Browse
You are looking at 31 - 40 of 1,482 items for
Diabetes and Endocrine Unit, National Hospital, Kandy, Sri Lanka
Search for other papers by G Amiyangoda in
Google Scholar
PubMed
Search for other papers by C N Antonypillai in
Google Scholar
PubMed
Search for other papers by S S C Gunatilake in
Google Scholar
PubMed
Search for other papers by T T Weerathunge in
Google Scholar
PubMed
Search for other papers by D Ediriweera in
Google Scholar
PubMed
Search for other papers by S G P D Kosgallana in
Google Scholar
PubMed
Search for other papers by R D P Jayawardana in
Google Scholar
PubMed
Search for other papers by H A N D Thissera in
Google Scholar
PubMed
Search for other papers by W J Emalka in
Google Scholar
PubMed
Search for other papers by H U Daraniyagala in
Google Scholar
PubMed
Refractory hypothyroidism is associated with high morbidity and increased healthcare expenditure. In general, the use of the levothyroxine absorption test looks promising in evaluating refractory hypothyroidism but has shown significant variability in protocols in multiple settings. We intended to assess the usefulness of the levothyroxine absorption test in a low-resource setting and to assess the factors associated with refractory hypothyroidism. A cross-sectional study among age-matched 25 cases of refractory hypothyroidism and 24 treatment-responsive hypothyroid controls was conducted. A supervised levothyroxine absorption test was performed with levothyroxine 1000 μg tablets after a 10-h fast, and serum free tetraiodothyronine (FT4) levels were measured at 0, 1, 2, 3, 4, and 5 h. Descriptive statistics, chi-square test, Student’s t-test, and logistic regression were used in the analysis. Results showed no significant difference in age, body weight, etiology of hypothyroidism, interfering medications, thyroxine storage, and ingestion technique in cases and controls. Cases had a longer duration of hypothyroidism and males had a higher peak FT4 concentration. During pooled analysis, serum FT4 peaked at 3 h with an increment of 149.4% (128.4–170.5%) from baseline and plateaued thereafter. The absolute value of FT4 at 3 h was 41.59 (s.d. 14.14) pmol/L (3.23 ng/dL). We concluded that there was no significant difference in the pattern of levothyroxine absorption in both groups. The most common cause of refractory disease was pseudo-malabsorption. Rapid supervised levothyroxine absorption test with two blood samples for FT4 at baseline and at the peak of absorption (3 h) is simple, convenient, and cost-effective, particularly in low-resource settings.
Search for other papers by Jie Yang in
Google Scholar
PubMed
Search for other papers by Min Lin in
Google Scholar
PubMed
Search for other papers by Xiaoyan Tian in
Google Scholar
PubMed
Search for other papers by Chujun Li in
Google Scholar
PubMed
Search for other papers by Haocun Wu in
Google Scholar
PubMed
Search for other papers by Ling Deng in
Google Scholar
PubMed
Search for other papers by Xuelan Li in
Google Scholar
PubMed
Search for other papers by Xin Chen in
Google Scholar
PubMed
Purpose: Our study aimed to assess the relationship between serum adipokines and insulin resistance (IR) in women with polycystic ovary syndrome (PCOS), as well as explore the predictive value of adipokines on IR in PCOS.
Methods: This was a prospective cross-sectional study. 154 women with PCOS were included from July 2021 to September 2022 who underwent gonadal steroid hormone measurement, lipid profile, oral glucose tolerance test and homeostasis model assessment (HOMA)-IR. Adiponectin (APN), leptin and secreted frizzled-related protein (Sfrp5) were measured by immunoturbidimetry and enzyme-linked immunosorbent assay. Women with PCOS were categorised based on the presence of IR.
Results: Women with PCOS with IR (n=99) had significantly lower APN level and APN to leptin ratio (A/L ratio) than those without IR (n=55), whereas serum levels of leptin and Sfrp5 were similar between the two groups. In multivariable linear regression analysis, serum log (APN) and log (A/L ratio) were associated with log(HOMA-IR), the association was statistically significant after adjusting for body mass index (BMI) and free androgen index. The area under the ROC curve (95% CI) for APN and A/L ratio were 0.726 (0.644–0.807; P<0.001) and 0.660(0.569–0.751; P<0.01), with cutoff values of 5.225 mg/L (Youden index ¼ 0.364) and 1.438 (Youden index ¼ 0.265) respectively.
Conclusion: Our study demonstrated that serum APN was negatively related to IR. Serum APN may be useful as a clinical marker for IR in women with PCOS. Our findings warrant further investigations into the function of APN in the pathogenesis of IR in women with PCOS.
