (IL-17) inhibitors on metabolic parameters remains inadequately characterized. This study evaluated the effects of IL-17 inhibitor therapy on glycemic control, lipid profiles, uric acid, and novel systemic inflammatory indices in psoriasis patients with metabolic comorbidities. Objective This 48-week single-center retrospective study included 30 patients with moderate-to-severe plaque psoriasis (Psoriasis Area and Severity Index [PASI] >= 10 with >= 1 metabolic comorbidity) receiving IL-17 inhibitors (June 2023-December 2024). Fasting glucose, lipid profiles, uric acid, serum beta 2-microglobulin, urinary albumin-to-creatinine ratio (UACR), homocysteine, systemic inflammation response index (SIRI), and systemic immune-inflammation index (SII) were assessed at baseline and weeks 12, 24, 36, and 48. The primary outcome was fasting glucose reduction >= 10% at week 48.Results After 48 weeks of treatment, PASI score decreased from 18.6 +/- 5.4 to 2.8 +/- 1.2 (P < 0.001). Fasting glucose decreased from 6.2 +/- 1.4 to 5.3 +/- 0.9 mmol/L (P < 0.001), triglycerides from 2.1 +/- 0.8 to 1.6 +/- 0.5 mmol/L (P = 0.002), uric acid from 435 +/- 52 to 378 +/- 41 mu mol/L (P < 0.001), and homocysteine from 14.2 +/- 3.5 to 10.8 +/- 2.6 mu mol/L (P < 0.001). SIRI decreased from 1.85 +/- 0.62 to 0.92 +/- 0.31 (P < 0.001), and SII from 680 +/- 145 to 420 +/- 98 (P < 0.001). Multivariate analysis suggested that SIRI reduction may be an independent predictor of glycemic improvement [odds ratio (OR) = 2.68, 95% confidence interval (CI): 1.21-5.93, P = 0.015] in this cohort. Conclusion This study suggests that IL-17 inhibitor therapy is associated with improvements in glycemic control, triglycerides, uric acid, homocysteine, and systemic inflammation in psoriasis patients with metabolic comorbidities. Preliminary evidence indicates that SIRI may serve as a practical clinical indicator for assessing metabolic improvement, although prospective validation is required. However, given the observational design, small sample size, lack of a control group, and absence of systematic data on lifestyle factors and direct measures of insulin resistance, these findings should be interpreted as hypothesis-generating and do not establish causality. Confirmation in larger prospective controlled studies is needed before any clinical recommendations can be made.
[1]Tianjin Acad Tradit Chinese Med, Affiliated Hosp, Dept Dermatol, Tianjin, Peoples R China.
[2]Tianjin Univ Tradit Chinese Med, Tianjin, Peoples R China.
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