Endocrine disorders in children can present with various oral manifestations that may impact overall health and quality of life. Despite this, awareness of these oral implications among patients and caregivers is often limited. Understanding this gap is essential for improving multidisciplinary care and oral health outcomes. This study aims to assess the awareness of oral health and dental care practices of children and caregivers with endocrine disorders. A cross-sectional study was conducted at the Paediatric Endocrinology Clinic of Lagos University Teaching Hospital (LUTH), Lagos, Nigeria. Ethical approval, informed consent, and assent were obtained. Fifty children aged 7-18 years with confirmed endocrine disorders and their caregivers were recruited. Data collection involved structured questionnaires and intraoral examinations. Statistical analysis was done with a level of significance set at p< 0.05. The mean age of patients was 11.52 ± 4.9 years, with females representing 54% of the participants. Type I Diabetes Mellitus was the most frequent endocrine condition (54%). Awareness of the oral implications of endocrine disorders was very low (12%). The majority of patients (70%) had never visited a dentist. Similarly, most caregivers (66.0%) had never visited a dentist. The presence of oral manifestations showed no statistically significant association with age group, sex, or caregiver educational level. Oral abnormalities are frequent among paediatric patients with endocrine conditions, yet both patients and caregivers demonstrate low awareness of these complications. Greater collaboration between endocrinologists and dental professionals, alongside promoting oral health education, is crucial to improving oral health outcomes in this population.
Type 1 diabetes mellitus characterized by insulin deficiency and hyperglycemia is associated with female subfertility. However, how hyperglycemia affects the hypothalamic-pituitary-ovarian-uterine axis remains poorly understood. In this study, we performed single-cell transcriptomic profiling of the hypothalamus, pituitary, ovary and uterus during the proliferative phase of the menstrual cycle in type 1 diabetic macaques to systematically characterize changes in tissue-specific cellular heterogeneity, gene expression, and intercellular communication networks under diabetic conditions. Our analysis revealed significant upregulation of the TNF signaling pathway across multiple tissues, concomitant with marked activation of inflammation-related pathways. Notably, the macrophage migration inhibitory factor signaling pathway exhibited a tissue-specific regulatory pattern, being significantly upregulated in the hypothalamus and pituitary but downregulated in the ovary and uterus, suggesting divergent inflammatory modulation along the reproductive endocrine axis in response to diabetes. Moreover, we observed that diabetes leads to reduced FSHR expression during granulosa cell differentiation, and this process is further exacerbated by the upregulated expression of SFRP4, a known antagonist of follicle-stimulating hormone signaling, resulting in diminished granulosa cell responsiveness to follicle-stimulating hormone. Consequently, this dysregulation is correlated with increased FSHB expression in pituitary gonadotropes, likely due to disrupted ovarian feedback signaling. Collectively, our findings provide a comprehensive landscape of cellular and molecular alterations in immune and endocrine compartments in the female reproductive system in diabetic states, advancing our understanding of immune‒endocrine cell crosstalk in the context of metabolic disease.