Search for other papers by Qian Yang in
Google Scholar
PubMed
Search for other papers by Qiannan Zhang in
Google Scholar
PubMed
Search for other papers by Fanfan Pan in
Google Scholar
PubMed
Search for other papers by Bingbing Zha in
Google Scholar
PubMed
Background: Signal transducer and activator of transcription 6 (STAT6) is an important nuclear transcription factor. Previous study demonstrated that blockading STAT6 can ameliorate thyroid function by reducing serum T3 and T4. Sodium/iodide symporter (NIS) is a key protein that mediates active iodine uptake and plays an important role in regulating thyroid function. This study explored the interaction between STAT6 and NIS.
Methods: Immunohistochemical staining was performed for detecting the expression of NIS in different tissues. Reverse transcription-polymerase chain reaction (RT-PCR) was performed for evaluating the mRNA level of NIS when Nthy-ori 3-1cells were incubated with IL4, TSH (Thyroid stimulating hormone) or monoclonal TSAb (thyroid-specific stimulatory autoantibody) for 24h. Quantitative RT-PCR,Western blot and immunofluorescence analysis were performed for detecting NIS expression after inhibiting STAT6 phosphorylation by AS1517499. Finally, we used Luciferase reporter assays to explore the ability of STAT6 to regulate the promoter activity of the NIS-coding gene.
Results: NIS was highly expressed in thyroid epithelial cells of EAGD mice or Graves' disease (GD) patients and TSAb increased the expression of NIS. We show that STAT6 phosphorylation inhibitor can attenuate the effect of TSAb on increasing NIS protein and mRNA levels. Finally, we confirm that transcription factor STAT6 can mediate NIS transcription and co-activator P100 protein can enhance STAT6-dependent transcriptional activation.
Conclusion: In Graves' disease, TSAb induces STAT6 signaling to upregulate NIS expression and STAT6 blockade ameliorates thyroid function via downregulation of the sodium/iodide symporter. Our study furthers understanding of the effects of STAT6 on thyroid function and reveals new avenues for GD treatment.
Department of Performance and Image-enhancing Drugs Research, Android Health Clinic, Utrecht, the Netherlands
Search for other papers by Peter Bond in
Google Scholar
PubMed
Department of Internal Medicine, Spaarne Gasthuis, Haarlem, the Netherlands
Search for other papers by Tijs Verdegaal in
Google Scholar
PubMed
Department of Performance and Image-enhancing Drugs Research, Android Health Clinic, Utrecht, the Netherlands
Search for other papers by Diederik L Smit in
Google Scholar
PubMed
Erythrocytosis, or elevated hematocrit, is a common side effect of testosterone therapy (TTh) in male hypogonadism. Testosterone stimulates erythropoiesis through an initial rise in erythropoietin (EPO), the establishment of a new EPO/hemoglobin ‘set point’, and a parallel decrease in the master iron regulator protein hepcidin, as well as several other potential mechanisms. Evidence shows an increased thrombotic risk associated with TTh-induced erythrocytosis. Several guidelines by endocrine organizations for the treatment of male hypogonadism recommend against starting TTh in patients presenting with elevated hematocrit at baseline or stopping TTh when its levels cannot be controlled. Besides dose adjustments, therapeutic phlebotomy or venesection is mentioned as a means of reducing hematocrit in these patients. However, evidence supporting the efficacy or safety of therapeutic phlebotomy in lowering hematocrit in TTh-induced erythrocytosis is lacking. In light of this dearth of evidence, the recommendation to lower hematocrit using therapeutic phlebotomy is notable, as phlebotomy lowers tissue oxygen partial pressure (pO2) and eventually depletes iron stores, thereby triggering various biological pathways which might increase thrombotic risk. The potential pros and cons should therefore be carefully weighed against each other, and shared decision-making is recommended for initiating therapeutic phlebotomy as a treatment in patients on TTh who present with increased hematocrit.
Search for other papers by Hanrong Zhang in
Google Scholar
PubMed
Search for other papers by Junxin Chen in
Google Scholar
PubMed
Search for other papers by Xin Chen in
Google Scholar
PubMed
Search for other papers by Chuimian Zeng in
Google Scholar
PubMed
Search for other papers by Pengyuan Zhang in
Google Scholar
PubMed
Search for other papers by Jiewen Jin in
Google Scholar
PubMed
Search for other papers by Haipeng Xiao in
Google Scholar
PubMed
Search for other papers by Yanbing Li in
Google Scholar
PubMed
Search for other papers by Hongyu Guan in
Google Scholar
PubMed
Search for other papers by Hai Li in
Google Scholar
PubMed
Background: Transforming growth factor beta receptor III (TGFBR3) has been shown to play a tumor suppressive role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains unknown.
