Horm. Metab. Res. [JOURNAL]
Sun
200 papers
Free Triiodothyronine Concentrations and Gestational Diabetes Mellitus: Unveiling the Correlation and Implications.
Zha H, Li S, Sun L … +2 more , Yu L, Yuan Q
Horm Metab Res · 2025 Feb · PMID 39929171 · Publisher ↗
Thyroid disease and gestational diabetes mellitus (GDM) are frequent complications during pregnancy. We observed the relationship between thyroid indicators and blood glucose to analyze whether thyroid function is associ...
Thyroid disease and gestational diabetes mellitus (GDM) are frequent complications during pregnancy. We observed the relationship between thyroid indicators and blood glucose to analyze whether thyroid function is associated with the development of GDM. We enrolled a total of 575 pregnant women diagnosed with GDM and 573 pregnant women without GDM. The correlation between thyroid indicators and blood glucose levels was established through correlation analysis. In addition, stratified analysis and restricted cubic spline curves were employed to describe the association between thyroid indicators and the incidence of GDM. We found no significant difference in urine iodine levels between the GDM and non-GDM groups throughout the second trimester. The levels of free triiodothyronine (FT3) and both fasting blood glucose and post-load blood glucose showed a robust positive connection. Thyroid-stimulating hormone (TSH) and free thyroxine (FT4), on the other hand, showed a weakly positive connection with these glucose values. A nonlinear correlation between FT3 and the risk of GDM was also found (pNonlinear=0.0007, p<0.0001). Particularly, those in the top quartile of FT3 had a 6.99-fold greater risk than those in the lowest. Notably, FT3 levels below 4.04 pmol/l were linked to a decreased chance of developing GDM, but levels over 4.04 pmol/l were linked to a greater risk. Our study successfully established the correlation between thyroid indicators and the risk of GDM. Notably, we discovered a non-linear association between FT3 levels and GDM. The study suggests that ensuring optimal thyroid function during pregnancy may decrease the likelihood of developing GDM.
Reassessing the Role of Morning Cortisol in Adrenal Insufficiency Diagnosis: Insights from a Multicentric Cohort.
Guia Lopes ML, Regala C, Limbert C … +4 more , Silva TN, Sequeira Duarte J, Leite V, Prazeres S
Horm Metab Res · 2025 Mar · PMID 39848260 · Publisher ↗
The diagnosis of adrenal insufficiency (AI) is challenging due to nonspecific symptoms. Measuring 8 AM serum cortisol levels is a common screening test, but its accuracy in predicting AI remains uncertain. This study aim...
The diagnosis of adrenal insufficiency (AI) is challenging due to nonspecific symptoms. Measuring 8 AM serum cortisol levels is a common screening test, but its accuracy in predicting AI remains uncertain. This study aimed to evaluate the predictive diagnostic value of basal morning cortisol levels in suspected AI cases and compare them with levels in healthy individuals. We have conducted a retrospective multicentric cohort study. The study included an epidemiological cohort (patients with AI suspicion) and a control cohort (healthy volunteers). In the epidemiological cohort an ACTH-stimulation test was performed to confirm (AI group) or exclude (non-AI group) the disease. We have included 273 individuals (168 suspected AI cases and 105 controls). Basal cortisol levels were higher in the control group compared to the AI-suspected group (9.9±3.2 μg/dl vs. 7.7±3.3 μg/dl, p<0.001), though both were below the 15 μg/dl recommended threshold for excluding AI. Within the epidemiological cohort, even after a propensity score matching, taking into consideration sex, age and AI symptoms complaints, no significant difference in basal cortisol levels was found between patients with and without AI [6.10 (4.43; 8.45) vs. 7.14 (4.68; 12.15), p=0.128]. Logistic regression and ROC curve analyses showed a low predictive value for basal cortisol, with a positive predictive value of 18.9% and low specificity. AI patients more frequently experienced hypotension and nausea, compared with non-AI patients. Morning cortisol levels alone are unreliable for diagnosing AI. Revising cortisol cutoffs and incorporating symptom-based criteria may improve diagnostic accuracy.
Correction: A Single-Center Pilot Study of Therapeutic Apheresis in Patients with Severe Post-COVID Syndrome.
