EP1755 - LBA_ECE_1325 - Altered myokine profile and reduced muscle strength in primary hyperparathyroidism: reversal after parathyroidectomy

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Abstract Background and Aim Primary hyperparathyroidism (PHPT) is associated with skeletal and neuromuscular manifestations; however, the potential role of myokines in PHPT-related muscle dysfunction remains poorly understood. We aimed to evaluate circulating myokine levels and muscle strength in patients with PHPT and to assess their changes after parathyroidectomy. Methods Fifty-seven patients with primary hyperparathyroidism (PHPT) and 50 age-, sex-, and body mass index (BMI)-matched healthy controls were included. Circulating levels of myostatin, follistatin, decorin, irisin, adiponectin, rantes, and resistin were measured. Muscle strength was assessed using handgrip dynamometry. A subgroup of 30 patients were reassessed after parathyroidectomy with a median follow-up of 134 days. Correlation analyses and adjusted group comparisons were performed. Results Patients with PHPT exhibited significantly higher circulating myostatin levels (30.3 ± 7.2 vs 23.7 ± 8.0 ng/mL, P < .001) and decorin levels (1081.3 vs 852.0 pg/mL, P = .003), accompanied by lower circulating follistatin levels (P = .048). Handgrip strength was also reduced in the PHPT group (24.1 vs 26.6 kgf, P = .03). Circulating myostatin levels showed positive correlations with both PTH (r = 0.346, P < .001) and serum calcium levels (r = 0.373, P < .001). After adjustment for age, sex, and BMI, PHPT status remained a significant determinant of circulating myostatin levels (ANCOVA F = 9.57, P = .003). Parathyroidectomy was associated with significant changes in circulating myokines and muscle strength, marked by a reduction in myostatin levels (30.7 ± 7.7 to 22.7 ± 9.9 ng/mL, P < .001) and concomitant increases in follistatin (P < .001), irisin (P = .003), and handgrip strength (P = .007). Conclusion PHPT is characterized by a distinct circulating myokine profile marked by increased myostatin and reduced follistatin levels, accompanied by impaired muscle strength. The reversal of these alterations after parathyroidectomy suggests a potentially reversible myokine-mediated mechanism underlying muscle dysfunction in PHPT and supports a role for the myostatin–follistatin axis in the neuromuscular manifestations of this disease.

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