Prolactinoma is the most common subtype of pituitary adenoma, and dopamine agonists are the gold standard for treatment, primarily cabergoline. Current guidelines suggest that transsphenoidal surgery could be offered, especially to young women with noninvasive microprolactinomas, due to its cost-effectiveness. Additionally, concerns regarding the long-term use of dopamine agonists and their lower remission rates have been raised. The SPARAGMOS trial (NCT07463235) will be an interventional, randomized, open-label, multicenter study utilizing a high dose of cabergoline for approximately 6 months to suppress prolactin levels, with the hypothetical goal of achieving greater tumor apoptosis and remission rates. Under this protocol, a remission rate of approximately 70% is hypothesized, similar to that achieved through neurosurgery in specialized pituitary centers or when cabergoline is carefully considered for withdrawal (i.e. treatment duration exceeding 2 years, low dosing, tumor shrinkage, and normoprolactinemia). The control group will receive cabergoline for 2 years at the lowest dose necessary to achieve normoprolactinemia, as per current guidelines. Under these conditions, the remission rate is expected to be low, around 30%. The findings from this trial have the potential to influence and redefine future therapeutic strategies for microprolactinoma.
BACKGROUND:Diabetic kidney disease (DKD) is a major complication of type 2 diabetes (T2D). Fibroblast growth factor 19 (FGF19) is a key metabolic regulator, but its relationship with DKD, as defined by estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (UACR), remains unclear. METHODS:This cross-sectional study included 330 T2D inpatients and 60 normal controls (NC group). Serum FGF19 levels were measured by ELISA. Renal function was evaluated according to eGFR (CKD-EPI equation) and UACR. Associations between FGF19 levels and renal parameters were analyzed according to Spearman's correlation, partial correlation, and multiple linear regression analyses adjusted for confounders. RESULTS:Serum FGF19 levels were lower in the T2D group than in the NC group (110.25 [68.40-169.32] vs. 242.06 [143.74-319.51] pg/mL, p < 0.001). Among those with T2D, patients with DKD had higher FGF19 levels than those without DKD (122.61 [83.38-189.02] vs. 106.97 [66.54-164.22] pg/mL, p = 0.023). In T2D patients, FGF19 was positively correlated with UACR (r = 0.185; p = 0.005) and inversely correlated with eGFR (r = -0.210; p = 0.001), and these correlations persisted after adjustment for confounders. In fully adjusted linear regression models, FGF19 remained independently associated with a higher UACR (β = 0.203, t = 2.286, p = 0.024) and a lower eGFR (β = -0.170, t = -2.542, p = 0.012). Restricted cubic spline analyses confirmed linear relationships between lnFGF19 and both lnUACR (p = 0.480) and eGFR (p = 0.162). CONCLUSION:Serum FGF19 levels are independently associated with DKD status in T2D patients; the serum FGF19 level is decreased in T2D patients but relatively elevated in those with DKD. FGF19 levels are independently associated with a higher UACR and a lower eGFR. Restricted cubic spline analyses confirmed linear, rather than nonlinear, associations. These cross-sectional findings suggest an association between FGF19 and diabetic kidney pathology, though the modest effect sizes and study design limit causal interpretation.
BACKGROUND:PCOS is a hormonal disorder with no medication, hence treatment is symptomatic. Letrozole plus chromium, L-arginine, or myoinositol was tested in PCOS-infertile women. METHODS:This prospective trial randomly assigned 240 PCOS patients (n = 60) to one of four groups: letrozole + chromium, L-arginine, myoinositol, or the control. Insulin resistance, testosterone, HOMA-IR, hirsutism, DHEA, and ovulatory function were examined before and after treatment. RESULTS:At each follow-up, all groups showed substantially different ovulation rates (p = 0.026, 0.039, and 0.008 at 1, 2, and 3 months, respectively). Weight, HOMA-IR, and hirsutism were decreased with chromium and myoinositol (p = 0.001). Chromium, myoinositol, and L-arginine significantly reduced testosterone. Myoinositol had the highest pregnancy rates at one and two months (36.7% and 41.9%, respectively). Conclusion: letrozole combined with chromium or myoinositol improves PCOS ovulation, HOMA-IR, and hirsutism.