Korth J, Steenblock C, Walther R … +3 more , Barbir M, Husung M, Velthof A
Horm Metab Res · 2024 Dec · PMID 39842465 · Publisher ↗
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Neutrophil Extracellular Traps (NETs) as a Potential Target for Anti-Aging: Role of Therapeutic Apheresis.
Jarzebska N, Rodionov RN, Voit-Bak K … +13 more , Straube R, Mücke A, Tselmin S, Rettig R, Julius U, Siow R, Gräßler J, Passauer J, Kok Y, Mavberg P, Weiss N, Bornstein SR, Aswani A
Horm Metab Res · 2025 Nov · PMID 39788160 · Full text
Neutrophil extracellular traps (NETs) are large structures composed of chromatin, histones and granule-derived proteins released extracellularly by neutrophils. They are generally considered to be a part of the antimicro...
Neutrophil extracellular traps (NETs) are large structures composed of chromatin, histones and granule-derived proteins released extracellularly by neutrophils. They are generally considered to be a part of the antimicrobial defense strategy, preventing the dissemination of pathogens. However, overproduction of NETs or their ineffective clearance can drive various pathologies, many of which are associated with advanced age and involve uncontrolled inflammation, oxidative, cardiovascular and neurodegenerative stress as underlying mechanisms. Targeting NETs in the elderly as an anti-aging therapy seems to be a very attractive therapeutic approach. Therapeutic apheresis with a specific filter to remove NETs could be a promising strategy worth considering.
Association Between Homocysteine and All-Cause Mortality Among Osteoarthritis Patients: A Cohort Study from the NHANES Database.
Shi Y, Lu M, He F … +3 more , Chen J, Zheng C, Lu L
Horm Metab Res · 2025 Feb · PMID 39662882 · Publisher ↗
This study explored the association between serum Hcy level and the all-cause mortality among osteoarthritis (OA) patients. This cohort study included patients diagnosed as OA from the National Health and Nutrition Exami...
This study explored the association between serum Hcy level and the all-cause mortality among osteoarthritis (OA) patients. This cohort study included patients diagnosed as OA from the National Health and Nutrition Examination Survey (NHANES) 1999-2006. Abbott Homocysteine assay, a fully automated fluorescence polarization immunoassay (FPIA) method, was used to measure the level of serum Hcy. Covariates included sociodemographic information, lifestyles, history of diseases and medications were extracted from the database. The weighted univariate, multivariate Cox proportional hazard models and restricted cubic splines (RCS) were utilized to explore the association between Hcy level and all-cause mortality in OA patients, with hazard ratios (HRs) and 95% confidence intervals (CIs). Subgroup analyses based on different age, gender, duration of OA, complications and C-reactive protein (CRP) were further assessed by this association. Totally 1384 OA patients were included in this study, of which 817 (59.03%) died by 31 December 2019. After adjusting all covariates, high Hcy level was associated with the high all-cause mortality among OA patients (HR=1.31, 95%CI: 1.02-1.67), especially in females (HR=1.43, 95%CI: 1.07-1.91), aged >60 years (HR=1.49, 95%CI: 1.14-1.94), duration of OA >10 years (HR=1.40, 95%CI: 1.01-1.95), with the history of hypertension (HR=1.37, 95%CI: 1.03-1.80), without the history of diabetes (HR=1.36, 95%CI: 1.01-1.82) or CRP >0.29 mg/l (HR=1.51, 95%CI: 1.04-2.19). High serum Hcy level was associated with high risk of all-cause mortality in OA patients. Our results suggest that serum Hcy is a promising biomarker for the prognosis of OA patients.
Clinical Application of Thyrotropin Receptor Antibodies.
Yang Y, Chen H
Horm Metab Res · 2025 Feb · PMID 39653332 · Publisher ↗
Thyrotropin receptor antibodies (TRAb) are specific for Graves' disease (GD) and play a crucial role in the pathogenesis of GD. TRAb assays have recently been greatly improved. This review discusses the clinical applicat...
