Hormone and Metabolic Research最新文献

Adrenalectomy and conservative management are therapeutic approaches for mild autonomous cortisol secretion; however, their comparative clinical impact in routine practice remains uncertain. We aimed to evaluate real-world hormonal, clinical, and metabolic outcomes according to the treatment strategy in patients with mild autonomous cortisol secretion. This single-center retrospective observational study included consecutive patients with adrenal incidentaloma fulfilling guideline-based diagnostic criteria for mild autonomous cortisol secretion between January 2015 and December 2024. Sixty-five patients with complete hormonal evaluation and follow-up data were analyzed and classified into surgery (n=23) and conservative (n=42) groups. Demographic characteristics, adenoma features, comorbidities, hormonal parameters, and metabolic outcomes were assessed at baseline and at the final follow-up. The median follow-up duration was approximately 3 years and similar between groups (p>0.05). At baseline, the body mass index, adenoma size, and cortisol levels after the 1-mg dexamethasone suppression test were significantly higher, while adrenocorticotropic hormone levels were lower in the surgery group (p=0.02, p=0.02, p=0.036, and p<0.01, respectively). During the follow-up, adrenocorticotropic hormone levels increased and post-dexamethasone suppression test cortisol levels significantly decreased after adrenalectomy (p=0.001 and p=0.036, respectively), whereas metabolic parameters and comorbidity profiles remained largely unchanged. In the conservative group, total cholesterol increased modestly over time (p=0.048), with no significant changes in other clinical outcomes. No significant difference in comorbidity progression was observed between treatment strategies. In this real-world cohort, adrenalectomy resulted in clear hormonal improvement without parallel short-term metabolic or clinical benefits compared with conservative management. These findings highlight the heterogeneous clinical expression of mild autonomous cortisol secretion and underscore the importance of individualized patient selection for surgery.

Primary hyperparathyroidism is an endocrine disorder characterized by chronic hypercalcaemia resulting from the unregulated excessive production of parathyroid hormone. This study aimed mainly to determine the clinical manifestations of primary hyperparathyroidism within the African population. This study was a systematic review carried out in strict compliance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The meta-analysis was executed utilizing Meta XL version 5.3, applying the DerSimonian Laird random-effects model. A total of 52 studies met the eligibility criteria, resulting in an overall sample size of 2,807 patients. The average age was 55.1 years. Seventy-nine percentage of the patients were women. Asymptomatic individuals represented 26% of the population. The most common symptoms include bone pain, lethargy, and features related to renal stones. Familial primary hyperparathyroidism is observed in 6% of patients. The majority of individuals diagnosed with primary hyperparathyroidism are women in their sixth decade. In contrast to developed countries, a considerable number of Africans suffering from primary hyperparathyroidism have already shown symptoms, which are frequently non-specific or have encountered complications before obtaining a diagnosis.

This retrospective study aimed to evaluate hematological and inflammatory markers as predictors of thyroid cancer in patients with atypia of undetermined significance thyroid nodules. A total of 174 patients with atypia of undetermined significance who underwent thyroidectomy were included. Pre- and postoperative immature granulocyte counts, neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio were analyzed after achieving euthyroid status. Propensity score matching for age and gender resulted in a final cohort of 128 patients (64 benign and 64 malignant). Static preoperative and postoperative immature granulocyte values did not differ significantly between the benign and malignant groups; however, the delta immature granulocyte value, defined as the change between pre- and postoperative measurements, was significantly lower in malignant cases (p=0.007). Receiver operating characteristic analysis demonstrated an area under the curve of 0.651 at a cut-off value of≤- 0.01, with a sensitivity of 46.2% and a specificity of 79.2%. Univariate logistic regression revealed that delta immature granulocytes independently predicted malignancy in the overall cohort (odds ratio=3.273 and p=0.007) and in patients younger than 55 years (odds ratio=5.082 and p=0.007), whereas this association was not observed in patients aged 55 years and older. The neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios were not significant predictors. These findings suggest that dynamic changes in immature granulocyte levels between the pre- and postoperative periods, rather than single-time-point measurements, may serve as a cost-effective and accessible complementary tool for malignancy prediction in atypia of undetermined significance thyroid nodules.

Hyperparathyroidism has been associated with an increased risk of stroke in several previous studies; but the findings have not been consistent, which prompts further investigation. This study aimed to elucidate the association between high serum parathyroid hormone levels and stroke through a systematic review and meta-analysis. PubMed, Embase, Scopus and Google Scholar were systematically searched up to May 2025 for relevant and original observational studies. Pooled odds ratios and hazard ratios were calculated with corresponding 95% confidence intervals, along with heterogeneity and publication bias. The combined search yielded 2,063 unique articles, and 14 studies were included in statistical analysis. Two associations were analysed: nine studies focused on comparing the risk of stroke between populations with normal and high parathyroid hormone levels and the remaining five studies focused on comparing the rate of hyperparathyroidism between populations with stroke and normal population. In the first group, subgroup analyses of studies reported that both hazard ratios and odds ratios demonstrated stroke to be more likely in groups with hyperparathyroidism (odds ratio: 1.49 and 95% confidence interval: 1.38-1.61; hazard ratio: 1.38 and 95% confidence interval: 1.09-1.75). In the second group, analysis demonstrated that groups with stroke are more likely to have higher level of parathyroid hormone (mean difference of parathyroid hormone levels: 10.30 pg/mL and 95% confidence interval: 1.60-19.00). There were no significant publication biases in any of the analyses (p> 0.05). This review is supportive of the association between hyperparathyroidism and stroke but does not establish a conclusive causal relationship.