The 2026 global consensus proposal published in The Lancet renamed Polycystic Ovary Syndrome (PCOS) to Polyendocrine Metabolic Ovarian Syndrome (PMOS), replacing an anatomically misleading, cyst-centered label with terminology grounded in the disorder's systemic endocrine-metabolic nature. Although PMOS corrects a long-standing mismatch between terminology and evidence, the philosophical, clinical, and social implications of this terminological shift have not been systematically examined. To critically evaluate the transition from PCOS to PMOS through the lenses of medical nosology, philosophy of language, and Kazem Sadegh-Zadeh's theory of fuzzy medical concepts, assessing both the scientific gains and the new epistemological, clinical, and social challenges introduced by the renaming. This is a conceptual and interpretive analysis rather than an empirical study. Competing models of disease classification (anatomical, symptom-based, eponymous, etiological, and mechanistic) are compared against the PMOS proposal. Sadegh-Zadeh's analytic philosophy of medicine, particularly his account of fuzzy medical concepts, is applied to assess whether PMOS achieves genuine conceptual closure. The analysis draws on the original Lancet consensus statement, empirical reproductive-outcome studies in PCOS, and a comparative precedent from the NAFLD-to-MASLD renaming, to evaluate clinical, psychological, and translatability implications. While PMOS represents a substantial scientific improvement by shifting emphasis from anatomical appearance to the disorder's lifelong metabolic and cardiovascular risks-including elevated odds of myocardial infarction and stroke-it introduces new risks of biomedical reductionism, this time centered on metabolic markers rather than ovarian anatomy. Psychological and social dimensions of the syndrome, including anxiety, depression, and body image distress, remain linguistically invisible in the new name. Retention of the word "ovarian," along with the acronym's phonetic proximity to "PMS," risks re-anchoring the condition to reproductive and gendered framings the renaming sought to escape. Applying Sadegh-Zadeh's framework, PMOS is best understood as an inherently fuzzy construct whose boundaries resist complete biomedical closure, with implications for clinical ownership, multidisciplinary care coordination, cross-cultural translatability, and the practical costs of transitioning established coding, literature, and patient-identity systems. PMOS marks meaningful scientific progress in aligning medical language with the systemic reality of the disorder, yet it is not a definitive terminological solution. Lasting semantic stability requires nomenclature that remains responsive to the multidimensional, lived experience of patients. The shift from PCOS to PMOS should therefore be understood not merely as a linguistic correction but as an ongoing reconstruction of disease ontology itself.
Corticotroph pituitary neuroendocrine tumours (PitNETs)/adenomas are heterogeneous sellar neoplasms. Currently established histopathological classification approaches are often considered limited in fully capturing the clinical and biological complexity of these tumours. Thus far, a molecular-based classification has not been established in corticotroph PitNETs. We compile molecular data of 270 corticotroph PitNETs (111 internal, 159 external), encompassing epigenome, transcriptome, and proteome profiles. Comprehensive integrative analyses are performed to identify, validate and characterise definitive molecular subgroups. Corticotroph PitNETs separate into four robust and clinicopathologically distinct molecular subgroups, which are broadly distinguishable by microscopy using SSTR1, GATA3 and SSTR5 immunohistochemistry. An integrated stratification model incorporating these molecular subgroups demonstrates significant prognostic utility. Our findings support the establishment of a refined molecular-based corticotroph PitNET classification, the full clinical value of which will require validation in prospective studies. To facilitate future research, we provide an easy-to-use epigenomic classifier for corticotroph PitNETs.
The effective extraction and sensitive detection of endocrine disruptive phenolic chemicals (EDPCs) in food matrices is of great importance for ensuring human health. This study develops a porous organic cage-based covalent organic framework (Cage-COF) as an advanced adsorptive material for solid-phase extraction (SPE) of EDPCs from milk samples. Interconnected 3D porous structure, large surface area (199 m2 g-1), electron-rich O, N heteroatoms and OH moieties endow Cage-COF with significantly enhanced active adsorption sites, leading to a highly effective affinity towards EDPCs. Theoretical calculation and control experiments clarified the interaction mechanism of pore filling, H bonds and π-π interaction between Cage-COF and EDPCs. A sensitive method for the quantification of four typical EDPCs at trace levels in whole milk and skim milk was established by coupling Cage-COF-based SPE and high performance liquid chromatography tandem mass spectrometry. The limits of detection for the EDPCs were between 0.01 and 0.06 ng mL-1, lower than that of most reported methods. Spiked recovery study gave the satisfactory recovery of 85% -115% and low relative standard deviations of 2.3% -9.0%. The distinguished adsorption performance of cage-based COFs unlocking their considerable untapped application potential in adsorption and separation.
Farooqi, Teichmann, and collaborators developed the Hormone Cell Atlas, a 14-million-cell dataset mapping hormone production and sensitivity across 47 human tissues. Their findings expand knowledge on sites of production and receiver cells, opening new avenues in endocrinology and metabolism.