Thyrotropin receptor antibodies (TRAb) are specific for Graves' disease (GD) and play a crucial role in the pathogenesis of GD. TRAb assays have recently been greatly improved. This review discusses the clinical application of TRAb in the differential diagnosis of hyperthyroidism, the prognosis of GD, GD in gestation and pediatrics, and GD related ophthalmopathy (GO). In addition to the classical competition and bioassays, a new bridging assay has emerged for TRAb assays. TRAb is the main pathogenic mechanism of hyperthyroidism in GD. Treated GD still has a high rate of recurrence and even a short-term surge of TRAb, leading to rapid deterioration of GO. Fetal goiter may be associated with elevated maternal TRAb during pregnancy, overtreatment may lead to fetal hypothyroidism. Pediatric patients with GD have high TRAb, poor remission from treatment, and insignificant manifestations of GO. TRAb is significantly correlated with GO activity and severity. Currently, TRAb assay has high specificity and sensitivity and can be used directly to identify the cause of hyperthyroidism. TRAb can be used to predict recurrence of drug treated GD or progression of GO after RAI therapy. TRAb should be measured regularly for GD in gestation to guide anti-thyroid medication to avoid thyrotoxicosis or hypothyroidism in the fetus. Monitoring TRAb in pediatric GD may help control the progression of GO. TRAb assay is an important guide for the treatment of GO.
Andrew Victor Schally - Nobel Prize Winner in Medicine, Legend and Pioneer in Endocrinology and a Great Friend and Supporter of the TransCampus.
Horm Metab Res · 2024 Dec · PMID 39653043 · Publisher ↗
Abstract loading — click title to view on PubMed.
A Single-Center Pilot Study of Therapeutic Apheresis in Patients with Severe Post-COVID Syndrome.
Korth J, Steenblock C, Walther R … +3 more , Barbir M, Husung M, Velthof A
Horm Metab Res · 2024 Dec · PMID 39653042 · Publisher ↗
After the COVID-19 pandemic, many patients have reported chronic fatigue and severe post-exertional malaise, with symptoms similar to those of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The accumulation...
After the COVID-19 pandemic, many patients have reported chronic fatigue and severe post-exertional malaise, with symptoms similar to those of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The accumulation of agonistic receptor autoantibodies targeting beta-adrenergic (β1 and β2) and muscarinic (M3 and M4) neurotransmitter receptors may play a crucial role in the pathomechanism of both ME/CFS and post-COVID conditions. Therapeutic apheresis has been suggested as an effective treatment option for alleviating and mitigating symptoms in this desperate group of patients. In this single-center pilot study, we analyzed autoantibodies in a cohort of 20 post-COVID patients before and after therapeutic apheresis. Apheresis resulted in a decline of β1 or β2 adrenergic receptor antibodies in all patients. Additionally, the majority of patients experienced a concurrent reduction in symptoms such as fatigue, physical activity restrictions, myalgia, post-exertional malaise, and concentration disorders. This study clearly demonstrates an association between autoantibodies and the clinical improvement of post-COVID patients. Even if future sham-controlled trials do not show a positive outcome, extracorporeal apheresis may still be valuable for this patient group by temporarily improving microperfusion and symptoms. Success in restoring patients to work and normal life, as observed in many individuals after therapeutic apheresis, should be recognized. Therefore, we believe that extracorporeal therapeutic apheresis, as part of a multimodal treatment, should be considered an early intervention for postinfectious syndromes in selected patients.
Prediction of the Survival Status, Immunotherapy Response, and Medication of Lung Adenocarcinoma Patients Based on Hypoxia- and Apoptosis-Related Genes.
Shi Z, Sang Z, Xiao J … +2 more , Hou J, Geng M
Horm Metab Res · 2025 Jan · PMID 39577840 · Publisher ↗
To predict patient survival prognosis, we aimed to establish a novel set of gene features associated with hypoxia and apoptosis. RNA-seq and clinical data of LUAD were sourced from The Cancer Genome Atlas (TCGA) and Gene...
