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Rohit Barnabas Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Swati Jadhav Department of Endocrinology, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, India

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Anurag Ranjan Lila Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Sirisha Kusuma Boddu Consultant Pediatric Endocrinology & Diabetes, Rainbow Children’s Hospital, Hyderabad, India

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Saba Samad Memon Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Sneha Arya Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Samiksha Chandrashekhar Hegishte Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Manjiri Karlekar Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Virendra A Patil Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Vijaya Sarathi Department of Endocrinology, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, India

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Nalini S Shah Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Tushar Bandgar Department of Endocrinology, Seth GS Medical College and KEM Hospital, Parel, Mumbai, India

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Background

The data on Leydig cell hypoplasia (LCH) resulting from biallelic Luteinizing hormone/chorionic gonadotropin receptor (LHCGR) inactivating variants is limited to case series.

Methods

We aim to describe our patients and perform systematic review of the patients with LHCGR inactivating variants in the literature. Detailed phenotype and genotype data of three patients from our centre and 85 (46,XY: 67; 46,XX: 18) patients from 59 families with LHCGR-inactivating variants from literature were described.

Results

Three 46,XY patients (age 6–18 years) from our center, with two reared as females, had two novel variants in LHCGR. Systematic review (including our patients) revealed 72 variants in 88 patients. 46,XY patients (n = 70, 56 raised as females) presented with pubertal delay (n = 41) or atypical genitalia (n = 17). Sinnecker score ≥3 (suggesting antenatal human chorionic gonadotropin (hCG) inaction) was seen in 80% (56/70), and hCG-stimulated testosterone was low (<1.1 ng/mL) in 77.4% (24/31), whereas puberty/postpubertal age, high luteinizing hormone (LH) (97.6%, 41/42) and low (<1.0 ng/mL) basal testosterone (94.9%, 37/39) was observed in most. Follicle stimulating hormone was elevated in 21/51 of these patients. Variants with <10% receptor function were exclusively seen in cohorts with Sinnecker 4/5 (10/15 vs 0/5, P = 0.033). 46,XX patients (n = 18) presented with oligo/amenorrhea and/or anovulatory infertility and had polycystic ovaries (7/9) with median LH of 10 IU/L (1.2–38).

Conclusion

In summary, this study comprehensively characterizes LHCGR variants, revealing genotype-phenotype correlations and informing clinical management of LCH. In 46,XY LCH patients, pubertal LH inaction is uniform with variable severity of antenatal hCG inaction. Few mutant LHCGR have differential actions for LH and hCG.

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G Amiyangoda Department of Pharmacology, Faculty of Medicine, University of Peradeniya, Sri Lanka
Diabetes and Endocrine Unit, National Hospital, Kandy, Sri Lanka

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C N Antonypillai Diabetes and Endocrine Unit, National Hospital, Kandy, Sri Lanka

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S S C Gunatilake Diabetes and Endocrine Unit, National Hospital, Kandy, Sri Lanka

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T T Weerathunge Department of Community Medicine, Faculty of Medicine, University of Colombo, Sri Lanka

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D Ediriweera Health Data Science Unit, Faculty of Medicine, University of Kelaniya, Sri Lanka

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S G P D Kosgallana Diabetes and Endocrine Unit, National Hospital, Kandy, Sri Lanka

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R D P Jayawardana Department of Biochemistry, National Hospital, Kandy, Sri Lanka

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H A N D Thissera Department of Biochemistry, National Hospital, Kandy, Sri Lanka

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W J Emalka Faculty of medicine, University of Peradeniya, Sri Lanka

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H U Daraniyagala Faculty of medicine, University of Peradeniya, Sri Lanka

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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.

