Search Results (559)

Neuropeptide Y (NPY) is a small signalling molecule produced by neurons through the cleavage of a precursor protein. It generally binds to and activates G protein-coupled receptors to modulate complex homeostatic processes and behaviours in animals. Mammals provide definitive proof of the role of NPY in the thyroid axis, but in reptiles, this link is unclear. We demonstrate that the thyroid axis responds to NPY administration in a dose-dependent manner, with a reduction in plasma TRH and TSH concentrations, and an increase in plasma T₃ and T₄ levels 2 and 24 h after administration, suggesting that NPY may activate the thyroid axis. This increase in thyroid hormones is supported by morphological findings in the thyroid gland, which show clear signs of stimulation demonstrated by a dose-dependent increase in the height of the follicular epithelium and the presence of numerous resorption vacuoles. Moreover, we investigated the 5-T₄ ORD (type II) Monodeiodinase activity at the hepatic level, showing that NPY increased hepatic T₃ levels and decreased hepatic T₄ levels, and suggesting an alternative mode of signalling by NPY on peripheral biosynthesis of thyroid hormones. Our study helps to address the current lack of research in the field of endocrinology concerning the effects of NPY on metabolism and thyroid function. Full article

Thyroid diseases in horses are rare and pose challenges for veterinarians due to the complexity of clinical and diagnostic approaches. This retrospective case series describes cases of equine thyroid disease in a referral hospital population. Files of horses examined for suspected thyroid disease at an equine university clinic between 2009 and 2024 were reviewed. Data from nine horses examined for suspected thyroid disease, including signalment, clinical presentation, laboratory results, imaging findings, fine needle aspirates, biopsies, diagnoses, and treatments, were summarised. Diagnoses included thyroid adenoma (n = 6), multiple thyroid cysts (possibly thyroid adenoma (n = 1)), non-thyroidal illness syndrome (NTIS, n = 1), and iodine deficiency goitre (n = 1). Diagnostic modalities varied, with, besides manual palpation performed in every patient, basal thyroid hormone measurement and ultrasonography being the most common. Low serum iodine concentrations were noted in four horses, yet iodine supplementation was inconsistently applied. Hemithyroidectomy was performed in four horses, enabling histopathological diagnosis (three out of four). Despite being rare, thyroid diseases in horses require consistent and thorough diagnostic approaches, including imaging, laboratory, and histopathological examinations. Improved screening tools and research could enhance the diagnostic accuracy and management of equine thyroid disorders. Full article

Objectives: Early and noninvasive detection of fibrotic interstitial lung disease (fILD) is a critical but unmet clinical necessity. This study aimed to evaluate the feasibility of using ^99mTc-HYNIC-Glu(PEG₄-oncoFAPi)₂ (denoted as ^99mTc-H-PoFP₂), a novel ^99mTc-labeled radiopharmaceutical that targets fibroblast activation protein (FAP), for single-photon emission computed tomography (SPECT) imaging of pulmonary fibrosis in a mouse model and preliminary clinical studies. Methods: ^99mTc-H-PoFP₂ could be conveniently afforded using a kit formula with high radiochemical purity and stability. The binding specificity and affinity of ^99mTc-H-PoFP₂ for FAP were validated by an in vitro binding assay. The in vivo characteristics of ^99mTc-H-PoFP₂ were also determined. Results: ^99mTc-H-PoFP₂ was eliminated quickly via the urinary system, leading to low normal tissue uptake and a high target/background ratio. SPECT imaging demonstrated significantly enhanced uptake of the ^99mTc-H-PoFP₂ in bleomycin-induced fibrotic lung tissues, with visual effects superior to those of normal mice. Thus, a pilot clinical study of ^99mTc-H-PoFP₂ SPECT/CT imaging was conducted in 12 patients diagnosed with fILD. The physiological biodistribution of ^99mTc-H-PoFP₂ in patients was predominantly observed in the kidneys, bladder, liver, and pancreas, with relatively minor accumulation in the thyroid, salivary glands, and spleen. fILD patients exhibited elevated pulmonary ^99mTc-H-PoFP₂ uptake in the affected lung regions. Furthermore, the uptake of ^99mTc-HPoFP₂ demonstrated moderate correlations with the results of pulmonary function tests (PFTs). A higher gender–age–physiology (GAP) index was associated with elevated standardized uptake value maximum (SUVmax) and target-to-background ratio (TBR) values. Conclusions: Collectively, this study demonstrates the potential of ^99mTc-HPoFP₂ for SPECT imaging and assessing fILD by targeting FAP overexpressed in fibrotic lung tissues. This strategy offers new possibilities for noninvasive and precise assessment of pulmonary fibrosis. Full article