To predict patient survival prognosis, we aimed to establish a novel set of gene features associated with hypoxia and apoptosis. RNA-seq and clinical data of LUAD were sourced from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, while hypoxia and apoptosis-related genes were obtained from the Molecular Signatures Database (MsigDB). A 13-gene-prognostic model incorporating hypoxia and apoptosis genes was developed using univariate/multivariate Cox regression, Nonnegative Matrix Factorization (NMF) clustering, and LASSO regression. Patients were divided into high-risk (HR) and low-risk (LR) groups according to the median risk score. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed distinct biological processes between HR and LR groups, including hormone regulation and lipid metabolism pathways. Single sample gene set enrichment analysis (ssGSEA) indicated elevated cell infiltration levels of Neutrophils and T_helper_cells in the LR group, while NK cells and Th1cells were higher in the HR group. Immunophenoscore (IPS) and tumor immune dysfunction and exclusion (TIDE) analyses suggested potential benefits of immunotherapy for LR group patients. In conclusion, this prognostic feature integrating hypoxia- and apoptosis-related genes offers insights into predicting survival, immune status, and treatment response in LUAD patients, paving the way for personalized treatment strategies.
Serum Homocysteine and Atrial Fibrillation Recurrence after Catheter Ablation: A Meta-Analysis of 11 Cohort Studies Involving 2147 Patients.
Li B, Zeng F, Zhao Q
Horm Metab Res · 2025 Mar · PMID 39577839 · Publisher ↗
The relationship between serum homocysteine (Hcy) levels and atrial fibrillation (AF) recurrence following catheter ablation remains unclear. This meta-analysis aims to investigate this association. Comprehensive searche...
The relationship between serum homocysteine (Hcy) levels and atrial fibrillation (AF) recurrence following catheter ablation remains unclear. This meta-analysis aims to investigate this association. Comprehensive searches in PubMed, Web of Science, Embase, Wanfang, and China National Knowledge Infrastructure (CNKI) databases identified relevant studies published up to May 25, 2024. Cohort studies that measured pre-ablation serum Hcy levels and reported AF recurrence post-ablation were included. Data were analyzed using random-effects models by incorporating the potential influence of heterogeneity, with odds ratios (ORs) and 95% confidence intervals (CIs) calculated for the association between serum Hcy levels and AF recurrence. Eleven retrospective cohort studies involving 2147 patients with AF who underwent catheter ablation were analyzed. Higher pre-ablation serum Hcy levels were associated with an increased risk of AF recurrence (OR for per 1 μmol/l increment of Hcy: 1.22, 95% CI: 1.17 to 1.28, p<0.001; I²=0%). Additionally, studies that categorized Hcy levels also found a higher risk of AF recurrence in patients with elevated Hcy (OR for patients with a high versus a low serum Hcy: 2.75, 95% CI: 2.02 to 3.75, p <0.001; I²=0%). Funnel plots and Egger's regression test indicated low risks of publication bias. In conclusions, elevated pre-ablation serum Hcy levels are significantly associated with an increased risk of AF recurrence post-catheter ablation. These findings suggest that Hcy could be a valuable biomarker for predicting AF recurrence and may inform pre-ablation risk stratification. Further prospective studies are warranted to confirm these results.
Diabetic Nephropathy: Pathogenesis, Mechanisms, and Therapeutic Strategies.
Dwivedi S, Sikarwar MS
Horm Metab Res · 2025 Jan · PMID 39572154 · Publisher ↗
Diabetic nephropathy represents a predominant etiology of end-stage renal disease (ESRD) on a global scale, significantly impacting the morbidity and mortality rates of individuals with diabetes. The primary objective of...
Diabetic nephropathy represents a predominant etiology of end-stage renal disease (ESRD) on a global scale, significantly impacting the morbidity and mortality rates of individuals with diabetes. The primary objective of this analysis is to furnish a comprehensive examination of the etiology, fundamental mechanisms, and treatment modalities for DN. The development of DN stems from a multitude of factors, encompassing a intricate interplay involving metabolic irregularities induced by hyperglycemia, alterations in hemodynamics, inflammatory responses, oxidative stress, and genetic susceptibility. Principal mechanisms encompass the generation of advanced glycation end products (AGEs), activation of protein kinase C (PKC), and overexpression of the renin-angiotensin-aldosterone system (RAAS). These processes precipitate glomerular hyperfiltration, hypertrophy, and eventually, fibrosis and scarring of the renal parenchyma. Initially, hyperglycemia triggers mesangial proliferation and thickening of the glomerular basement membrane in the incipient stages of DN, subsequently leading to progressive glomerular sclerosis and tubulointerstitial fibrosis. Inflammatory cascades, notably involving cytokines like TGF-β and NF-κB, play pivotal roles in the advancement of DN by fostering the accumulation of extracellular matrix and renal fibrosis. Inflammation pathways, particularly those involving cytokines like TGF-β and NF-κB, play essential roles in diabetic nephropathy progression by stimulating extracellular matrix accumulation and renal fibrosis. The presence of oxidative stress, worsened by dysfunctional mitochondria, contributes further to renal injury via lipid peroxidation and DNA damage. Current therapeutic approaches for diabetic nephropathy concentrate on optimizing glycemic control, controlling hypertension, and suppressing the renin-angiotensin-aldosterone system. Among antihypertensive medications, ACE inhibitors and angiotensin II receptor blockers are crucial for decelerating disease advancement.