Thyroid nodules are among the most frequently encountered endocrine abnormalities, affecting up to two-thirds of adults in iodine-sufficient regions. Although thyroid-stimulating hormone (TSH) and genetic mutations have long been implicated in their pathogenesis, emerging evidence reveals a multifactorial interplay between inflammatory, hormonal, toxic, and micronutrient influences that extend beyond the classical model. This narrative review examines the converging biological pathways that contribute to thyroid nodule formation, emphasizing the integrative roles of inflammation, estrogen signaling, environmental endocrine disruptors, and micronutrient imbalance in altering thyroid cellular homeostasis. Chronic low-grade inflammation and oxidative stress create a permissive microenvironment for thyrocyte proliferation and clonal expansion. Estrogen receptor activation-amplified by insulin and IGF-1 signaling-enhances vascular and proliferative responses within thyroid tissue, contributing to the female predominance of nodular disease. Exposure to heavy metals and xenoestrogens disrupts thyroid peroxidase activity, deiodinase regulation, and immune tolerance, while deviations in iodine, selenium, zinc, and vitamin D status further impair redox balance and DNA repair mechanisms. Together, these factors promote a spectrum of structural changes ranging from microscopic hyperplasia to clinically significant nodules. Thyroid nodules represent a visible manifestation of intersecting metabolic and environmental stressors rather than a single endocrine defect. Integrating insights from molecular endocrinology, environmental toxicology, and nutritional science may advance early detection and preventive strategies targeting the inflammatory-hormonal-toxic axis of thyroid disease.

Metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated steatohepatitis are increasingly concerning health issues, especially in people with type 2 diabetes mellitus, where metabolic problems drive liver disease progression. While lifestyle changes remain essential, new drug strategies-particularly sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists-have gained growing interest for their potential to protect the liver. This review examines how sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists might help treat metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated steatohepatitis, focusing on their mechanisms of action, study evidence, and results from meta-analyses. A thorough search of the literature found studies on how these drugs affect insulin sensitivity, liver fat, and inflammation. Preclinical models show that they can lower liver fat, reduce oxidative stress, and decrease fibrosis markers. Clinical trials and meta-analyses support their potential to improve liver enzyme levels, decrease liver fat, and slow fibrosis growth. Overall, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists appear promising in the management of metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated steatohepatitis, especially in type 2 diabetes mellitus patients. Still, more long-term research studies are needed to confirm how well they work, how safe they are, and the best way to use them, either alone or in combination with other treatments. These drugs may represent important advances in the treatment of liver diseases linked to metabolic problems.

Metabolic alterations characterize a large subset of those with post-acute COVID-19 syndrome, and similar symptoms affect those with post-acute COVID-19 vaccination syndrome. These symptoms are characterized by the triumvirate of post-acute COVID-19 (vaccination) syndrome symptoms: post-exertional malaise, fatigue, and cognitive impairment, commonly referred to as brain fog. These symptoms can be recreated through perturbations that disrupt mitochondria, and spike protein has been observed to disrupt mitochondria in vitro, providing mechanistic support for this relationship. Post-acute COVID-19 (vaccination) syndrome patients suffer from a severely decreased lactate threshold and can experience symptoms of overexertion even at low power output. Furthermore, biopsies have revealed disrupted mitochondria, and energetics and physiological studies have shown that lipid oxidation constitutes a significantly reduced fraction of total energy production/consumption in post-acute COVID-19 (vaccination) syndrome patients. This review explores the therapeutic axes of lactate, carbon dioxide, and fatty acid oxidation for resolving the energy production challenges in post-acute COVID-19 (vaccination) syndrome, suggesting interventions that increase the lactate threshold, increase tissue oxygenation (paradoxically through increasing partial pressure of CO₂), and increase the rates at which lipids are oxidized relative to carbohydrates. Analogies from the world of exercise science are introduced, comparing post-acute COVID-19 (vaccination) syndrome to an overabundance of fast-twitch muscle fibers, with oxygenation similar to that experienced at high altitude, and presenting as an inverse 'fat adaptation' phenomenon, as observed in endurance athletes, especially those adopting low-carbohydrate diets.

