Psoriasis is a complex chronic immunologically mediated disease that may involve skin, nails, and joints. It is characterized by hyperproliferation, deregulated differentiation, and impaired apoptosis of keratinocytes. Sphingolipids, namely ceramide, sphingosine-1-phosphate, sphingosine, sphingomyelin, and sphinganine-1-phosphate, are signal molecules that may regulate cell growth, immune reactions, and apoptosis. Fifteen patients with psoriasis and seventeen healthy persons were enrolled in the study. Skin samples were taken from psoriatic lesions and non-lesional areas. Tissue concentration of ceramides, sphingosine-1-phosphate, sphingosine, sphingomyelin, and sphinganine-1-phosphate was measured by liquid chromatography. We assessed that all levels of ceramides, sphingosine-1-phosphate, sphingosine, sphingomyelin, and sphinganine-1-phosphate were higher in lesioned psoriatic skin than in non-affected skin. The profile of bioactive lipids in the lesional skin of patients with psoriasis differed significantly from non-involved psoriatic skin and skin in healthy subjects.

Psoriasis is a chronic, complex, immunological disorder, which may lead to many different systemic complications. Sphingolipids, including ceramide, are bioactive lipids, which take part in the regulation of immune reactions, cell growth, and apoptosis. Twenty psoriatic patients and twenty-eight control subjects were included in the study. Skin (both lesional and non-lesional) and serum samples were collected from both the control group and the psoriatic patients. The levels of sphingosine (SFO), sphingosine-1-phosphate (S1P), sphingomyelin, sphinganine (SFA), sphinganine-1-phosphate (SFA1P), and ceramide (CER) were assessed in both tissue (t) and serum (s) samples using high-performance liquid chromatography (HPLC). We identified elevated serum levels of SFO, S1P, SFA, and SFA1P in psoriatic patients when compared to healthy individuals. As far as the lesional skin and serum of psoriatic patients are concerned, we demonstrated positive associations between CER_t and CER_s, SFA_t and CER_s, and SFO_t and CER_s. Additionally, we found negative correlations in the non-lesional skin and serum of psoriatic patients, including SFO_t vs. SFO_s, CER_t vs. SFA_s, CER_t vs. SFO_s, and SFO_t vs. SFA_s. Finally, we observed a positive correlation between S1P and SFA1P in both the serum samples of psoriatic patients and the serum samples of the control group. In this study, we did not observe any correlations between psoriasis area and severity index (PASI) scores and sphingolipid levels. In conclusion, our findings indicate an interplay between skin and serum lipids in psoriatic patients, which is not observed in healthy individuals.

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.

Cancer remains a primary global health and economic challenge, characterized by complex mechanisms of carcinogenesis and metastasis. Central to these processes is the dysregulation of matrix metalloproteinases, a family of zinc-dependent proteases. While traditionally recognized for their role in extracellular matrix remodeling, MMPs are now understood as versatile regulators of both intra- and extracellular signaling. This review explores the characteristics and diverse functional roles of MMPs in representative cancers, highlighting their transition from simple matrix degraders to complex modulators of the tumor microenvironment. Current evidence indicates that non-selective inhibition of all MMPs is unlikely to be an effective therapeutic strategy. Instead, a more targeted approach focusing on specific MMPs and disease stages may be required.

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.