Endocrine Connections最新文献

Background: Patients with adrenal insufficiency require glucocorticoid replacement therapy either as hydrocortisone in multiple-daily doses or as low-dose prednisolone once daily. Data on the long-term safety, cardiovascular risk, and quality-of-life (QoL) outcomes of prednisolone remain limited.

Methods: In this prospective longitudinal cohort study, patients with adrenal insufficiency underwent a pre-specified switch from multiple-daily dose hydrocortisone to once-daily low-dose prednisolone (2-4 mg) as part of routine clinical care and followed up for at least four months. Cardiovascular risk was assessed using anthropometric and biochemical markers (lipid profile, HbA1c, C-reactive protein, blood pressure, and waist and hip circumference). QoL was evaluated using a modified SF-36 questionnaire. Baseline and follow-up measures were compared using paired t-tests or non-parametric equivalents.

Results: Of the 62 enrolled patients, 48 completed follow-up. The mean age was 54.5 ± 13 years; 56% were female; and 83% had secondary adrenal insufficiency. After at least four months on prednisolone, weight decreased significantly (90.6-89.6 kg, P = 0.007), accompanied by a reduction in systolic blood pressure (-5 mmHg, P = 0.032). Lipid parameters, HbA1c, and CRP remained unchanged (P > 0.05). Energy scores improved significantly (+9 points, P = 0.003), and patients reported increased treatment convenience (P = 0.002).

Conclusion: Low-dose once-daily prednisolone offers comparable cardiovascular risk to hydrocortisone while improving treatment convenience, systolic blood pressure, and SF-36 subjective energy scores. These findings support the use of prednisolone as a potentially preferable alternative in patients with adrenal insufficiency.

Objective: This study aimed to investigate the association between fasting glucagon levels and the risk of comorbid stroke in hospitalized patients with type 2 diabetes mellitus (T2DM).

Methods: This study included 1,745 T2DM patients hospitalized at Tianjin Medical University General Hospital from September 1, 2022, to September 30, 2025. Patients were divided into a T2DM group and a T2DM with stroke group based on the presence of stroke. Fasting glucagon levels and other clinical data were collected. Binary logistic regression models were used to analyze the relationship between fasting glucagon and stroke risk.

Results: Among female T2DM patients, fasting glucagon levels were significantly higher in the T2DM with stroke group compared to the T2DM group (13.38 vs 11.56 pmol/L, P = 0.011). Multivariable logistic regression analysis showed that after adjusting for multiple confounding factors, including age, diabetes duration, BMI, hypertension, eGFR, HbA1c, dyslipidemia, and medication use, higher fasting glucagon levels are independently associated with the presence of comorbid stroke in female T2DM patients (model 3: Q4 vs Q1: OR = 2.396, 95% CI: 1.075-5.339, P = 0.037). In addition, the prevalence of stroke increased with ascending quartiles of glucagon levels in female patients (P = 0.023). However, no significant association was observed between fasting glucagon levels and stroke risk in male patients.

Conclusion: This study demonstrates that among hospitalized female patients with T2DM, higher fasting glucagon levels are independently associated with the presence of comorbid stroke. This association suggests a potential link between glucagon and cerebrovascular diseases in this population, warranting further investigation to explore its role.

Objective: To identify factors independently associated with quality-of-life (QoL) impairment in Graves' hyperthyroidism (GH) patients and develop a clinically applicable nomogram for outpatient settings.

Methods: A total of 402 GH patients were recruited from the outpatient clinic of Endocrinology Department of Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, from January 2024 to June 2025. Participants were surveyed using a general information questionnaire, the Thyroid-specific Patient-Reported Outcome Short-Form (ThyPRO-39), the Pittsburgh Sleep Quality Index (PSQI), the Hamilton Depression Scale (HAMD), and the Hamilton Anxiety Scale (HAMA). Univariate and multivariate analyses identified independent predictors of QoL impairment. A nomogram was developed and validated using the area under the receiver operating characteristic curve (AUC), bootstrap-calibrated plots, and decision curve analysis (DCA). An online dynamic calculator (dynnom) was also developed to facilitate clinical application.

Results: Multivariate analysis revealed that thyroid eye disease (TED), goiter, sleep disturbances, anxiety, and depressive symptoms were independent predictors of QoL impairment. The nomogram demonstrated an excellent discriminative ability: AUC was 0.886 in the training group and 0.844 in the validation group. Bootstrap calibration showed good consistency between predicted and observed probabilities. DCA revealed favorable net clinical benefit across a 0.2-0.6 threshold range. The associated online calculator further improved clinical usability.