Polybrominated diphenyl ethers (PBDEs) are neuroendocrine-disrupting chemicals that produce adverse neurodevelopmental effects. PBDEs have been implicated as risk factors for autism spectrum disorder (ASD), which is characterized by abnormal psychosocial functioning and is commonly comorbid with cognitive deficits and sensory abnormalities. Here, we used a mouse model with translationally relevant exposure to establish direct causal evidence that maternal transfer of a commercial mixture of PBDEs, DE-71, produces ASD-relevant behavioral and neuroendocrine deficits in male offspring. C57Bl6/N mouse dams were exposed to a commercial PBDE mixture, DE-71, via oral administration of 0 (vehicle control, VEH/CON), 0.1 (L-DE-71), or 0.4 (H-DE-71) mg/kg b.w./day for 10 weeks, spanning from 3 weeks prior to gestation through the end of lactation at postnatal day (PND) 21. Mass spectrometric analysis indicated a dose-dependent transfer of PBDEs (in ppb) to brains of F1 male offspring at PND 30, with reduction in levels by PND 110. DE-71-exposed adult F1 male offspring displayed ASD-relevant abnormal neurobehavioral phenotypes, including impaired social novelty preference (SNP) despite intact general sociability and exaggerated repetitive behavior. There were also milder effects on long-term social recognition memory (SRM). DE-71-exposed mice also displayed altered olfactory discrimination of social odors without altered odor preference for non-social odors, impaired novel object recognition memory, and reduced open field habituation relative to VEH/CON. However, no changes were observed in sensorimotor, anxiety-, or depressive-like behaviors. At the molecular level, DE-71-exposed males displayed deregulated gene markers of prosocial neuropeptides, oxytocin, vasopressin, and PACAP systems in hypothalamic and forebrain regions. Oxt was upregulated in the paraventricular nucleus (PVN); Avp was upregulated in the PVN and bed nucleus of the stria terminalis (BNST) but downregulated in the lateral septum (LS); Avp1ar and Adcyap1 were upregulated in the BNST; and Adcyap1r1 was upregulated in the PVN, supraoptic nucleus (SON), and BNST. Peripheral OXT was increased in L-DE-71 males, while no changes in plasma AVP were observed. These findings demonstrate that developmental PBDE exposure produces enduring behavioral and neuroendocrine phenotypes that resemble core domains of ASD, which may result from early neurodevelopmental reprogramming within central social and memory networks.
Real-world comparative outcomes of endoscopic retrograde cholangiopancreatography-based endoscopic therapy vs. pancreatic surgery in chronic pancreatitis (CP) remain incompletely defined. We performed a retrospective comparative effectiveness study using the TriNetX US Collaborative Network. Adults with CP undergoing endoscopic therapy or pancreatic surgery were identified, and propensity score matching generated 1451 patients in each cohort. Outcomes were assessed from 1-1095 days after the index event, using risk-based analyses as the primary comparative summaries and Kaplan-Meier analyses as secondary time-to-event summaries. Outcomes included chronic opioid prescriptions, opioid use disorder (OUD), celiac plexus block/neurolysis, pain codes, acute pancreatitis, exocrine and endocrine pancreatic insufficiency, emergency visits, and all-cause mortality. Mean follow up was 771.494 days for endoscopy and 827.285 days for surgery. New chronic opioid prescriptions occurred in 146/1092 (13.4%) endoscopic vs. 79/1032 (7.7%) surgical patients (odds ratio [OR] 1.862, 95% confidence interval [CI] 1.396-2.484; P<0.001; hazard ratio [HR] 1.861, 95%CI 1.415-2.448). Acute pancreatitis occurred in 167/530 (31.5%) vs. 65/565 (11.5%) patients (OR 3.539, 95%CI 2.578-4.858; P<0.001; HR 3.341, 95%CI 2.506-4.453). Exocrine pancreatic insufficiency occurred in 200/1213 (16.5%) vs. 132/1206 (10.9%) patients (OR 1.606, 95%CI 1.269-2.034; P<0.001; HR 1.585, 95%CI 1.272-1.975). Endocrine pancreatic insufficiency, mortality, emergency visits, and OUD did not differ significantly between cohorts. Endoscopic therapy was associated with higher chronic opioid prescribing, acute pancreatitis, celiac plexus block/neurolysis, and exocrine pancreatic insufficiency. These findings are associative and should be interpreted in the context of residual confounding and coding-based outcome ascertainment.
