Insulin Resistance in Patients with Soft Tissue Rheumatism

Background: Soft tissue rheumatism (STR), including plantar fasciitis and supraspinatus tendinopathy, is a leading cause of musculoskeletal pain. Emerging evidence links insulin resistance (IR) and related metabolic disturbances to tendon and fascial pathology through low-grade inflammation, adipokine imbalance, and altered collagen turnover. However, the diagnostic utility of IR indices and the therapeutic value of targeting IR in STR remain uncertain. Objective: To investigate the prevalence of insulin resistance in patients with STR, specifically plantar fasciitis and supraspinatus tendinopathy. Patients and Methods: A case–control study was conducted on 53 overweight or obese patients with STR and 50 age- and sex-matched healthy controls. Anthropometric measures (neck circumference, waist circumference, BMI) and metabolic indices (fasting insulin, fasting glucose, HOMA-IR, insulin/HDL ratio, lipid profile) were assessed. Ultrasound was performed to evaluate tendon and fascia thickness. Associations between STR, insulin resistance, central adiposity, and metabolic parameters were analyzed. Results: STR patients had significantly higher fasting insulin (12.5 vs 6.5 μIU/mL, p < 0.001) and HOMA-IR (2.87 ± 1.37 vs 1.30 ± 0.56, p = 0.01) than controls. The insulin/HDL ratio was also elevated (0.296 vs 0.140, p < 0.001). Neck circumference (38.6 vs 34.6 cm, p < 0.001) and waist circumference (103.3 vs 98.8 cm, p = 0.005) were greater in cases. Ultrasound revealed increased plantar fascia and supraspinatus tendon thickness in STR patients. HOMA-IR correlated positively with tendon/fascia thickness and pain severity. Moreover, metabolic syndrome (62.3% vs 44.0%) and prediabetes (26.4% vs 14.0%) were more frequent in STR, highlighting a strong metabolic link. Conclusion: STR, including plantar fasciitis and supraspinatus tendinopathy, is strongly associated with insulin resistance and central adiposity, independent of BMI. Simple clinical measures such as neck circumference and HOMA-IR may help identify at-risk patients, underscoring the metabolic contribution to STR pathogenesis.