The ubiquitous environmental pollution with micro- and nano-sized plastic particles (MNPs) is a current and significant problem today. At the same time, lung cancer is responsible for the largest number of cancer-related deaths worldwide. Many research groups have investigated the relationship between lung cancer development and exposure to MNPs in recent years. Studies have demonstrated that these particles could enter the respiratory system in a variety of ways—both directly through inhaled air and through the bloodstream, and through internalization in the intestines and other digestive organs. Data regarding the possibility of their aggregation in the respiratory system, thyroid gland, and brain are also concerning, as the harmful effects of MNPs have been proven to depend on their concentration and exposure time. The primary response of cells to plastic particles is an increase in oxidative stress. This is generated both by the cell itself (especially macrophages) and induced by damage caused by mechanical damage to cellular organelles by MNPs. The consequences of MNP exposure can include metabolic disturbances, DNA damage, and mutations, ultimately inducing neoplastic transformation in healthy cells. This can lead to changes in tissue architecture and increase their susceptibility to other pathogens, such as pathogenic microorganisms or heavy metals. These, in turn, can be internalized along with MNPs, forming a corona surrounding them. Full article

Congenital hypothyroidism (CH) is one of the most common endocrine disorders of childhood. The primary form of CH is attributable to thyroid dysgenesis (agenesis, hypoplasia, or ectopy) in 65–85% of cases, with the remaining cases being attributed to dyshormogenesis. Thyroid dysgenesis was considered a sporadic disease. However, the recent advantages of molecular techniques have significantly contributed to the understanding of the pathogenesis of the disease. The higher prevalence of congenital malformations and syndromes in patients with CH compared to the general population supports the genetic basis. This narrative review aims to provide an overview of the identified and potential genetic causes of thyroid dysgenesis. Mutations in ten genes involved in thyroid gland development during embryogenesis, TSHR, PAX8, NKX2-1, NKX2-5, FOXE1, JAG1, NTN1, GLIS3, CDC8A, and TUBB1, have been identified in cohorts of patients with thyroid dysgenesis. However, most cases remain unexplained. Novel candidate genes have been proposed. The extant evidence suggests that the pathogenesis of thyroid dysgenesis involves a spectrum of genetic etiologies, ranging from monogenic to multigenic, and that epigenetic or environmental factors may also contribute. As molecular techniques are continuously refined, future studies are expected to elucidate the complex genetic background of thyroid dysgenesis. Full article

Background: Subclinical hyperthyroidism grade 1 (SCH G1, TSH > 0.1 mU/L) is common in patients with thyroid unifocal autonomy (UFA) and associated with cardiovascular risks and increased mortality. While ¹³¹I radioiodine therapy (¹³¹I-RIT) effectively treats UFA, it frequently induces hypothyroidism, partly due to extra-nodular absorbed dose (AD) enhanced by residual TSH stimulation. Objective: We hypothesized that short-term LT3-induced TSH suppression at the time of RIT would promote long-term euthyroidism. Patients and Methods: A retrospective study was conducted on 95 UFA patients with SCH G1 (2001–2024). Patients underwent baseline and post-LT3 thyroid scintigraphy, and then received ¹³¹I-RIT with individualized dosimetry. Long-term bioclinical follow-up was achieved. Results: Short-term low-dose LT3 suppression caused no adverse events and significantly reduced TSH (0.45 to 0.047 mU/L). Whole-gland ¹²³I uptake decreased moderately (11.0 to 8.4%), while extra-nodular lobe uptake dropped markedly (1.77 to 0.73%) (all p < 0.0001). This focused activity on the UFA (2.5-fold increase), maintaining mean UFA AD (about 260 Gy) but reducing extra-nodular AD (61 to 37 Gy, p < 0.0001). Despite low ¹³¹I doses (mean 181 MBq), a dose–response relationship was observed: higher AD correlated with greater nodular lobe volume reduction (p < 0.033). At the 88-month follow-up, 93% of patients achieved normal thyroid function; one had persistent SCH G1, two were borderline hypothyroid, and two required LT4. Conclusions: ¹³¹I-RIT under brief LT3-induced TSH suppression induces sustained euthyroidism in SCH G1 with UFA. This simple, low-risk strategy reduces radioprotection concerns and is under evaluation to determine cardiovascular benefits. Full article