Association of Circulating Homocysteine Level with the Risk of Nephropathy in Type 2 Diabetes Mellitus: A Meta-Analysis.
Zhu M, Fan Y
Horm Metab Res · 2025 Feb · PMID 39572153 · Publisher ↗
The objective of the study was to explore the association between homocysteine (Hcy) levels and the risk of type 2 diabetic nephropathy (T2DN). PubMed, Web of Science, Cochrane Library, and Embase databases were searched...
The objective of the study was to explore the association between homocysteine (Hcy) levels and the risk of type 2 diabetic nephropathy (T2DN). PubMed, Web of Science, Cochrane Library, and Embase databases were searched to collect literature on the association between Hcy levels and the risk of T2DN. The retrieval period was from the establishment of the database to September 10, 2024. Stata 15.0 statistical software was used for data analysis. Type II diabetes without nephropathy was considered the control group, and microalbuminuria and macroalbuminuria were included in the experimental group. Fourteen articles were included in this meta-analysis. The results of the meta-analysis showed that compared with the control group, the level of Hcy in the T2DN group with microalbuminuria [Weighted mean difference (WMD)=2.50, 95% confidence interval (CI): 1.49-3.51, p<0.001] and the group with macroalbuminuria (WMD=3.38, 95% CI: 1.95-4.82) was significantly increased. Compared with the T2DN microalbuminuria group, the Hcy level in the T2DN macroalbuminuria group was considerably higher (WMD=2.12, 95% CI: 0.80-3.44, p<0.001). High homocysteine levels were associated with an increased risk of T2DN (OR=1.36, 95% CI: 1.20-1.54, p<0.001). In conclusion, circulating Hcy levels are significantly associated with the severity of T2DN. In addition, there was a significant association between high Hcy levels and an increased risk of T2DN.
The Prognostic Impact of Radioiodine Therapy in Patients with Papillary Thyroid Cancer.
Schott M, Schott-Ohly P, Krieg S … +4 more , Thomaschky C, Wieltsch JH, Petrovitch A, Krieg A
Horm Metab Res · 2024 Nov · PMID 39510099 · Publisher ↗
Radioiodine (RAI) therapy after surgery, is an important component for the treatment of patients with papillary thyroid cancer (PTC), the most common thyroid cancer. In this study we sought to evaluate the cancer-specifi...
Radioiodine (RAI) therapy after surgery, is an important component for the treatment of patients with papillary thyroid cancer (PTC), the most common thyroid cancer. In this study we sought to evaluate the cancer-specific survival (CSS) impact of RAI in specific thyroid cancer subgroups. The Surveillance, Epidemiology, and End Results (SEER) database were used to identify patients with PTC who underwent surgery between 2000 and 2019. Patients not treated with RAI were compared to those treated with RAI using propensity score matching (PSM) on the basis of identical inclusion criteria. A total of 106 333 patients were identified from the SEER database. RAI therapy was associated with improved CSS in the matched cohort (HR: 0.83; 95% CI: 0.72-0.96, p=0.01) but not in the unmatched data set (HR: 1.46; 95% CI: 1.30-1.64, p<0.001) among all PTC patients regardless of disease stage. Detailed analyses, however, showed that only patients with high-risk disease (pT3N1, pT4N1) experienced the greatest benefit in CSS. In the lower disease stages, no significant differences were recognized in the group of PTC patients with or without RAI therapy. One exception: in the group of PTC patients in stage pT1bN0, a significant difference was seen towards RAI. This is, however, most likely due to the large number of patients investigated. In summary, RAI therapy should not be used in low-risk PTC patients and might be used to some extent in intermediate-risk PTC patients. The histological suptype of the tumor needs to be considered in this context.