INTRODUCTION:Thyroid cancer (TC) represents the most frequently diagnosed malignancy of the endocrine system, with its incidence continuing to increase worldwide. Multimerin 1 (MMRN1), a glycoprotein implicated in various cancers, exhibits context-dependent roles, but its function in TC remains unexplored. The Hippo pathway, a key regulator of cell proliferation and apoptosis, is frequently dysregulated in TC. We hypothesized that MMRN1 inhibits TC progression by activating the Hippo signaling pathway. METHODS:Bioinformatics analysis of GSE33630 identified differentially expressed genes (DEGs) in TC. MMRN1 expression was validated in TC cell lines (BCPAP, TPC-1, IHH-4, HTH83) and normal thyroid cells (NTHY-ORI3.1) via RT-qPCR and Western blot. Functional assays assessed proliferation, migration, and invasion. Hippo pathway activity was evaluated after MMRN1 modulation. Oxidative stress and ferroptosis markers (ROS, SOD, CAT, GSH, MDA, GPX4, TF, TFR1) were analyzed. RESULTS:MMRN1 was downregulated in TC tissues and cell lines. Overexpression of MMRN1 suppressed TC cell proliferation, migration, and invasion while promoting apoptosis. Mechanistically, MMRN1 activated Hippo signaling, increasing p-MST1/2, p-LATS1/2, and p-YAP levels. Verteporfin reversed these effects. Additionally, MMRN1 modulated oxidative stress markers (including ROS and the indirect lipid peroxidation marker MDA) and altered GPX4 activity and iron metabolism, suggesting enhanced ferroptosis sensitivity. CONCLUSION:MMRN1 acts as a tumor suppressor in TC by activating the Hippo pathway and modulating oxidative stress and ferroptosis. These findings highlight MMRN1 as a potential therapeutic target for TC treatment.
BACKGROUND:Testosterone therapy induces well-known changes in body composition in transgender men; however, its short-term cardiometabolic effects remain incompletely characterized. This study aimed to evaluate body composition and cardiometabolic changes during testosterone therapy over a 12-month period. METHODS:This retrospective observational study included 15 transgender men initiating intramuscular testosterone therapy who were followed for 12 months. Anthropometric measurements, body composition, blood pressure, and laboratory parameters including lipid profile, fasting glucose, HbA1c, plasma atherogenic index (PAI), and triglyceride-glucose (TyG) index were assessed at baseline and at 12 months. All participants initiated intramuscular depot testosterone therapy administered every 28 days. None of the participants underwent oophorectomy during the study period. RESULTS:Total testosterone levels increased significantly from 40.82 ± 19.46 ng/dL to 338.06 ± 205.02 ng/dL (p < 0.001), while estradiol levels remained stable. Systolic blood pressure and mean arterial pressure showed mild but non-significant increases during follow-up. Body weight, body mass index, and fat-free mass increased significantly, while body fat percentage decreased. HDL cholesterol levels decreased (59.7 ± 11.2 to 52.3 ± 13.2 mg/dL, p = 0.019), and triglyceride levels showed a non-significant upward trend. The PAI increased from 0.08 ± 0.24 to 0.23 ± 0.25 (p = 0.017), and the TyG index rose from 8.02 ± 0.43 to 8.21 ± 0.39 (p = 0.016). Blood pressure parameters did not change significantly. CONCLUSIONS:In transgender men without oophorectomy, testosterone therapy was associated with favorable changes in body composition alongside modest shifts in cardiometabolic indices over a 12-month period. These findings suggest that simple indices such as PAI and TyG may be useful for monitoring early cardiometabolic changes attributable to exogenous testosterone therapy. Larger prospective studies are warranted to confirm these observations.
BACKGROUND:Thyroid cancer (TC), the most common endocrine malignancy, is closely linked to aging. In this study, we estimated DNA methylation (DNAm) age in TC tissues versus adjacent non-cancerous thyroid tissues using TCGA and GSE97466 datasets. METHODS:We employed multi-tissue DNAm age estimators, specifically Horvath's clock and the Bayesian Neural Network (BNN) clock, to quantify epigenetic aging in TC and adjacent normal tissues from the TCGA and GSE97466 cohorts. We further integrated genomic, transcriptomic, and mutational analyses, including assessments of senescence-associated secretory phenotype (SASP), immune cell infiltration, and thyroid differentiation, to elucidate the associations between DNAm age acceleration and various cancer-related features. RESULTS:Our results revealed marked DNAm age acceleration in TC tissues relative to controls, with both models yielding significantly higher DNAm age estimates in tumors. Although DNAm age correlated strongly with chronological age in control tissues (R ≈ 0.94), this association was notably diminished in TC tissues (R ≈ 0.62). Moreover, TC tissues with accelerated DNAm age exhibited higher telomerase-associated gene expression score, heightened SASP signaling, and distinct immune profiles characterized by elevated M2 macrophages and reduced activated NK cells. Genomic analysis further showed a higher prevalence of BRAF mutations and lower thyroid differentiation scores (TDS) in the accelerated subgroup. No significant associations were detected between DNAm age and clinicopathological parameters or overall survival. CONCLUSIONS:Our findings provide valuable insights into the complex interplay between epigenetic regulation, immune dysfunction, and genomic instability in thyroid cancer, highlighting promising avenues for future research and therapeutic intervention.
