Fibroblasts are crucial in tissue engineering because of their ability to synthesize the extracellular matrix (ECM) and secrete growth factors. Orbital fibroblasts (OFs) from patients with thyroid eye disease (TED) exhibit enhanced fibroblastic properties, making them ideal candidates for regenerative medicine in ocular tissue. In the present study, we investigated the effect of nanoperlite on TED OFs. Nanoperlite, with its unique properties including high silica (SiO2) content, holds promise for enhancing fibroblast functions. Nanoperlite was prepared and characterized in terms of particle size and chemical composition. A sample of orbital adipose tissue was taken from a TED patient during orbital decompression surgery and OFs were expanded in vitro. The cells were then treated with nanoperlite at concentrations of 1 and 10 μg/mL for 24 h, and gene expression related to the fibrogenesis process was assessed using real-time PCR. Nanoperlite at 1 μg/mL significantly increased the expression of TGF-β, CD90, α-SMA, ZEB1, β-Catenin, and Snail genes in OFs. However, at 10 μg/mL, this effect was not observed. This study highlights nanoperlite's potential to enhance fibroblast activity specifically at the concentration of 1 μg/mL. This effect can potentially aid tissue engineering strategy for periorbital tissue repair and eyelid reconstruction. However, further research is needed to fully elucidate its therapeutic potential and safety profile.

The 'Thyroid: Year in Review', presented at the AACE 2026 annual meeting, synthesized practice-influencing peer-reviewed clinical research published between March 1, 2025, and February 15, 2026. This narrative review, based on that presentation, highlights two overarching themes in clinical thyroidology: precision medicine and de-escalation when appropriate. In thyroid dysfunction, recent studies support lean body mass-based levothyroxine dosing and the metabolic integration of liothyronine. The management of thyroid nodules and differentiated thyroid cancer has shifted toward de-escalation, favoring non-surgical interventions, active surveillance for low-risk malignancies, selective omission of radioactive iodine, de-escalation of surveillance strategies, and the complementary use of artificial intelligence with molecular testing to improve diagnostic accuracy in indeterminate nodules. This review summarizes these findings and their implications for contemporary evidence-based endocrine practice.

Recently, the incidence of thyroid diseases has been on the rise. While standardized diagnosis and treatment generally yield excellent prognoses, the association between thyroid disorders and cognitive function remains a topic of significant interest. Cognitive function includes memory, language, visuospatial ability and executive function. Cognitive dysfunction refers to the impairment of one or more of the above, including mild cognitive impairment (MCI) and dementia. More and more studies have shown that thyroid disease is associated with cognitive dysfunction. Clinically, some patients present with noticeable symptoms such as memory loss and inattention, which severely impede their daily social functioning. There is a consensus on the view that thyroid hormone deficiency during the neonatal or embryonic period can cause disorders in the central nervous system, resulting in severe cognitive impairment such as persons with congenital hypothyroidism, but there is disagreement on the relationship between adult thyroid diseases, including clinical hyperthyroidism, hypothyroidism, subclinical hyperthyroidism, subclinical hypothyroidism and cognitive dysfunction. The inconsistencies in research conclusions are attributed to complex factors. Differences in age stratification constitute an important confounding factor for thyroid-related cognitive impairment; various neuropsychological assessment tools show obvious discrepancies in the sensitivity of detecting cognitive damage, which can directly affect the evaluation of research outcomes. Meanwhile, methodological heterogeneity among studies is also a key inducement for the inconsistent findings on the association between clinical thyroid dysfunction and cognitive function in adults. Therefore, this article mainly reviews the relationship and research progress between thyroid function and cognitive dysfunction in adults. From this review, we conclude that obvious thyroid dysfunction is obviously related to cognitive function, mainly focusing on attention and memory. Treatment would improve cognition to some extent, but wouldn't fully restore it. The relationship between subclinical thyroid dysfunction and cognitive function is still of important significantly.

Therapeutic plasma exchange is a second-line therapy for severe hyperthyroidism when anti-thyroid drugs (ATD) are contraindicated or ineffective. We report five patients (three males, two females, age range: 30-70 years old): ATD-induced agranulocytosis (n = 2); ATD-induced cholestatic hepatitis (n = 1); refractory hyperthyroidism with large goiter (n = 1); thyroid storm during pregnancy (n = 1). A total of six TPE sessions were performed (five with fresh frozen plasma, one with 5% albumin). Among sessions with quantifiable baseline fT4, levels decreased by a mean of 39.0% per session; two sessions had baseline fT4 above the assay's upper limit of quantification, precluding exact calculation, though both showed reductions of at least 50%. Four patients underwent successful thyroidectomy; one continued medical management. No intraoperative thyroid storms occurred. TPE could be an effective bridging strategy for patients with severe hyperthyroidism and ATD intolerance.

Thyrotoxic hypokalemic paralysis is a rare complication of hyperthyroidism, characterized by acute, reversible episodes of muscle weakness associated with severe hypokalemia, secondary to intracellular potassium redistribution mediated by excess thyroid hormones and activation of the Na+/K+ - ATPase pump. Its incidence is approximately 0.2% and it occurs predominantly in males. In this report, we describe four cases of hypokalemic paralysis associated with thyrotoxicosis. All patients were male, aged between 21 and 37 years. The predominant clinical presentation was acute-onset muscle weakness, mainly proximal, with greater involvement of the lower limbs. In three of the four cases, paralysis was the main initial manifestation of hyperthyroidism due to Graves' disease. Potassium replacement combined with antithyroid therapy and beta-blockers resulted in complete resolution of the muscle weakness and adequate disease control in all patients. Therefore, thyrotoxic hypokalemic paralysis should be considered among the differential diagnoses in patients presenting with muscle weakness, as well as among the complications associated with hyperthyroidism.