Effects of Growth Hormone on Osteoarthritis Development.
Sun L, Gang X, Li F … +3 more , Guo W, Cui M, Wang G
Horm Metab Res · 2024 Nov · PMID 39510098 · Publisher ↗
Osteoarthritis (OA), a chronic joint disease characterized by primary or secondary degeneration of articular cartilage and bone dysplasia, is associated with various risk factors and is the leading cause of musculoskelet...
Osteoarthritis (OA), a chronic joint disease characterized by primary or secondary degeneration of articular cartilage and bone dysplasia, is associated with various risk factors and is the leading cause of musculoskeletal pain and disability, severely impacting the quality of life. Growth hormone (GH), secreted by the anterior pituitary gland, is essential in mediating the growth and development of bone and cartilage. Reportedly, osteoarthritis increases, and the growth hormone decreases with age. A negative correlation between GH and OA suggests that GH may be related to the occurrence and development of OA. Considering that abnormal growth hormone levels can lead to many diseases related to bone growth, we focus on the relationship between GH and OA. In this review, we will explain the effects of GH on the growth and deficiency of bone and cartilage based on the local pathological changes of osteoarthritis. In addition, the potential feasibility of treating OA with GH will be further explored and summarized.
Influence of Mitochondrial NAD(P) + Transhydrogenase (NNT) on Hypothalamic Inflammation and Metabolic Dysfunction Induced by a High-Fat Diet in Mice.
Santos GL, Dias Costa EF, Dalla Costa AP … +8 more , Zanesco AM, Simoes MR, Rogério F, Demolin DMR, Navarro CDC, Velloso LA, Francisco A, Castilho RF
Horm Metab Res · 2025 Mar · PMID 39481390 · Publisher ↗
The mitochondrial protein NAD(P) transhydrogenase (NNT) has been implicated in the metabolic derangements observed in obesity. Mice with the C57BL/6J genetic background bear a spontaneous mutation in the gene and are kn...
The mitochondrial protein NAD(P) transhydrogenase (NNT) has been implicated in the metabolic derangements observed in obesity. Mice with the C57BL/6J genetic background bear a spontaneous mutation in the gene and are known to exhibit increased susceptibility to diet-induced metabolic disorders. Most of the studies on NNT in the context of diet-induced obesity have compared C57BL/6J mice with other mouse strains, where differences in genetic background can serve as confounding factors. Moreover, these studies have predominantly employed a high-fat diet (HFD) consisting of approximately 60% of calories from fat, which may not accurately mimic real-world fat-rich diets. In this study, we sought to examine the role of NNT in diet-induced hypothalamic inflammation and metabolic syndrome by using a congenic mice model lacking NNT, along with a HFD providing approximately 45% of calories from fat. Our findings indicate that mice lacking NNT were more protected from HFD-induced weight gain but presented a worse performance on glucose tolerance test, albeit not in insulin tolerance test. Interestingly, the brown adipose tissue of HFD-fed mice presented a greater mass and a higher whole-tissue ex-vivo oxygen consumption rate. Also, HFD increased the expression of the inflammatory markers , and in the hypothalamus of mice. In conclusion, our study highlights the importance of NNT in the context of diet-induced obesity and metabolic syndrome, indicating its contribution to mitigate hypothalamic inflammation and suggesting its role in the brown adipose tissue increased mass.
The Value of lncRNAs as a Biomarker for the Diagnosis of Gestational Diabetes: A Meta-Analysis.
Fan Y, Chen X, Yang S … +4 more , Tu H, Zhang Y, Wang M, Jiang J
Horm Metab Res · 2025 Jan · PMID 39401523 · Publisher ↗
Gestational diabetes mellitus (GDM) is a common metabolic disorder in pregnancy and leads to serious harm to the mother and the fetus. A variety of lncRNAs play a key role in GDM. This meta-analysis was performed to expl...