Variants in LHX3, encoding a LIM-homeodomain transcription factor essential for pituitary and neuronal development, are a rare cause of combined pituitary hormone deficiency (CPHD). Affected patients typically exhibit deficiencies of growth hormone (GH), thyrotropin (TSH), prolactin (PRL), and gonadotropins, often accompanied by cervical spine rigidity or sensorineural hearing loss. A 4.8-year-old boy presented with short stature and central hypothyroidism. Combined deficiencies of GH, TSH, and PRL were documented, while ACTH secretion remained intact. Cranial magnetic resonance imaging showed normal pituitary morphology. Neck mobility and audiological evaluation were unremarkable. A targeted next-generation sequencing panel for panhypopituitarism was non-diagnostic. Whole-exome sequencing (WES) was performed at 10.5 years of age. WES identified a novel homozygous LHX3 c.575 G > A, p.(Arg192His) variant located within the homeodomain. Segregation analysis confirmed parental heterozygosity. A younger sister carrying the same homozygous variant exhibited a similar endocrine phenotype. Growth velocity normalized on recombinant human GH replacement. This case expands the phenotypic spectrum of LHX3-related CPHD by demonstrating that a homeodomain missense variant may produce isolated endocrine deficiencies without structural, auditory, or motor abnormalities, and underscores the value of serial genetic re-evaluation in unexplained CPHD.
Metabolic dysfunction that results from complex interactions between genetics, metabolism, and environmental factors has emerged as a major global health concern. Endocrine-disrupting chemicals (EDCs), known for their ability to interfere with hormones and signalling cascades, are increasingly recognized for their role in promoting metabolic dysfunction. Bisphenol A (BPA), a widely used EDC, exhibits systemic toxicity, disrupting endocrine regulation while interfering with metabolism and energy homeostasis. However, the molecular mechanisms underlying BPA-induced metabolic dysfunction remain poorly understood, highlighting the need for robust in vivo models with measurable endpoints to evaluate its effects. Here, we developed a functional disease model using Drosophila melanogaster to investigate metabolic disruption following developmental exposure to BPA. Male flies exposed to BPA exhibited key metabolic dysfunction phenotypes, including reduced satiety (hyperphagia), elevated triacylglyceride (TAG) levels, impaired TAG mobilization under nutrient stress, and hypertrophy of lipid droplets. Protein-protein interaction (PPI) network analysis identified overlapping genes between obesity-associated and BPA-responsive datasets. Candidate genes- AKH, AKHR, Foxo, Akt, Hnf4, FASN1, Upd2, Lsd, adp, and ERR showed significant misregulation at transcript and protein levels, supporting in silico predictions. Our findings establish Drosophila as a promising model for xenobiotic-induced metabolic dysfunction and a translational platform for mechanistic studies and future applications.
Perioperative dexamethasone is commonly used in enhanced recovery protocols, yet its safety in adrenalectomy remains underevaluated. We report a 33-year-old woman who developed postoperative adrenal crisis-like deterioration 54 hours after right adrenalectomy for a radiologically and biochemically non-functioning adrenal tumor on basal preoperative testing. A single 5 mg intravenous dose of dexamethasone was administered intraoperatively for antiemetic prophylaxis. During clinical deterioration, the patient exhibited marked suppression of ACTH and cortisol, consistent with pharmacological glucocorticoid effects in the perioperative period. However, the clinical presentation was non-specific and alternative postoperative complications, including infection, thromboembolic disease, and metabolic disturbances, could not be fully excluded. The patient improved following combined supportive therapy and stress-dose hydrocortisone. Preoperative endocrine evaluation did not include a 1 mg overnight dexamethasone suppression test, and mild autonomous cortisol secretion could not be excluded. Dynamic assessment of adrenal reserve was not performed preoperatively. This case highlights that perioperative dexamethasone may be temporally associated with postoperative endocrine perturbations that mimic adrenal crisis in susceptible patients. However, causality cannot be established, and careful differential diagnosis is essential in the postoperative setting following adrenal surgery.