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Zeting Li Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Ling Pei Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Huangmeng Xiao Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Nan Chen Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Fenghua Lai Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Shufang Yue Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Changliu Xu Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Yanbing Li Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Haipeng Xiao Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Xiaopei Cao Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Glucose-like peptide-1 (GLP-1) is a vital hormone in the intestines that regulates glucose metabolism. Although pancreatic-derived factor (PANDER) overexpression is known to suppress GLP-1, the underlying mechanisms are unclear. Our study aims to uncover how PANDER influences GLP-1 synthesis and secretion. We established a PANDER overexpression model in STC-1 intestinal cells, confirming its inhibitory effect on GLP-1 secretion. This effect was reversed in PANDER-knockout cells. Additionally, a negative correlation between PANDER and GLP-1 was observed in patients with a history of gestational diabetes. Subsequently, through whole transcriptome gene sequencing in PANDER-overexpressed STC-1 cells, we discovered that the activation of IL-6 and its related STAT3 signaling pathway was significantly inhibited, and this finding was validated by Western blotting and quantitative reverse transcription PCR. Finally, rescue experiments confirmed that the IL-6-related STAT3/Akt/GSK3β/β-catenin signaling pathway mediates the negative regulatory effect of PANDER on GLP-1. Taken together, our data identify IL-6 as a bridge connecting PANDER and GLP-1 in the STC-1 cells, demonstrating potential therapeutic targets for diabetes treatment by targeting the PANDER–IL-6–GLP-1 axis.

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Peter Bond Department of Internal Medicine, Elisabeth TweeSteden Hospital, Tilburg, the Netherlands
Department of Performance and Image-enhancing Drugs Research, Android Health Clinic, Utrecht, the Netherlands

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Tijs Verdegaal Department of Internal Medicine, Elisabeth TweeSteden Hospital, Tilburg, the Netherlands
Department of Internal Medicine, Spaarne Gasthuis, Haarlem, the Netherlands

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Diederik L Smit Department of Internal Medicine, Elisabeth TweeSteden Hospital, Tilburg, the Netherlands
Department of Performance and Image-enhancing Drugs Research, Android Health Clinic, Utrecht, the Netherlands

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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.

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Shanhong Li Department of Medical Informatics, Medical School of Nantong University, Nantong, Jiangsu Province, China

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Jincheng Tao Department of Medical Informatics, Medical School of Nantong University, Nantong, Jiangsu Province, China
Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China

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Jie Tang Department of Medical Informatics, Medical School of Nantong University, Nantong, Jiangsu Province, China

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Yanting Chu Department of Medical Informatics, Medical School of Nantong University, Nantong, Jiangsu Province, China

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Huiqun Wu Department of Medical Informatics, Medical School of Nantong University, Nantong, Jiangsu Province, China

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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.

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Yi Wang Y Wang, Department of Endocrinology, Genetics and Metabolism , Beijing Children's Hospital Capital Medical University, Beijing, China

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Yingying Xu Y Xu, Department of Pediatrics, Sun Yat-Sen University, Guangzhou, China

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Rongrong Xie R Xie, Department of Endocrinology, Children’s Hospital of Soochow University, Suzhou, China

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Bing Yan Cao B Cao, Department of Endocrinology, Genetics and Metabolism, Beijing Children's Hospital Capital Medical University, Beijing, China

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Yuan Ding Y Ding, Department of Endocrinology, Genetics and Metabolism, Beijing Children's Hospital Capital Medical University, Beijing, China

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Jiayun Guo J Guo, Department of Endocrinology, Genetics and Metabolism, Beijing Children's Hospital Capital Medical University, Beijing, China

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Xiaoqiao Li X Li, Department of Endocrinology, Genetics and Metabolism, Beijing Children's Hospital Capital Medical University, Beijing, China

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Xiaolin Ni X Ni, Department of Endocrinology, Genetics and Metabolism, Beijing Children's Hospital Capital Medical University, Beijing, China

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Zheng Yuan Z Yuan, Department of Endocrinology, Genetics and Metabolism, Beijing Children's Hospital Capital Medical University, Beijing, China

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Linqi Chen L Chen, Department of Endocrinology, Children’s Hospital of Soochow University, Suzhou, China

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Liyang Liang L Liang, Department of Pediatrics, Sun Yat-Sen University, Guangzhou, China

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Chunxiu Gong C Gong, Department of Endocrinology, Genetics and Metabolism, Capital Medical University, Beijing, 100054, China

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Objective: Rapid-onset obesity with hypoventilation, hypothalamic dysfunction, and autonomic dysregulation (ROHHAD) is rare, and manifestations of autonomic dysregulation are diverse and may be overlooked. We aimed to evaluate the incidence of these manifestations.