INTRODUCTION:Androgen receptor (AR) gene mutations are a common cause of 46, XY disorders of sex development (DSD), resulting in varying degrees of androgen insensitivity. This study aims to comprehensively evaluate the clinical features, hormone profiles, and AR gene variants of patients diagnosed with Androgen Insensitivity Syndrome (AIS), and to analyze the distribution of these variants across different functional domains. MATERIALS AND METHODS:This retrospective, single-center study analyzed 16 cases of 46, XY DSD, all of whom were found to have AR variants from a single tertiary center in Turkey. Patients were evaluated based on their complaints, hormonal measurements, clinical features, and genetic diagnoses. Patients were classified as having Complete, Partial, or Mild AIS. The variants were categorized based on their location within the functional domains: The Ligand Binding Domain (LBD) and the N-terminal Domain (NTD). RESULTS:Patients were classified as having CAIS (8/16), PAIS (6/16), MAIS (1/16), and suspected diagnosis (1/16). The most common clinical finding was cryptorchidism (11/16). Ten different AR variants were detected: eight missense (p.Pro392Ser, p.Ala749Val, p.Val890Met, p.Asp733Asn, p.Arg856His, p.Arg856Cys, p.Glu494Ala, and p.Glu710Lys), one nonsense (p.Lys659Ter), and with p.Lys659Ter, p.Glu494Ala and being novel. A CAIS associated with p.Pro392Ser has been reported, and intrafamily variability has been documented in variants such as p.Arg856His and p.Pro392Ser. Most variants (10/16 patients) localized to the LBD. Individuals harboring LBD variants demonstrated lower external genital scores and shorter phallus lengths compared to those with NTD variants. T/DHT ratio was available in 11 patients and did not yield false-positive AIS diagnoses. Marked intrafamilial phenotypic variability was observed. CONCLUSION:This study expands the AR variant spectrum in AIS and represents one of the more comprehensively characterized cohorts from our country. While LBD variants were more often associated with severe phenotypes and NTD variants with milder presentations, marked phenotypic variability was observed. Nevertheless, considerable phenotypic variability, including marked intrafamilial heterogeneity, was evident. The T/DHT ratio provided supportive biochemical information but did not replace the need for molecular confirmation. Molecular confirmation remains essential, and multidisciplinary, patient-centered management is warranted.
Cortisol and vitamin D are known to influence plasma glucose, but their relationship with glycemia, assessed by continuous glucose monitoring, remains unclear for healthy adults. This study compared these relationships between 32 young (26.0 ± 4.8 years) and 25 older (67.3 ± 4.8 years) healthy volunteers. Cortisol was determined at bedtime, awakening, and 30 min (T30) and 60 min (T60) post-awakening. Older adults had higher fasting glucose but lower cortisol concentration at T30 than young adults. In young adults, night- and daytime mean glucose and fasting glucose correlated negatively with cortisol at T30, while glycemic variability correlated positively with cortisol at T60. Vitamin D correlated negatively with nighttime mean glucose in the young group. In conclusion, glucose concentration and glycemic variability are associated with the cortisol response the following morning. The lack of these associations in older adults could be explained by their higher fasting glucose concentrations resulting in a lower morning cortisol response.
BACKGROUND:Chronic low-grade inflammation contributes to the development and complications of type 2 diabetes (T2D). Nutritional ketosis improves glycemic control and weight, but its broader immunomodulatory effects are less well defined. METHODS:In this post-hoc analysis, adults with T2D (n = 195) or prediabetes (n = 89) in a two-year continuous care intervention (CCI) with individualized carbohydrate reduction emphasizing nutritional ketosis were compared with T2D participants receiving usual care (UC, n = 63). Serum was collected at baseline, 1, and 2 years for high-sensitivity CRP, 15 cytokines/adhesion molecules, and comprehensive blood count (CBC)-derived indices. Linear mixed-effects models evaluated longitudinal changes, while regression (including least absolute shrinkage and selection operator, LASSO) examined associations with mean β-hydroxybutyrate (BHB), weight change, HbA1c, and HOMA-IR. RESULTS:Nineteen of 21 markers declined at 1 year in CCI, largely sustained at 2 years; UC showed no changes. Higher BHB predicted reductions in WBC, ICAM-1, VEGF-A, and systemic immune-inflammation index (SII), while weight loss correlated with IL-6, IL-18, IL-1β, and TNF-α. CONCLUSION:CCI induced broad, durable anti-inflammatory effects, supporting its role in lowering systemic inflammation and cardiometabolic risk.