Background and objectives: The identification and preservation of the parathyroid glands (PGs) are of paramount importance in thyroid surgery. Permanent hypoparathyroidism represents a significant post-operative complication that may result from the surgeon’s failure to accurately identify the PGs or their associated blood supply. Post-operative hypocalcemia (POH) represents the most common surgical complication following thyroid surgery and is the primary factor influencing the post-operative course, causing the requirement of frequent electrolyte monitoring and of supportive therapies, precluding the possibility of early discharge, and resulting also in significant healthcare costs. Near-infrared autofluorescence (NIRAF) employs the intrinsic capacity of PGs to emit fluorescent light when exposed to light within the NIR spectrum. In the context of thyroid surgery, NIRAF represents a safe method with no documented risks to the patient. Materials and Methods: A retrospective analysis was conducted on 383 patients who underwent thyroid surgery at our Institution, either with (n = 27) or without (n = 356) intraoperative NIRAF, focusing on its efficacy in reducing the incidence of POH. Conclusions: Our results suggest that the systematic integration of NIRAF within non-high-capacity centres for cervical surgery, owing to its usefulness in identifying PGs intraoperatively, may strongly contribute to a reduction in the incidence of POH (45.8% without vs. 18.5% with NIRAF; p = 0.0078). This, in turn, has the potential to contribute to a decrease in overall healthcare expenditure. Full article

In birds, light can penetrate the cranial bones and reach deep brain regions, where non-visual photoreceptors, especially in the hypothalamus, detect spectral and photoperiodic cues. Alongside retinal photoreception, deep-brain light sensing contributes to circadian entrainment and regulates melatonin secretion by the pineal gland. These light-driven pathways modulate endocrine activity, playing a key role in muscle development. This review explores how monochromatic light-emitting diode (LED) illumination, particularly green and blue wavelengths, affects the somatotropic axis (growth hormone-releasing hormone [GHRH]-growth hormone [GH]-insulin-like growth factor 1 [IGF-1]), the gonadal axis (gonadotropin-releasing hormone [GnRH]-luteinizing hormone [LH]/follicle-stimulating hormone [FSH]-sex steroids [testosterone, estrogen, progesterone]), the thyroid axis (thyrotropin-releasing hormone [TRH]-thyroid-stimulating hormone [TSH]-thyroxine [T₄]/triiodothyronine [T₃]), and the hypothalamic-pituitary-adrenal (HPA) axis (corticotropin-releasing hormone [CRH]-adrenocorticotropic hormone [ACTH]-corticosterone). Green light enhances early-stage muscle growth via GHRH and IGF-1 upregulation, while blue light supports later myogenic activity and oxidative balance. Light schedules also influence melatonin dynamics, which in turn modulate endocrine axis responsiveness to photic cues. Furthermore, variations in photoperiod and exposure to artificial lights at night (ALAN) affect thyroid activity and HPA axis reactivity, influencing metabolism, thermoregulation, and stress resilience. Together, ocular and intracranial photoreception form a complex network that links environmental light to hormonal regulation and muscle growth. These insights support the strategic use of LED lighting to optimize broiler performance and welfare. Full article

Thyroid cancer (TC) represents the most prevalent endocrine malignancy, with papillary thyroid cancer (PTC) comprising approximately 80% of cases and accounting for the majority of annual incidence and mortality. PTC is generally confined to the thyroid gland and demonstrates an excellent prognosis after surgery, with a five-year survival rate exceeding 90%. Nevertheless, recurrence can occur, and the ten-year survival rate for the advanced PTC is below 50%. Even after effective successful surgical intervention, many still require ongoing surveillance, additional treatment, and lifelong thyroid hormone replacement, while facing the potential adverse effects such as hormone fluctuations, surgical complications, and sequelae of radioactive iodine exposure. Naturally occurring compounds have demonstrated anti-cancer properties and hence the potential to be used as therapeutic options, impacting the same drivers and pathways involved in the tumorigenesis of thyroid cancer. This narrative review focuses on the natural compounds’ convergence on molecular nodes of PI3K/Akt, MAPK, and JAK/STAT to overcome therapeutic resistance and restore apoptosis, highlighting their potential in advanced and recurrent PTC. Full article