Methods: Patients with ROHHAD syndrome reported before and after 2019 were divided into Groups 1 and 2. Patients who were diagnosed at three regional hospitals in China were included in Group 3. We collected the age of each specific term of the ROHHAD (neurogenic tumor, NET) acronym and the detailed manifestations of each term, and compared them among the three groups.

Results: A total of 16 patients were diagnosed within the 2-year period. Two had neurogenic tumors and cognitive and behavioral abnormalities before developing rapid obesity. At least 93.8% of the patients had ≥ 4 symptoms of autonomic dysregulation. When comparing autonomic dysregulation among Groups 1–3, the rates of cardiovascular manifestations were NA vs. 12.8% vs. 81.2%; gastrointestinal disturbances were 11.4% vs. 8.5% vs. 62.5%; strabismus was 25.7% vs. 12.8% vs. 62.5%; sleep disturbance was NA vs. 6.4% vs. 50.0%; and abnormal pain threshold was NA vs. 10.6% vs. 25.0% (all p<0.05). The rates of cognitive and behavioral abnormalities were NA vs 29.8% and 87.5% (p<0.01).

Conclusions: Rapid-onset obesity is not always the first sign of ROHHAD syndrome. Higher rates of autonomic dysregulation and cognitive and behavioral abnormalities with multiple manifestations of autonomic dysregulation coexisted in our cohort, indicating that evaluations of autonomic function and the limbic system should be strengthened when assessing this condition.

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Hui Li Department of Thyroid Surgery, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/Hunan Cancer Hospital, Changsha, Hunan, P. R. China.

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Peng Wu Department of Thyroid Surgery, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/Hunan Cancer Hospital, Changsha, Hunan, P. R. China.

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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.

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Nishchil Patel N Patel, Endocrinology and Diabetes, University Hospitals Plymouth NHS Trust, Plymouth, PL6 8DH, United Kingdom of Great Britain and Northern Ireland

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Kagabo Hirwa K Hirwa, Department of Endocrinology, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Gemma Gardner G Gardner, Endocrinology and Diabetes, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Kirsten Pearce K Pearce, Department of Neuroradiology, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Jinny Jeffery J Jeffery, Department of Biochemistry, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Fizzah Iqbal F Iqbal, Morriston Hospital, Swansea, United Kingdom of Great Britain and Northern Ireland

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Daniel Flanagan D Flanagan, Department of Endocrinology, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Aim: To define functional and anatomical pituitary disease following ICI therapy and describe any change in pituitary function with time.

Methods: Retrospective observational audit of patients on ICI therapy in our centre between 2013 and 2023. We reviewed all patients on ICI therapy under the oncology department at University Hospital Plymouth, and identified individuals referred to endocrinology with suspected adrenal insufficiency. Patients were established on adrenal steroid replacement and subsequently underwent formal pituitary testing. Pituitary disease was evidenced by low ACTH, other pituitary dysfunction and/or abnormalities on pituitary imaging.

Results: 954 patients received ICI therapy during the study period, and 37 developed HPA axis dysfunction. Median interval of onset of symptoms was 4 months. There was no recovery in cortisol or ACTH for any individual on repeated testing. Other permanent anterior pituitary hormone defects were unusual. Hypophysitis associated with immunotherapy appears to specifically target corticotrophs with no evidence of recovery. There was a specific abnormality seen in MRI scans of 7 of 27 patients who had scans, appearing to be a particular feature of immune mediated hypophysitis. These were confined to the anterior aspect of the pituitary as striations and were not visible on any scans performed more than three months after disease onset.