BACKGROUND:Tauroursodeoxycholic acid (TUDCA) has been shown to improve endothelial dysfunction in type 2 diabetes mellitus (T2DM). However, its role in attenuating endothelial insulin resistance in diabetes is not well understood. OBJECTIVES:This study aimed to investigate TUDCA's potential therapeutic effect on endothelial insulin resistance and its underlying mechanisms. METHODS:Twenty-seven male Sprague Dawley rats were categorized into control (CON, n = 9), diabetes (DM, n = 9), and diabetes treated with TUDCA (DMT, n = 9). Diabetes was induced using a high-fat diet and low-dose streptozotocin. TUDCA (150 mg/kg) was administered to the DMT group during the last two weeks of a 15-week study. Aortic tissues were analyzed for insulin-mediated relaxation, endoplasmic reticulum (ER) stress markers [inositol-requiring kinase 1 (IRE-1), protein kinase-like ER kinase (PERK), and binding immunoglobulin protein (BIP)], end othelial function markers [endothelial nitric oxide synthase (eNOS), protein kinase B (Akt), and insulinreceptor substrate-1 (IRS-1)], oxidative stress [superoxide dismutase activity (SOD) and malondialdehyde level (MDA)] and inflammation [tumor necrosis factor-alpha (TNF-a)] markers. RESULTS:Insulin-mediated relaxation was impaired in diabetic rats (-56.7%) compared to controls (0%), accompanied by elevated ER stress markers and reduced eNOS, Akt, and IRS-1 expression. TUDCA treatment improved relaxation responses (-6.2%) significantly reduced ER stress markers and restored the expression of endothelial markers.
BACKGROUND:Thyroid cancer (THCA) is one of the most common endocrine malignancies, with a significant increase in incidence over the past few decades. ETS variant transcription factor 4 (ETV4) is a member of the ETS family of transcription factors, which play crucial roles in tumorigenesis. However, the precise mechanisms by which ETV4 contributes to THCA progression remain largely unexplored. METHODS:The expression levels of ETV4, programmed death-ligand 1 (PD-L1), signal transducer and activator of transcription 6 (STAT6), and solute carrier family 7 member 11 (SLC7A11) were analyzed using quantitative reverse transcription PCR (qRT-PCR) and western blotting assays. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Reactive oxygen species (ROS) levels and apoptosis were evaluated by flow cytometry. Colorimetric assays were employed to measure malondialdehyde (MDA) levels, glutathione (GSH) levels, iron (Fe2+) levels, and lactate dehydrogenase (LDH) cytotoxicity. Enzyme-linked immunosorbent assay (ELISA) was used to quantify interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin-2 (IL-2) levels. The interaction between ETV4 and STAT6 was confirmed using a dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay. RESULTS:ETV4 expression was upregulated in THCA tissues and cells. Its knockdown increased ROS, MDA, and Fe2+, decreased GSH and SLC7A11, and reduced PD-L1 expression. Silencing ETV4 enhanced CD8+ T cell cytotoxicity and elevated secretion of IFN-γ, TNF-α, and IL-2, while promoting apoptosis. STAT6 expression was upregulated in THCA tissues and positively correlated with ETV4 expression. Mechanistically, ETV4 transcriptionally activated STAT6 in FTC-133 cells, and STAT6 overexpression inhibited ferroptosis and promoted immune escape by interacting with ETV4. CONCLUSION:ETV4 transcriptionally activated STAT6 to inhibit ferroptosis and promote immune escape in THCA. Targeting the ETV4-STAT6 axis may offer a novel therapeutic strategy, potentially inhibiting ferroptosis and enhancing immune response in THCA patients.