Thyroid storm is a rare but life-threatening endocrine emergency characterized by extreme thyrotoxicosis and multi-organ dysfunction. Prompt recognition and rapid, coordinated management are essential to reduce its high mortality. This consensus statement, developed by experts in endocrinology and acute care, provides practical recommendations for the diagnosis and treatment of thyroid storm. Diagnosis remains clinical, aided by validated scoring systems such as the Burch-Wartofsky and Japanese Thyroid Association/Japan Endocrine Society criteria, which also predict outcomes. Management requires a multidisciplinary approach in high-dependency or intensive care settings, incorporating supportive measures, aggressive treatment of precipitating factors, and targeted therapies. Core treatments include beta-blockade, high-dose antithyroid drugs, corticosteroids, and iodide, with careful attention to timing and contraindications. Adjunctive therapies such as cholestyramine, lithium, plasmapheresis and extracorporeal membrane oxygenation (ECMO), as well as surgical thyroidectomy in selected cases, may be required for refractory disease. This guidance also highlights the need for definitive management of underlying hyperthyroidism after stabilization. By summarizing current evidence and expert consensus, this document aims to standardize care, support clinical decision-making, and improve outcomes in patients presenting with thyroid storm.
Emerging contaminants, such as antibiotics, antidepressants, non-steroidal anti-inflammatory drugs, analgesics, hormones, pesticides, and microplastics, pose a growing threat to aquatic ecosystems, primarily affecting macroinvertebrates, which are crucial as bioindicators of water quality. This study aims to evaluate the effects of these contaminants on the physiological and bioindicator responses of macroinvertebrates through a systematic review following the PRISMA methodology and a principal component analysis of standardised, categorised data to identify patterns in sublethal effects. It was found that anti-inflammatories, such as ketoprofen, and antidepressants, such as fluoxetine, alter the reproduction of Daphnia magna, reducing the number of offspring and affecting community structure. Non-steroidal anti-inflammatory drugs, such as ibuprofen, affect the locomotion of Gammarus pulex, reducing their speed and mobility, thereby disrupting their feeding and refuge-seeking behaviour. Analgesics, such as diclofenac, reduce the reproduction and abundance of aquatic species, including Neocaridina denticulata, thereby impacting biodiversity. Hormones, such as 17α-ethinylestradiol, interfere with the endocrine system of Mytilus galloprovincialis, thus altering reproduction. Pesticides, such as imidacloprid, favour tolerant species, including Asellus aquaticus, thereby affecting the structure of aquatic communities. Microplastics also alter the locomotion of Gammarus pulex, disrupting their ecological functions. In conclusion, emerging contaminants alter macroinvertebrate communities and compromise traditional water quality indices (BMWP, ASPT, EPT, SPEAR, and AMBI). It is necessary to adapt these indices by incorporating sensitivity weights and a functional approach to achieve more accurate assessments of water quality.
The conspecific alarm substance (CAS), a chemical compound likely based on glycosaminoglycans, purines, and nitrogen oxide-based pterins, is a natural stressor released by specialized epidermal cells damaged by injury or attack in fish, inducing hormonal and behavioral changes in conspecifics. Its effects in the reproductive context are poorly understood, but previous studies have demonstrated earlier spawning in broodstock exposed to CAS and an influence on the larval length of the offspring, potentially linked to increased cortisol transfer. In this study, 53 sexually mature specimens of Astyanax bimaculatus (18 males and 35 females) were exposed to CAS for 6 min, before hormonal induction by intraperitoneal injection of carp pituitary extract solution. The CAS substance was extracted by injuring the skin of donor conspecific animals, by superficial cuts of the epidermis, using scissors. After hormonal induction, the animals were paired for courtship. Following semi-natural reproduction, we assessed spawning time, embryonic development, hatching rate, larval anomalies in the first 18 h, initial larval linear morphometry in the first 72 h, and offspring survival for 7 days. The exposed animals spawned 1 h earlier than the non-exposed breeders. Despite this, embryonic development, hatching rate, larval anomalies, and survival were similar for the offspring resulted from the exposed and non-exposed groups, and the offspring of stressed breeders showed significantly shorter total length, improved cephalic development, a thicker dorsal muscle region, and greater yolk consumption 48 h after hatching. The scarcity of research on the physiological consequences of CAS on fish reproduction limits the interpretation of intergenerational findings. The precocity of gamete release suggests CAS as a potential trigger of reproduction in the species, but the results in the progeny remain inconclusive. Further studies, including endocrine assessments, are needed to confirm or refute the intergenerational patterns induced by CAS.