Conclusions: The nomogram integrating TED, goiter, sleep, and emotional factors provides a reliable tool for early identification of GH patients at high risk of QoL impairment in outpatient settings. Future external multicenter validation is needed to improve its generalizability.

Background: This study evaluated the effects of vitamin D supplementation on oxidative stress, inflammation, and pregnancy outcomes in women with gestational diabetes mellitus (GDM).

Methods: In a randomized, double-blind, placebo-controlled trial, 229 women with GDM were assigned to receive 200 IU of vitamin D twice daily or a placebo for 6 weeks alongside standard care. Biomarkers and pregnancy outcomes were assessed.

Results: Vitamin D supplementation significantly increased serum 25(OH)D and calcium levels, improved oxidative stress markers (increased GSH and decreased MDA), and reduced hs-CRP compared to placebo. The vitamin D group had a lower neonatal birth weight and a reduced incidence of macrosomia. No significant differences were found in fasting glucose changes or most other obstetric outcomes.

Conclusion: A 6-week vitamin D supplementation in women with GDM improved vitamin D status, ameliorated oxidative stress and inflammation, and was associated with reduced neonatal birth weight and macrosomia, without significantly affecting glycemic control.

RTN4IP1 encodes a mitochondrial oxidoreductase essential for coenzyme Q biosynthesis; pathogenic variants have been reported mainly in optic neuropathy and encephalopathy. We describe a 30-year-old woman carrying three novel pathogenic RTN4IP1 variants by exome sequencing (c.1163G>A p.Arg388Gln, c.949A>C p.Met317Leu, and c.1109T>C p.Phe370Ser), who presented with panhypopituitarism, optic nerve hypoplasia, corpus callosum agenesis, bicuspid aortic valve disease, seizures, and muscle pain, already on conventional hormone replacement. Coenzyme Q10 (CoQ10) (200 mg) was administered orally for six months; outcomes were assessed using BPI, WOMAC, TUG, LEFS, grip-strength dynamometry, SF-36, CPK, and LDH, and after six months of daily 200 mg CoQ10, the patient showed marked reductions in pain (BPI 4 → 0.8; -80%) and muscle-damage markers (CPK 254 → 110 U/L) together with gains in grip strength (+49%) and lower-extremity function (LEFS 31 → 60; +94%). SF-36 domains related to physical health showed marked gains, while emotional scores remained stable. This is the first report linking RTN4IP1 mutations to endocrine failure and suggesting a therapeutic role for CoQ10 in mitochondrial-related endocrine disease.

Background: Age at puberty determines timing of pubertal growth spurt. Whether the intensity of the peri-pubertal growth velocity is also affected by pubertal timing in boys remains to be elucidated.

Objective: To study changes in growth velocity in relation to pubertal timing, Insulin-like Growth Factor-I (IGF-I) and fasting insulin in healthy boys.

Design, setting and participant: Longitudinal study with biannual assessment of testicular volume (TV), growth velocity, IGF-I and fasting insulin levels. Peak height velocity (PHV) was calculated. 105 boys (947 examinations) were included. Pubertal onset was available in 62 boys - the rest remained prepubertal throughout the study period or were in puberty at baseline.

Results: Age at pubertal onset (TV > 3 ml) was negatively correlated with PHV (ρ = -0.48; p < 0.001). The early (age of onset < 33,3 percentile) tertile of maturing boys had significantly higher growth velocity (mean Δ 0.48 (0.14 - 0.82) cm/year; p < 0.006) than late maturing boys (> 66,7 percentile) over the 6 years peri-pubertal period. However, the late maturing boys remained significantly taller throughout the study (p < 0.05). IGF-I levels were similar between the 3 groups of boys. In all boys, the increase in growth velocity was associated with a larger increase in IGF-I (p < 0.001) during the first 2 years of puberty.

Conclusion: Early maturation was associated with increased growth velocity and PHV in healthy boys. However, it was not sufficient to compensate for the shorter total growth period. IGF-I was positively associated with growth velocity.