PURPOSE:This review aims to discuss the prevalence, risk factors, and management of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) in patients with end-stage renal disease (ESRD) on hemodialysis. METHODS:A comprehensive literature review of retrospective studies, case reports, and clinical guidelines was conducted. RESULTS:DKA and HHS incidence is lower in ESRD patients due to delayed insulin clearance and regular dialysis. Management requires cautious fluid administration, reduced insulin infusion rates, conservative potassium replacement, and gradual correction of hyperosmolarity. Emergency hemodialysis may be necessary for severe acidosis or hyperkalemia. CONCLUSION:Treatment must be individualized. Emerging strategies, including extended dialysis sessions and closed-loop insulin delivery, require further validation.
INTRODUCTION:The pancreas is innervated by a complex network including vagal, sympathetic, and spinal sensory pathways but recent studies suggest that the trigeminal system, known for its role in sensory perception, may also contribute to pancreatic innervation. METHODS:This review explores the hypothesis that the trigeminal system, via sensory neuropeptides such as calcitonin gene-related peptide and substance P, plays a role in pancreatic sensory innervation. Several hypotheses are proposed to explain this potential role, including embryological development, antidromic activity, and neurotransmitter actions. RESULTS:Neuropeptides, found in pancreatic tissues, may influence blood flow, inflammation, and pain perception, as well as modulate pancreatic functions such as enzyme secretion and insulin release. Understanding the interplay between the trigeminal system and the pancreas could provide insights into the pathophysiology of conditions like pancreatitis and diabetes. DISCUSSION:Targeting these pathways might offer new therapeutic strategies for managing pancreatic disorders, especially pain control and inflammation.
OBJECTIVE:We aimed to determine the relationship between obstructive sleep apnea (OSA) and diabetes in Korean adults. METHODS:This study used data from the 8th Korea National Health and Nutrition Examination Survey (2019-2021). A total of 11,439 adults aged ≥40 years were included. The obstructive sleep apnea was evaluated using the Snoring, Tiredness during the daytime, Observed apnea, high blood Pressure, Body mass index, Age, Neck circumference, and Gender (STOP-BANG) criteria. RESULTS:The prevalence of diabetes was 18.3% and a high risk for OSA was 7.3%. The prevalence of diabetes differed depending on the OSA risk, with the high-risk group demonstrating a significantly higher adjusted odds ratio for diabetes (2.78, 95% confidence interval = 2.24-3.44) compared with the low-risk group for OSA. Additionally, we identified a dose-response relationship, where the risk of diabetes increased as the number of risk factors for OSA increased (p < 0.001). CONCLUSION:People at high risk for OSA had a higher prevalence of diabetes than those who were not at risk. Given the increasing burden of diabetes and the potential association of OSA with other essential health conditions, further research is needed to evaluate the benefits of diabetes prevention or blood glucose testing in patients with OSA.
OBJECTIVE:Herein, we aimed to reveal the factors affecting the early treatment responses and the normalization process of thyroid hormone levels in childhood Graves' disease.. METHODS:This retrospective study included 46 pediatric patients who were diagnosed with Graves' disease and started treatment during a period of 10 years, and whose at least one of their free T3 (fT3) or free T4 (fT4) levels decreased to the reference range during follow-up. RESULTS:The normalization time of fT3 and fT4 were 5 (3-8) and 3.5 (2-7) weeks after the treatment initiation, respectively. Gender, age, pubertal status, presence of goiter, ophthalmopathy or tachycardia, basal thyroid hormone levels, initial dose of methimazole, and addition of beta-blockers did not show an effect on the normalization time of either fT3 or fT4 (p > 0.05). In those under the age of 12 (n = 15) with a high TRAb titer (>10 IU/L), the time for normalization of fT3 was longer (p = 0.024), and in those with ophthalmopathy, this process was longer for fT4 (p = 0.017). CONCLUSIONS:By these results, we showed that early treatment response and the normalization period of thyroid hormones were not related to the initial treatment dose.
OBJECTIVE:Orexin-A (OXA) is a hypothalamic neuropeptide implicated in glucose regulation and insulin sensitivity. Given the central role of insulin resistance in polycystic ovary syndrome (PCOS), this study evaluated serum OXA levels in women with PCOS. METHODS:This cross-sectional case-control study included 88 women with PCOS and 88 age- and body mass index-matched controls. Serum OXA levels were quantified using a commercial ELISA kit. RESULTS:Serum OXA levels were significantly lower in women with PCOS than in controls (321.53 ng/L vs. 385.06 ng/L, p = 0.012). A significant negative correlation was observed between the modified Ferriman-Gallwey score and serum OXA level. In the ROC analysis, a serum OXA level of 369.55 ng/L yielded a sensitivity of 55.7% and a specificity of 55.7% (AUC: 0.610) for detecting PCOS. CONCLUSIONS:Serum OXA concentrations were reduced in women with PCOS. Whether this reduction contributes to PCOS pathogenesis or reflects a secondary alteration remains uncertain.