Zoledronate is most effective when bone turnover is elevated, as in postmenopausal women. Individuals with type 2 diabetes mellitus show lesser bone mineral density gains compared to non-diabetes mellitus individuals with zoledronate, and fractures often occur despite preserved bone mineral density. It is unclear whether zoledronate reduces fracture risks in type 2 diabetes mellitus. This study aimed to evaluate skeletal outcomes, including fracture incidence, over 5 years in postmenopausal osteoporotic women with and without type 2 diabetes mellitus. This prospective cohort included postmenopausal women with bone mineral density T-scores of≤-2.5 at the lumbar spine, femoral neck, or hip. Participants were classified as type 2 diabetes mellitus or non-diabetes mellitus. All received annual zoledronate (4 mg), daily calcium (1000 mg), and cholecalciferol (500 IU), with standardized fall-prevention measures. Fracture history was recorded at follow-up visits, and annual spine radiographs were performed to detect morphometric vertebral fractures. Women completing≥5 years of follow up were included in the final analysis. The primary end point was fracture incidence; secondary end points were changes in bone mineral density and bone turnover markers. Of 221 women enrolled, 150 completed 5 years (63 type 2 diabetes mellitus and 87 non-diabetic mellitus; median age 59 y). The baseline bone mineral density was similar, but bone turnover markers were lower in type 2 diabetes mellitus. At a minimum of 60 months follow up, 20 new fractures occurred in 15 women: 8 (12.7%) with type 2 diabetes mellitus and 7 (8.0%) without. The relative risk (RR) was 1.58 (95% confidence interval: 0.60-4.13; p=0.2). Both groups showed comparable bone mineral density improvements. Despite differences in baseline bone turnover, fracture incidence did not differ significantly between postmenopausal women with and without type 2 diabetes mellitus treated with annual zoledronate over a 5-year follow-up. However, the low number of fracture events and wide confidence intervals limit definitive inference.

In type 2 diabetes mellitus, the prevalence at diagnosis, incidence, and remission of erectile dysfunction are unknown. We evaluated the prevalence, incidence, remission, and predictors of erectile dysfunction in newly diagnosed and uncomplicated type 2 diabetic men. We consecutively enrolled 549 diabetic men without complications. Erectile dysfunction was diagnosed using the International Index for Erectile Function 5 questionnaire. Patients were followed up for 64.2±22.1 months. At baseline, 133 patients had erectile dysfunction and 416 patients did not. The prevalence of erectile dysfunction was 24.2%. Among the 416 patients without erectile dysfunction at baseline, 67 (16.1%) patients developed erectile dysfunction at follow-up, with an erectile dysfunction incidence of 2.3%/y. Among the 133 patients with erectile dysfunction at baseline, 27 (20.3%) patients had remission at follow-up, with an erectile dysfunction remission rate of 0.9%/y. Multivariate analysis showed that age>60 years, total testosterone levels of<2.8 ng/mL and uric acid levels of>6 mg/dL were predictors of erectile dysfunction at diagnosis. Predictors of erectile dysfunction incidence were age>60 years, smoking and low total testosterone levels, whereas total testosterone levels of>2.8 ng/mL predicted erectile dysfunction remission. No significant association between therapeutic patient education and erectile dysfunction was observed. In conclusion, one quarter of men with newly diagnosed and uncomplicated type 2 diabetes has erectile dysfunction at diagnosis. The incidence of erectile dysfunction was 2.3%/y, while remission was 0.9%/y. Older age, low total testosterone levels, and hyperuricemia were associated with erectile dysfunction at diabetes diagnosis, while older age, smoking, and total testosterone levels were the longitudinal predictors of erectile dysfunction.

Normocalcemic primary hyperparathyroidism is thought to be an early form of hypercalcemic primary hyperparathyroidism. However, some studies have shown progression to hypercalcemia, hypercalciuria or kidney stones, bone loss and fractures in a proportion of patients over time, whereas other studies have not observed such outcomes. The aim of this study was to investigate the clinicopathological features and natural history of the disease in a large patient population and to provide clinicians with strong evidence-based recommendations. This is a nationwide, multicenter, observational, retrospective cohort study. Tertiary healthcare endocrinology departments were the setting for this study. Data from different regions of Turkey, including 527 patients, were included in this study. A total of 123 patients were not eligible for inclusion, and the remaining 404 patients were included in the final analysis. All laboratory assessments, dual-energy X-ray absorptiometry and renal ultrasound were performed locally at each center at baseline and several times during follow-up. The mean age was 54.63±11.41 years. As expected, there was a female predominance of 362 (89.4%). A total of 376 patients were followed up for 1 year and 252 patients for 3 years. Forty-seven out of 404 patients (11.6%) developed hypercalcemia within 3 years. Twenty-eight patients became hypercalcemic within the 1^st year, and 19 patients became hypercalcemic within 3 years. Among the 47 patients, only four patients had a calcium level above 11 mg/dL during the follow-up. Nephrolithiasis was detected in 50 patients (12.6%). There was no significant difference in calcium, parathyroid hormone, 25-hydroxyvitamin D, or urinary calcium levels or the presence of nephrolithiasis. Bone mineral density assessments revealed that only 90 patients (28.5%) had normal bone mineral density. A total of 135 (42.7%) patients had osteopenia, and 91 (28.8%) patients had osteoporosis at least one site at presentation. This study revealed that patients with normocalcemic primary hyperparathyroidism have significant adverse skeletal outcomes, a slight increase in kidney stones. Only a small proportion of patients develop hypercalcemia, and the risk of developing significant hypercalcemia that would alter the patient's treatment management is much lower.