Gestational diabetes mellitus (GDM) is a common metabolic disorder in pregnancy and leads to serious harm to the mother and the fetus. A variety of lncRNAs play a key role in GDM. This meta-analysis was performed to explore the potential value of lncRNAs in GDM diagnosis. Articles correlated with lncRNA and GDM were screened from Embase, Medline, EBSCO, PubMed, Chinese National Knowledge Infrastructure, and WanFang databases. Summary receiver operator characteristic (SROC) was performed to evaluate the pooled area under curve (AUC). Forest plot was conducted to calculate the sensitivity, specificity, diagnostic likelihood ratio (LR), diagnostic score, and diagnostic odds ratio (DOR). Deeks' funnel plot was utilized to evaluate the publication bias. Eleven articles containing 12 tests (1060 GDM patients and 1066 controls) were included in this meta-analysis. AUC (0.89, 95%CI=0.86-0.92), sensitivity (0.84, 95%CI=0.80-0.87), and specificity (0.81, 95%CI=0.77-0.85)of the SROC curve showed a high diagnostic value of lncRNA for GDM. Positive LR (PLR 4.40, 95%CI=3.45-5.60) and negative LR (NLR 0.20, 95%CI=0.15-0.26) results indicated that the diagnosis of lncRNA for GDM had low clinical utility. Diagnostic score (3.09, 95%CI=2.62-3.57) and DOR (22.04, 95%CI=13.68-35.51) results suggested lncRNAs have good discriminative effect on GDM. Heterogeneity was significantly higher, but not induced by the subgroups. LncRNAs had high diagnostic value and good discriminative effect for GDM, but the clinical utility was not high. This meta-analysis study offers a potential target for GDM diagnosis.
Denosumab for Management of Hypercalcemia in Primary Hyperparathyroidism.
Zhao Y, Zhang F, Zhang S … +5 more , Zhang X, Gao L, Ren Q, Han X, Ji L
Horm Metab Res · 2024 Dec · PMID 39393416 · Publisher ↗
Denosumab is a completely human monoclonal high-affinity antibody that binds to the nuclear factor kappa-B ligand (RANKL) and is widely used to treat osteoporosis. Furthermore, it can potentially lower serum calcium leve...
Denosumab is a completely human monoclonal high-affinity antibody that binds to the nuclear factor kappa-B ligand (RANKL) and is widely used to treat osteoporosis. Furthermore, it can potentially lower serum calcium levels by inhibiting osteoclast activation and preventing bone calcium from being released into the blood. This review aimed to provide evidence of the efficacy and safety of denosumab in treating hypercalcemia in primary hyperparathyroidism (PHPT). PubMed and the Cochrane Library were searched for published studies that described denosumab for hypercalcemia management in PHPT. Data were extracted by two independent investigators and analyzed using SPSS 23. The risk of bias was assessed by NIH Quality Assessment Tool. In total, 161 patients with PHPT from 18 studies were included in this review. The average age was 61 (47-72) years and the highest serum calcium was 3.76 (3.11-4.20) mmol/l. We found that denosumab can effectively reduce the serum calcium level by a median reduction of 0.5 mmol/l within 3 days. Significant reduction was maintained for 14 days. The serum calcium-lowering effect weakened after one month. In conclusion, denosumab has a potential clinical value in treating hypercalcemia in patients with PHPT.
Improvement of Bone Metabolism in Prepubertal Girls with Turner Syndrome Following Long-term Pegylated Growth Hormone Treatment.
Gao X, Cao B, Chen J … +3 more , Liu M, Peng Y, Gong C
Horm Metab Res · 2025 Feb · PMID 39393415 · Publisher ↗
The study aims to assess the improvement in bone metabolism in prepubertal girls with Turner Syndrome (TS) after long-term polyethylene glycol recombinant human Growth Hormone (PEG-rhGH) treatment. A 12-month longitudina...