Background: Hashimoto’s thyroiditis (HT) is characterised by chronic inflammation of the thyroid gland. The impact of a health-promoting diet and probiotics on health and quality of life, as well as on the anti-thyroid peroxidase antibody (anti-TPO), is increasingly being researched. However, the relevance of these factors to the course of HT is yet to be fully established. Objective: The aim of this study was to assess the impact of a 12-week nutritional intervention, comprising a rational, health-promoting diet supplemented with the probiotic strain Lactiplantibacillus plantarum 299v (Lp299v), on eating habits, nutritional status, health and quality of life in patients diagnosed with HT. Methods: The 12-week study involved 64 female patients with HT, divided into two groups: the NE+Lp299v group, which received nutritional education and Lp299v (n = 32); and the NE+placebo group, which received nutritional education and placebo (n = 32). Before and after the intervention, anthropometric parameters, body composition analysis, blood pressure, blood anti-TPO levels, dietary habits, quality of life, and gastrointestinal symptoms were assessed. Results: The NE+Lp299v intervention improved overall quality of life (60.94 pts. vs. 35.94 pts.), including 12 of 14 domains, and the diet quality index (11.03 pts. vs. 18.50 pts.). The NE+placebo group improved overall quality of life (54.69 pts. vs. 39.84 pts.), including 3 of 14 domains, and the diet quality index (12.34 pts. vs. 19.18 pts.). Anti-TPO blood levels and body mass index did not improve in either group. Conclusions: Lp299v can enhance the efficacy of nutritional education in improving the quality of life of individuals diagnosed with HT. However, these benefits appear to be independent of anti-TPO levels. Full article

Background/Objectives: Thyroid dysfunction (hypo- and hyperthyroidism) and cancer incidence have increased over the past decades, possibly linked to environmental contributions from endocrine disrupting chemicals (EDCs). Glyphosate is one of the most widely used herbicides globally and has endocrine-disruptive properties. Because of the sensitivity of the thyroid gland to endocrine disruption and the increased glyphosate exposure worldwide, this comprehensive review aimed to summarize studies investigating the link between glyphosate/glyphosate-based herbicides (GBHs) and thyroid dysfunction in human, animal, and in vitro studies. Methods: PubMed, Scopus, and Embase were used to search for original studies assessing glyphosate or GBH exposure and thyroid-related outcomes through December 2024. Data were extracted on study design, population or model, exposure, and thyroid outcomes. A total of 28 studies, including 9 human, 3 in vitro, and 16 animal studies were included. Results: Human studies showed mixed findings with some suggesting associations between glyphosate exposure and altered thyroid hormone levels, while others found no significant effects. Animal studies, particularly in rodents and amphibians, showed thyroid hormone disruption and altered gene expression, especially after perinatal or developmental exposure. In vitro studies reported changes in thyroid-related gene transcription and cell viability, however at concentrations exceeding those seen in humans. Conclusions: While there is some evidence that glyphosate may disrupt thyroid function, differences in study populations, exposure assessment methods, species models, and exposure doses complicated the comparison and summarization of the results. Further mechanistic and longitudinal studies are needed to clarify the thyroid-specific risks of glyphosate exposure. Full article

Background: Chronic autoimmune thyroiditis, also known as Hashimoto’s thyroiditis (HT) or chronic lymphocytic thyroiditis whose pathophysiology includes both cellular (T-cell mediated) and humoral (B-cell mediated) immune responses, leads to the destruction of thyroid follicular cells and progressive fibrosis of the thyroid gland. While hypothyroidism is a common autoimmune disease, athletes may experience unique challenges related to its diagnosis and management within the context of training programme, competition and anti-doping regulations. In turn, it is known that moderate physical exercise can have a positive effect on the immune system, while excessive exercise can cause unfavourable changes in this system. Therefore, we aimed (1) to identify the interplay between physical activity and autoimmune thyroid disease, (2) to quantify changes in thyroid function associated with physical activity, and (3) to explain the underlying mechanisms of autoimmune thyroiditis in athletes. Methods: The medical database PubMed/MEDLINE was searched in the time period 2004–2025, where 12 publications met the inclusion criteria and were ultimately included for further evaluation according to the RAMESES (Realist and Meta-narrative Evidence Syntheses: Evolving Standards). Results: The reviewed studies have clearly indicated that physical exercise has a beneficial effect on thyroid function, and two studies reported that non-excessive physical exercise leads to a decrease in TPO-Ab concentrations. Conclusions: The beneficial effect of physical exercise on thyroid function and immune response underlines the need for further well-designed studies to formulate specific guidelines for patients with HT, as well as for athletes with autoimmune thyroid disease. Similarly, there is a need to evaluate the prevalence of thyroid hormone use among amateur and professional athletes in order to establish prevention strategies. Full article