Primary hyperparathyroidism (PHPT), increasingly diagnosed in its asymptomatic form, is associated with clinically significant neuromuscular dysfunction. Growing evidence indicates that skeletal muscle is a direct target of parathyroid hormone (PTH), with chronic PTH excess impairing mitochondrial bioenergetics, promoting proteolysis, and altering muscle-bone-adipose endocrine crosstalk. Experimental studies confirm PTH receptor type 1 (PTHR1) expression in muscle fibers and satellite cells, while transcriptomic analyses of PHPT muscle reveal dysregulation of calcium signaling and oxidative metabolic pathways. Clinically, patients with PHPT, irrespective of hypercalcemia, demonstrate reduced grip strength, slower gait speed, impaired chair-stand performance, and diminished postural stability. Parathyroidectomy improves several of these deficits, with studies reporting increases in grip strength, knee extension force, ambulatory capacity, and, in some cohorts, improved muscle composition and metabolic gene expression. However, available data are heterogeneous and derived primarily from small cohorts with variable functional measures. Current evidence implicates PTH-mediated skeletal muscle dysfunction as a reversible component of PHPT, yet key mechanistic and clinical gaps remain. Standardized functional assessments and larger prospective studies are needed to clarify biological pathways, identify predictors of postoperative recovery, and inform the integration of muscle health into PHPT management. The focus of this review was to explore evidence linking PTH excess and skeletal muscle pathophysiology and review the relationship between PHPT and parathyroidectomy on physical function.

Background: Epidermal growth factor (EGF) plays a crucial role in cellular growth, differentiation, and pancreatic β-cell maintenance. Despite reports on EGF deficiency in diabetic animal models, its relevance in type 2 diabetes (T2D), particularly in relation to obesity, remains underexplored. The present study aimed to evaluate plasma EGF levels in individuals with and without T2D, assess its associations with glycaemic status and clinical parameters, and evaluate the influence of obesity on these relationships.

Methods: A total of 838 eligible participants were selected from the Kuwait Diabetes Epidemiology Program. Of those, 428 were included in a 1:1 case-control analysis (214 T2D and 214 non-diabetics). EGF was measured in plasma using ELISA. Associations between EGF with glycaemic and clinical variables were evaluated using Pearson's correlation, multiple linear regression, and logistic regression analyses.

Results: Plasma EGF levels were significantly lower in individuals with T2D compared to non-diabetics (P < 0.001). Among non-diabetics, obese participants had a significantly lower EGF level than their non-obese counterparts (P = 0.03), while no such difference was observed in T2D. EGF negatively correlated with fasting blood glucose in both non-diabetics (P = 0.004) and T2D individuals (P < 0.001). In T2D, EGF negatively correlated with haemoglobin A1C (HbA1C) (P = 0.001), triglyceride (TG) (P = 0.021), and waist-to-hip ratio (WHR) (P = 0.014). Logistic regression confirmed that lower EGF levels were independently associated with T2D but not with general obesity (OR = 0.996, P = 0.001).

Conclusion: Reduced EGF levels are associated with poor glycaemic control in T2D. These findings highlight EGF's potential as a biomarker for glycaemic dysregulation and support further investigation into its role in diabetes pathophysiology and complications.

Purpose: Ketosis-prone diabetes (KPD) is a new subtype of diabetes distinct from traditional type 2 diabetes, and the role of muscle mass in KPD remains unclear. Serum creatinine-to-cystatin C ratio (CCR) has been identified as a marker of muscle mass. The present study aims to investigate the value of CCR in newly diagnosed KPD.

Methods: Two hundred and ninety patients with newly diagnosed T2D were included in the study and were divided into T2D (n = 195) and KPD (n = 95) groups according to the occurrence of ketosis. The cutoff value of CCR in identifying KPD was analyzed by receiver operating characteristic (ROC) curves. Logistic regression was used to assess the relationship between CCR and KPD and the independent influences on KPD.

Results: The serum CCR level of the KPD group was significantly higher than that of the T2D group. After adjustment for all confounders, the risk of KPD was significantly increased with elevated CCR levels. The optimal cutoff value for CCR was 69.775 for male and 63.365 for female, with areas under the ROC curve of 0.639 for male and 0.648 for female. Postprandial blood glucose and CCR were independent risk factors, whereas age and postprandial C-peptide were independent protective factors for the KPD.

Conclusion: High levels of CCR are significantly associated with the odds of KPD, suggesting that higher muscle mass (estimated by CCR) may be linked to higher KPD incidence. Our study suggests that CCR may be a useful marker for the incidence of KPD, providing new insights into the mechanisms of KPD.