Data on redox homeostasis and matrix metalloproteinase (MMP) activity in parathyroid adenoma are limited, although chronic inflammation and oxidative stress may contribute to the pathophysiology of primary hyperparathyroidism. In this prospective pre–post study, we assessed systemic redox status, nitrosative stress markers, and circulating MMP activity in 52 patients with parathyroid adenoma before and six months after parathyroidectomy and in 52 age- and sex-matched controls. Before surgery, patients had lower total antioxidant capacity (TAC), and higher total oxidant status (TOS) and oxidative stress index (OSI) compared to the controls. Six months after surgery, TAC returned to control levels, whereas TOS and OSI remained elevated. Nitric oxide (NO) levels decreased after parathyroidectomy, and peroxynitrite (ONOO⁻) levels at follow-up were higher than in controls. Postoperatively, the plasma activity of all six investigated MMPs (MMP-1, -2, -7, -9, -11, and -13) was lower than in the controls, whereas significant pre- to postoperative decreases were observed only for MMP-7 and MMP-11. Thus, six months after parathyroidectomy, several systemic redox, nitrosative, and MMP parameters still differed from those in the controls. Longer follow-up is required to determine whether these abnormalities normalize and to establish their clinical significance.

Thyroid diseases encompass a broad spectrum of autoimmune, inflammatory, and neoplastic disorders, yet current diagnostic approaches provide limited insight into innate immune activation and tumor-associated inflammatory remodeling. Damage-associated molecular patterns (DAMPs) and neutrophil extracellular traps (NETs) have emerged as interconnected mediators of sterile inflammation with potential relevance to thyroid carcinogenesis, disease progression, and biomarker development. This narrative review synthesized literature identified through PubMed/MEDLINE and Scopus to evaluate the biological, diagnostic, and translational significance of DAMP- and NET-associated pathways in thyroid diseases, with particular emphasis on thyroid cancer. DAMPs such as high-mobility group box 1 (HMGB1), S100A8/A9, serum amyloid A, heat shock proteins, and extracellular nucleic acids may sustain inflammatory signaling through pattern-recognition receptors and contribute to tumor proliferation, angiogenesis, immune modulation, and therapeutic resistance. In parallel, circulating analytes associated with NET biology—including nonspecific cell-free DNA (cfDNA) and nucleosomes, pathway-associated citrullinated histone H3 (CitH3), and composite myeloperoxidase–DNA (MPO–DNA) complexes—have shown associations with thyroid malignancy, dedifferentiated disease, metastatic presentation, and greater disease severity. Experimental data further suggest that aggressive thyroid cancer cells, particularly anaplastic thyroid carcinoma, can induce extracellular trap formation and exploit neutrophil-derived signals to support tumor growth. However, limited disease specificity, assay heterogeneity, and the predominance of small or exploratory cohorts currently restrict clinical implementation. Future strategies should prioritize standardized, prospective validation of multimarker panels integrating DAMP- and NET-related analytes with imaging, cytology, molecular diagnostics, and clinicopathological risk stratification to determine whether they provide incremental value for diagnosis, prognostication, and longitudinal monitoring in thyroid cancer.