Thyroid amyloidosis is a rare condition associated with thyroid pathologies such as medullary carcinoma, papillary carcinoma, amyloid goitre, and benign lesions, with a clinically palpable goitre being exceptionally uncommon. As a result, many cases of benign thyroid enlargement caused by amyloid deposits remain undiagnosed. A 28-year-old male patient noticed progressive neck circumference enlargement, voice alteration, decreased appetite, weight loss, dysphagia, fever, and night sweats. Fine-needle aspiration biopsy of the thyroid gland did not reveal the cause of the goitre. A total thyroidectomy was performed. Histopathological examination confirmed advanced thyroid amyloidosis. Full article

This study investigated the morphometric characteristics of adenohypophyseal thyrotrophs and circulating thyroid hormone profiles in dromedary camels (Camelus dromedarius) in relation to age and lactation status. Clinically healthy Brela breed camels were divided into lactating female, and non-lactating female groups across two age categories (5–10 years and ≥11 years), with fifty animals per group. Blood samples were collected before slaughter and pituitary glands were collected post-slaughter and processed for immunohistochemical detection of thyroid-stimulating hormone (TSH) using anti-porcine TSHβ antibody, while morphometric measurements of thyrotrophs were conducted through image analysis. Plasma concentrations of TSH, triiodothyronine (T₃), and thyroxine (T₄) were quantified using validated ELISA and enzyme immunoassay kits. Group differences were analyzed using one-way ANOVA followed by post hoc comparisons, with statistical significance set at p < 0.05. Morphometric analysis revealed that lactating female camels exhibited significantly higher thyrotroph counts compared with non-lactating counterparts, whereas non-lactating females displayed larger cell and nuclear dimensions. Age influenced these patterns, with older camels showing hypertrophied thyrotrophs but reduced functional plasticity compared to younger animals. Plasma hormone assays demonstrated that non-lactating camels had higher TSH and T₄ concentrations, while lactating camels maintained elevated T₃ levels, suggesting enhanced peripheral conversion of T₄ to T₃ during milk production. Additionally, younger camels exhibited higher T₃ concentrations than older animals, indicating age-related decline in thyroidal activity. These findings highlight the dynamic regulation of the hypothalamic–pituitary–thyroid axis in camels, demonstrating how lactation and age shape thyroidal morphology and function to meet diverse physiological demands. These findings not only broaden the comparative endocrinology of underexplored species but also provide physiopathological insights relevant to farm animal management, lactation efficiency, and adaptive metabolism in harsh environments. Full article

IgG4-related disease (IgG4-RD) is a subacute, progressive, multisystemic autoinflammatory condition which presents with nonspecific symptoms like weight loss, fatigue and myalgia, and is marked by lymphoplasmacytic infiltrates rich in IgG4-positive plasma cells. IgG4-RD can involve various organs including the pancreas, bile ducts, thyroid, salivary and lacrimal glands, retroperitoneum, kidneys, lungs and CNS, often mimicking malignancy. A rigorous literature review was conducted. Articles on IgG4 disease, CD-19 and the MITIGATE trials were studied and included in the review. Glucocorticoids remain first-line therapy, but adverse effects and relapses are common. Rituximab, an anti-CD20 agent, is effective but may leave CD20-negative plasmablasts intact, contributing to relapse. In contrast, CD19-targeting therapies like inebilizumab offer more comprehensive B-cell depletion, including plasmablasts, potentially reducing relapses, fibrosis progression and long-term organ damage. MITIGATE trials showed promise in the use of an anti-CD-19 agent in preventing IgG4 disease flares and prolonging the time to first flare. Full article