The study aims to assess the improvement in bone metabolism in prepubertal girls with Turner Syndrome (TS) after long-term polyethylene glycol recombinant human Growth Hormone (PEG-rhGH) treatment. A 12-month longitudinal prospective study was conducted with 28 prepubertal girls diagnosed with TS. Participants were divided into two groups: 18 received PEG-rhGH therapy (0.1-0.25 mg/kg/week) and 10 did not. Anthropometric measurements, bone turnover markers (BTMs), and serum levels of IGF-1, calcium, and phosphate were collected at baseline and after 12 months. BTMs included bone alkaline phosphatase (BAP), Type I collagen propeptide (CICP), Type I collagen telopeptide (CTX), and fibroblast growth factor 23 (FGF23). After 12 months of PEG-rhGH therapy, the treatment group showed significant increases in growth velocity (GV) and height standard deviation scores (HtSDS). Serum IGF-1 levels increased rapidly within one month and remained elevated. BTMs indicated enhanced bone formation, significantly increasing BAP and CICP, while CTX levels remained low. FGF23 levels initially rose slightly but declined below baseline by 12 months. Elevated blood phosphate levels were observed. PEG-rhGH therapy in children with TS significantly improves linear growth and enhances bone formation markers, benefiting bone metabolism.
Effect of Low Dose Glucocorticoid Inhalation on Bronchopulmonary Dysplasia in Premature Infants.
Li X, Liu H
Horm Metab Res · 2025 Feb · PMID 39348827 · Publisher ↗
The aim of the study was to explore the effect of low dose glucocorticoid on bronchopulmonary dysplasia in premature infants, to provide new ideas for clinical prevention and cure of bronchopulmonary dysplasia in prematu...
The aim of the study was to explore the effect of low dose glucocorticoid on bronchopulmonary dysplasia in premature infants, to provide new ideas for clinical prevention and cure of bronchopulmonary dysplasia in premature infants. The 144 cases of premature infants were divided into 72 each: control group and experimental group. Control group received routine clinical prevention and cure, while experimental group was received low dose glucocorticoid on the basis of control group. The serum interleukin-10 (IL-10) , interleukin-8 (IL-8), and transforming growth factor-1 (TGF-β1) before and after treatment were compared between two groups. The incidence and severity of bronchopulmonary dysplasia was compared between two groups. The mechanical ventilation time, oxygen inhalation time and hospitalization time in two groups were recorded, and the body mass, head circumference and body length at 30 days after birth were assessed in both groups. After treatment, the serum IL-10 level in experimental group was increased and IL-8, TGF-β1 levels were decreased compared with control group (p <0.05). The incidence rate of bronchopulmonary dysplasia in experimental group was 13.89% and the disease severity in experimental group was significantly reduced (p<0.05). Both groups exhibited no notable adverse reactions (p>0.05). Low-dose glucocorticoids have a significant preventive and therapeutic effect on bronchopulmonary dysplasia in preterm infants, and have a high safety, showing high clinical application value for bronchopulmonary dysplasia in preterm infants.
Loxenatide Alleviates High Glucose-Induced Pancreatic β-Cell Senescence via Regulating the PERK/eIF2α Pathway.
Yuan J, Wang Y, Wang D … +2 more , Yan H, Wang N
Horm Metab Res · 2024 Dec · PMID 39333044 · Publisher ↗
Glucagon-like peptide-1 (GLP-1) receptor agonists are effective hypoglycemic agents for type 2 diabetes mellitus (T2DM). It was reported that T2DM was implicated in pancreatic β-cell senescence. Whether loxenatide regula...
Glucagon-like peptide-1 (GLP-1) receptor agonists are effective hypoglycemic agents for type 2 diabetes mellitus (T2DM). It was reported that T2DM was implicated in pancreatic β-cell senescence. Whether loxenatide regulates cellular senescence of pancreatic β-cells is to be investigated. Our results revealed that high glucose (HG)-induced cellular senescence and elevated expression of SASP factors inhibited cell proliferation and stimulated DNA damage, which were reversed by loxenatide treatment. In addition, HG induction resulted in promoted insulin secretion and insulin synthesis of pancreatic β-cells and loxenatide treatment further strengthened these influences. In addition, loxenatide could inactivate the PERK/eIF2α signaling pathway via decreasing the levels of p-PERK and p-eIF2α in HG-induced pancreatic β-cells. Furthermore, CCT020312, an activator of the PERK/eIF2α signaling pathway, abolished loxenatide-mediated inhibiting cellular senescence, elevating cell proliferation and improving DNA damage and enhancing insulin secretion of HG-induced pancreatic β-cells. In conclusion, our results indicated that loxenatide impeded cellular senescence, promoted cell proliferation, improved DNA damage, enhanced insulin secretion and insulin synthesis of HG-induced pancreatic β-cells through modulating the PERK/eIF2α signaling pathway.
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