Method: TGFBR3 expression levels in PTC were analyzed utilizing TCGA and GEO database. Edu, wounding healing and Transwell assays were used to evaluate cell proliferation, migration and invasion. Transcriptome sequencing, qRT-PCR and Western blotting were used to detect the underlying mechanism of TGFBR3 in PTC progression.
Result: This study demonstrated that TGFBR3 expression was significantly down-regulated in PTC compared to normal thyroid tissues. Low expression of TGFBR3 was associated with poor prognosis of patients with PTC. Furthermore, TGFBR3 expression positively correlated with thyroid differentiation score. In investigating the biological impact of TGFBR3 over-expression in PTC cell lines, we found that the proliferation, migration and invasion of PTC cells were significantly inhibited in response to TGFBR3 overexpression. Moreover, we also demonstrated that overexpression of TGFBR3 inhibited PI3K/AKT pathway and epithelial mesenchymal transformation processes. Lastly, TGFBR3 expression was found to be involved in tumor immune infiltration, highlighting its potential influence on immune dynamics within the tumor microenvironment in PTC.
Conclusion: TGFBR3 plays a tumor suppressive role in PTC progression by inhibiting PI3K/AKT pathway and EMT.
Search for other papers by Shanhong Li in
Google Scholar
PubMed
Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
Search for other papers by Jincheng Tao in
Google Scholar
PubMed
Search for other papers by Jie Tang in
Google Scholar
PubMed
Search for other papers by Yanting Chu in
Google Scholar
PubMed
Search for other papers by Huiqun Wu in
Google Scholar
PubMed
The global burden of controlling and managing diabetes mellitus (DM) is a significant challenge. Despite the advancements in conventional DM therapy, there remain hurdles to overcome, such as enhancing medication adherence and improving patient prognosis. Digital therapeutics (DTx), an innovative digital application, has been proposed to augment the traditional disease management workflow, particularly in managing chronic diseases like DM. Several studies have explored DTx, yielding promising results. However, certain concerns about this innovation persist. In this review, we aim to encapsulate the potential of DTx and its applications in DM management, thereby providing a comprehensive overview of this technique for public health policymakers.
Search for other papers by Hui Li in
Google Scholar
PubMed
Search for other papers by Peng Wu in
Google Scholar
PubMed
Background
Epigenetics, which involves regulatory modifications that do not alter the DNA sequence itself, is crucial in the development and progression of thyroid cancer. This study aims to provide a comprehensive analysis of the epigenetic research landscape in thyroid cancer, highlighting current trends, major research areas, and potential future directions.
Methods
A bibliometric analysis was performed using data from the Web of Science Core Collection (WOSCC) up to 1 November 2023. Analytical tools such as VOSviewer, CiteSpace, and the R package ‘bibliometrix’ were employed for comprehensive data analysis and visualization. This process identified principal research themes, along with influential authors, institutions, and countries contributing to the field.
Results
The analysis reveals a marked increase in thyroid cancer epigenetics research over the past two decades. Emergent key themes include the exploration of molecular mechanisms and biomarkers, various subtypes of thyroid cancer, implications for therapeutic interventions, advancements in technologies and methodologies, and the scope of translational research. Research hotspots within these themes highlight intensive areas of study and the potential for significant breakthroughs.
Conclusion
This study presents an in-depth overview of the current state of epigenetics in thyroid cancer research. It underscores the potential of epigenetic strategies as viable therapeutic options and provides valuable insights for researchers and clinicians in advancing the understanding and treatment of this complex disease. Future research is vital to fully leverage the therapeutic possibilities offered by epigenetics in the management of thyroid cancer.
Search for other papers by Junhui Zhang in
Google Scholar
PubMed
Search for other papers by Hongyan Zhang in
Google Scholar
PubMed
Search for other papers by Bao Guo in
Google Scholar
PubMed
Search for other papers by Jun Yang in
Google Scholar
PubMed
Search for other papers by Renxiang Yu in
Google Scholar
PubMed
Search for other papers by Wenxiu Chen in
Google Scholar
PubMed
Search for other papers by Muxin Zhai in
Google Scholar
PubMed
Search for other papers by Cao Yuhan in
Google Scholar
PubMed
Search for other papers by Yajing Liu in
Google Scholar
PubMed
Search for other papers by Qiang Hong in
Google Scholar
PubMed
Search for other papers by Fenfen Xie in
Google Scholar
PubMed
The elevated level of hepatic oxidative stress (OS) in polycystic ovary syndrome (PCOS) is one of the important causes of liver abnormalities. Therefore, decreasing the level of hepatic OS in PCOS is beneficial to reduce the risk of PCOS-related liver diseases. Melatonin (MT), recognized as a potent antioxidant. Nevertheless, the efficacy of MT in alleviating hepatic OS associated with PCOS is yet to be established, and the precise mechanisms through which MT exerts its antioxidant effects remain to be fully elucidated. The aim of this study was to explore the potential mechanism by which MT reduces hepatic OS in PCOS. First, we detected elevated OS levels in the PCOS samples. Subsequently, with MT pretreatment, we discovered that MT could significantly diminish the levels of OS, liver triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT) and aspartate aminotransferase (AST),while concurrently ameliorating mitochondrial structural damage in PCOS liver. Furthermore, we identified elevated autophagy levels in the liver of PCOS rats and an inhibition of the Keap1-Nrf2 pathway. Through MT pretreatment, the expression of LC3 was significantly decreased, while the Keap1-Nrf2 pathway was activated. Our study showed that MT could affect the Nrf2 pathway dependent on the P62/LC3 autophagy pathway, thereby attenuating hepatic OS in PCOS. These findings offer novel insights and research avenues for the study of PCOS-related liver diseases.
Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
Search for other papers by Agata Hanna Bryk-Wiązania in
Google Scholar
PubMed
Search for other papers by Mari Minasyan in
Google Scholar
PubMed
Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
Search for other papers by Alicja Hubalewska-Dydejczyk in
Google Scholar
PubMed
Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
Search for other papers by Aleksandra Gilis-Januszewska in
Google Scholar
PubMed
Objective
Cushing’s syndrome (CS) is associated with an 18-fold greater risk of venous thromboembolism (VTE). We aimed to identify factors which provoke VTE among patients with CS and VTE and to describe the anticoagulant regimen used in these cases.
Methods
In this retrospective observational study, patients included in the European Registry on CS (ERCUSYN) in Krakow center, Poland, were followed for the occurrence of VTE and anticoagulant treatment. We identified factors provoking VTE according to the International Society of Thrombosis and Hemostasis (ISTH), along with factors included in the Padua score and CS-VTE score.
Results
Of the 128 patients followed for a median of 4.3 years, there were nine patients who experienced ten VTE episodes (prevalence of 7.8% and incidence of 13.4 per 1000 patient-years). All VTEs were classified as provoked according to the ISTH guidance, predominantly due to the transient major and minor (50% and 20%, respectively) factors, while they were less commonly due to persistent (30%) factors. In 2/9 patients, we could not identify any risk factor for VTE according to the Padua score, while in 2/6 patients according to the CS-VTE score. Patients were mostly anticoagulated with vitamin K antagonists (4/8 patients), followed by direct oral anticoagulants (3/8) and low-molecular-weight heparin (1/8). The median duration of anticoagulation was 2.75 years and exceeded beyond the primary treatment in 28% of episodes provoked by transient factors.
Conclusion
Further, multicenter studies are required to create a validated thrombotic risk score and guidelines regarding VTE treatment in CS patients.
Search for other papers by Waleed K W Al-Badri in
Google Scholar
PubMed
Search for other papers by Hinke Marijke Jellema in
Google Scholar
PubMed
Search for other papers by Arnaud R G G Potvin in
Google Scholar
PubMed
Search for other papers by Ruth M A van Nispen in
Google Scholar
PubMed
Search for other papers by Peter H Bisschop in
Google Scholar
PubMed
Search for other papers by Peerooz Saeed in
Google Scholar
PubMed
Purpose
This review aims to discuss the psychological aspects of Graves’ ophthalmopathy (GO), estimate the prevalence of depression and anxiety disorders in GO, examine whether these psychiatric disorders are more prevalent in GO than in Graves’ disease (GD) without eye disease, and evaluate the main contributors for depression and anxiety in GO.
Methods
A review of the literature.
Results
Both depression and anxiety are associated with GO. The prevalence of depression and anxiety disorders specifically in GO patients was estimated at 18–33% and 26–41%, respectively. The reported prevalence in GD patients ranged from 9% to 70% for depression and from 18% to 88% for anxiety disorders. Significantly higher levels of depression and anxiety were found in GD patients compared with patients with non-autoimmune hyperthyroidism. Conflicting results have been reported regarding the association of antithyroid autoantibodies with depression and anxiety disorders. Serum thyroid hormone levels do not correlate with the severity of depression and anxiety. An improvement of psychiatric symptoms is observed in hyperthyroid patients after treatment of thyrotoxicosis. Moreover, depression and anxiety are significantly related to impaired quality of life (QoL) in GO. Exophthalmos and diplopia were not associated with depression nor anxiety, but orbital decompression and strabismus surgery do seem to improve QoL in GO patients.
Conclusions
The results of this review suggest that altered thyroid hormone levels and autoimmunity are prognostic factors for depression and anxiety in GO. With regard to the visual and disfiguring aspects of GO as contributing factors for depression and anxiety, no decisive conclusions can be made.