The human gut microbiota represents a complex ecosystem of trillions of microorganisms with profound implications for neurological health. Emerging evidence demonstrates that dysbiosis, an imbalance in microbial composition and function, plays a crucial role in the pathogenesis of neurodegenerative diseases and age-related cognitive decline. This chapter summarizes current knowledge of the microbiota-gut-brain axis (MGBA) and elucidates how intestinal microbes and their metabolites communicate with the central nervous system via neural, immune, endocrine, and metabolic pathways. We examine the mechanistic links between gut dysbiosis and specific neurodegenerative conditions, including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and Multiple sclerosis (MS). Furthermore, we explore age-related changes in the microbiota and their contributions to neuroinflammation, immunosenescence, and cognitive decline. Finally, we evaluate therapeutic interventions targeting the microbiota, including probiotics, prebiotics, synbiotics, and dietary modulation as promising strategies to prevent and ameliorate neurodegenerative pathology. The chapter provides a comprehensive summary of how microbiota-targeted approaches may delay ageing and neurodegeneration.
This study aims to systematically assess the association between exposure to endocrine-disrupting heavy metals (Pb, Hg, or Cr) and the risk of polycystic ovary syndrome (PCOS) through a meta-analysis of observational studies. Meta analysis Materials, Setting, Methods: We thoroughly explored PubMed, Embase, and the Cochrane Library for studies released until April 2023, using MeSH terms and keywords related to heavy metals and PCOS. Inclusion criteria encompassed observational studies reporting blood or urinary concentrations of Pb, Hg, or Cr in PCOS cases versus healthy controls. Seven Asian studies involving 897 reproductive-aged women were included. Whole-blood levels of Pb were significantly higher in PCOS (SMD=0.494, 95% CI: 0.227-0.761, p = 0.0003; I² = 99%), while serum or urinary levels showed no difference. Whole blood analysis provided more biologically relevant data for Pb exposure assessment due to its high binding affinity for hemoglobin. No statistically significant associations were observed for Hg exposure across biological matrices: serum (SMD = 2.047, 95% CI: -2.382 to 6.476, p = 0.365), whole blood (SMD = 0.831, 95% CI: -0.740 to 2.401, p = 0.300), or urine (SMD = 0.110, 95% CI: -0.253 to 0.473, p = 0.553). PCOS women had significant increased Cr across biological matrices (serum: SMD=0.287, 95%CI: 0.085-0.632, p <0.001; whole blood: SMD=0.506, 95% CI: 0.184-0.828, p =0.002) with minimal heterogeneity (I² = 0%). This meta-analysis identifies Pb and Cr exposure as a potential risk factor for PCOS in Asian populations. In contrast, Hg exhibited no statistically significant associations. These findings highlight the need for metal-specific prevention strategies in reproductive health.