BACKGROUND:Testosterone plays multifaceted roles in cardiovascular health. However, the prospective sex-specific impact of serum testosterone on atherosclerotic cardiovascular disease (ASCVD) risk remains unclear. METHODS:This prospective study included 2978 participants (1184 men and 1794 women) with a followed-up 10.66 years. The Cox proportional hazards model was employed to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for ASCVD events according to testosterone tertiles. Additionally, structural equation modeling was used to investigate whether hypertension and metabolic factors mediate the association between serum testosterone levels and ASCVD risk. RESULTS:During follow-up, 142 and 203 ASCVD events occurred in men and women, respectively. Compared with participants in the lowest serum testosterone tertile, men in the highest tertile exhibited a reduced ASCVD risk (HR: 0.59, 95% CI: 0.38-0.90), while women in the highest tertile showed an increased risk of ASCVD (HR: 1.79, 95% CI:1.26-2.55). Structural equation modeling revealed that in men, the association between testosterone and ASCVD risk was indirectly mediated by metabolic factors (β = -0.119). Among women, the results indicated a total effect of testosterone on ASCVD risk (β = 0.051), comprising a significant direct positive effect (β = 0.056) and a negative indirect effect mediated by hypertension and metabolic factors (β = -0.005). CONCLUSIONS:Elevated serum testosterone levels are associated with a reduced risk of ASCVD in men but an increased risk in women.
BACKGROUND:Sleep Apnea Syndrome (SAS) is a common problem in acromegaly. This study examines changes in apnea hypopnea index (AHI) and sleep quality following treatment for acromegaly. METHODS:Subjects with active acromegaly underwent polysomnography to identify SAS and Pittsburgh Sleep Quality Index (PSI) questionnaire for the assessment of subjective sleep quality at baseline, which were repeated after treatment. RESULTS:Twenty patients were recruited. Obstructive SAS was present in 85% and poor sleep quality was reported in 65% patients. AHI positively correlated with age, duration of disease, male gender, and PSQI score. After treatment, there was a significant decrease in tumor volume (72%) and insulin-like growth hormone (IGF-1) levels (44%), although IGF-1 normalization was seen in only 34% subjects. There was a significant reduction in mean AHI (35 ± 20 vs 23 ± 19; p = 0.008) and mean PSQI (7.8 ± 3.9 vs 5.6 ± 3.6; p = 0.002) after treatment. CONCLUSION:Mean AHI and mean PSQI improved significantly after treatment, although normalization of IGF-1 was seen in only one-third of patients.
INTRODUCTION:Continuous glucose monitoring (CGM) demonstrates significant benefits in glycemic control for both type 1 and type 2 diabetes, including reductions in HbA1c, increased time-in-range, and decreased hypoglycemia. METHODS:In this article, we review the recent American Diabetes Association guidelines recommending real-time CGM for adults with type 2 diabetes, including those not using insulin. RESULTS:While acknowledging the documented advantages, CGM remains underutilized, with many barriers, particularly in primary care settings and among racially diverse or lower socioeconomic populations. DISCUSSION:This review outlines positive strategies to address barriers to CGM-adoption, optimize glycemic control and thereby potentially reduce cardiovascular-kidney-metabolic complications.
INTRODUCTION:A leading endocrine illness affecting women of reproductive age is autoimmune thyroid disease (AITD), which can have a significant impact on the course of a pregnancy. Thyroid dysfunction is more likely to occur during pregnancy due to hormonal and immunological changes. Women are more susceptible to thyroid dysfunction during pregnancy because of physiological changes that increase the need for thyroid hormones. METHODS:This review summarizes the most recent research on alterations in thyroid function during pregnancy, investigates the mechanisms underlying autoimmune thyroid imbalance and its effects on reproduction, and emphasizes the importance of early detection and specialized clinical management. RESULTS:Infertility, miscarriage, preterm birth, and decreased fetal development are among the negative reproductive consequences that can result from AITD, which affects up to 2-5% of pregnant women and is frequently asymptomatic and undetected. DISCUSSION:To maximize outcomes for both the mother and the fetus, early detection and specialized clinical management are essential, particularly because AITD is often asymptomatic and can go undetected during pregnancy.