Carbohydrate antigen 19-9 (CA19-9) is a well-established tumour marker primarily associated with pancreaticobiliary and gastrointestinal malignancies. Its elevation in benign gynaecological conditions, particularly in isolated ovarian endometriosis (OE) without malignancy, is rare and can pose a significant diagnostic challenge. In this case report, a 44-year-old female was found to have significantly elevated CA19-9 (up to 2453.1 U/mL), accompanied by left lower abdominal dull pain and weight loss. She was first diagnosed with an ovarian cyst more than 20 years ago, which resolved during pregnancy and recurred postpartum with no special intervention due to the absence of clinical symptoms. Extensive workup, including gastroenterological endoscopy and abdominal magnetic resonance imaging (MRI), excluded gastrointestinal malignancies. Laparoscopy followed by pathological examination confirmed the diagnosis of an ovarian endometriotic cyst (chocolate cyst). Postoperatively, the patient received standardised endocrine therapy, and follow-up assessments showed that serum CA19-9 levels returned to the normal range with no evidence of lesion recurrence. For female patients with elevated CA19-9 combined with a long-standing ovarian cyst and pelvic symptoms, ovarian malignancy should be suspected after excluding gastrointestinal lesions. However, benign diseases should also be considered. The final diagnosis should be based on comprehensive clinical evaluation, additional laboratory and imaging findings, and ultimately confirmed by pathological biopsy. Clinicians need to strengthen the cognitive understanding of this atypical manifestation to reduce misdiagnosis.
Various pharmacological properties and therapeutic effects were shown for Allium cepa L. (Liliaceae), (A. cepa) or onion and its derivatives including their effects on oxidative stress in different conditions. In this article, an update and comprehensive review of antioxidant effects of A. cepa and A. cepa-associated phytochemicals as well as the underlying molecular mechanisms are provided. The literature on antioxidant effects of A. cepa published between 2015 and the end of July 2025 was searched on database like PubMed, WOS, Science direct and Scopus. A. cepa and its constituents showed antioxidant in various conditions such as cardiovascular, endocrine and metabolic, gastrointestinal and liver, immunological, hematological and autoimmune, urogenital, neurologic and respiratory disorders as well as cancer and neoplasia. The antioxidant effects of A. cepa and its derivatives were achieved by decreasing lipid peroxidation (LPO), malondialdehyde (MDA), nitric oxide (NO), and endothelial nitric oxide synthase (eNOS), inhibiting NADPH oxidase (NOX) activity but enhancing antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione peroxidase omega (GSPO), thioredoxin reductase (TrxR), glutathione-S-transferase (GST) and glutathione reductase (GR) activities and thiol levels. Therefore A. cepa and A. cepa-associated phytochemicals showed potent antioxidant effects indicating their possible therapeutic value for treatment of disorders associated with oxidative stress.
Endocrine conditions such as thyroid disorders can significantly impact maternal and child health. Key determinants such as environmental setting and presence of iodine can influence the incidence of thyroid disorders. Individuals living in coastal regions are exposed to iodine rich foods in comparison to those residing in inland areas, which is a possible differentiating factor in the occurrence of thyroid based diseases in these individuals. Despite this possible relationship, very few studies have investigated the burden of thyroid diseases amongst coastal and inland populations. The study aims to systematically explore the prevalence of thyroid disorders in coastal and inland regions to understand the impact of differences in diet, environmental determinants, demographic variation and access to healthcare services on thyroid disease occurrence. Databases such as PubMed, Google Scholar and Scopus were used to identify articles in accordance with the PRISMA 2020 guidelines. Twenty three articles were selected based on them being in the English language, full length studies published between January 2017 and September 2023 and had reported on prevalence of thyroid diseases in inland and/or coastal areas. The review identified that a higher prevalence of thyroid cancer and thyroid nodules were seen amongst coastal populations, while goiter and hypothyroidism were seen in inland and mountainous areas. These differences were influenced by the iodine status of the region, consumption of seafood, presence of environmental pollutants like bisphenol A and polychlorinated biphenyls, iodization of salt, socioeconomic conditions and healthcare access. Female gender and older age was found to be significantly associated with greater burden of disease in both areas of study. The geographical location or setting is a vital determinant of the distribution of thyroid disorders, mainly through the influence of iodine intake and exposure to environmental pollutants. Regular monitoring of environmental pollutants, early detection of cases, universal iodization of salt and proactive supplementation of iodine may lead to decreased prevalence of thyroid disorders and its consequences. Longitudinal studies in this field can help identify the causal pathways emerging from socioeconomic factors and environmental determinants to thyroid disorders.