Conclusion: These data show that immune related (IR) hypophysitis is a common complication of immune checkpoint inhibitor therapy. This may result in an imaging abnormality within the areas of the pituitary richest in corticotrophs. The endocrine consequence of this is a permanent defect in ACTH and therefore cortisol production.

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Shuqi Li S Li, Department of Endocrinology, Zhongshan Hospital Fudan University, Shanghai, China

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Chenye Shi C Shi, Department of General Surgery, Zhongshan Hospital Fudan University, Shanghai, China

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Haifu Wu H Wu, Department of General Surgery, Zhongshan Hospital Fudan University, Shanghai, China

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Hongmei Yan H Yan, Department of Endocrinology, Zhongshan Hospital Fudan University, Shanghai, China

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Mingfeng Xia M Xia, Department of Endocrinology, Zhongshan Hospital Fudan University, Shanghai, China

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Heng Jiao H Jiao, Department of General Surgery, Zhongshan Hospital Fudan University, Shanghai, China

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Yang He Y He, Department of Endocrinology, Zhongshan Hospital Fudan University, Shanghai, China

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Ming Zhong M Zhong, Department of Critical Care Medicine, Zhongshan Hospital Fudan University, Shanghai, China

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Wenhui Lou W Lou, Department of General Surgery, Zhongshan Hospital Fudan University, Shanghai, China

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Xin Gao X Gao, Department of Endocrinology, Zhongshan Hospital Fudan University, Shanghai, China

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Hua Bian H Bian, Department of Endocrinology, Zhongshan Hospital Fudan University, Shanghai, China

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Xinxia Chang X Chang, Department of Endocrinology, Zhongshan Hospital Fudan University, Shanghai, China

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Background: Bariatric surgery induces significant weight loss, increases insulin sensitivity and improves dyslipidemia. As one of the most widely performed bariatric surgeries, laparoscopic sleeve gastrectomy (LSG) is thought to improve metabolic profile along with weight loss. The objective of this study was to evaluate longitudinal changes in serum metabolite levels after LSG and elucidate the underlying mechanisms of metabolic improvement.

Methods: Clinical metabolic parameters and serum samples were collected preoperatively and at 1, 3, and 6 months postoperatively from nine patients with obesity undergoing LSG. Serum metabolites were measured using non-targeted metabolic liquid chromatography-mass spectrometry (LC-MS) method.

Results: During the 1, 3, and 6 months postoperative follow-up, the BMI, HOMA-IR, liver fat content showed a gradual descending trend. A total of 328 serum metabolites were detected and 38 were differentially expressed. The up-regulated metabolites were mainly enriched in ketone body metabolism, alpha linolenic acid and linoleic acid metabolism, pantothenate and CoA biosynthesis, glycerolipid metabolism, fructose and mannose degradation, while the down-regulated metabolites were closely related to caffeine metabolism, oxidation of branched chain fatty acids, glutamate metabolism, and homocysteine degradation. Notably, nine metabolites (oxoglutarate, 2-ketobutyric acid, succinic acid semialdehyde, phthalic acid, pantetheine, eicosapentaenoate, 3-hydroxybutanoate, oxamic acid, and dihydroxyfumarate) showed persistent differential expression at 1, 3, and 6 months follow-up. Some were found to be significantly associated with weight loss, insulin resistance improvement and liver fat content reduction.

Conclusions: This finding may provide a new perspective for revealing novel biomarkers and mechanisms of metabolic improvement in obesity and related comorbidities.

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Junhui Zhang J Zhang, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China

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Hongyan Zhang H Zhang, Department of Histology and Embryology, Anhui Medical University, Hefei, China

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Bao Guo B Guo, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China

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Jun Yang J Yang, Anhui Medical University, Hefei, China

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Renxiang Yu R Yu, Anhui Medical University, Hefei, China

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Wenxiu Chen W Chen, Department of Histology and Embryology, Anhui Medical University, Hefei, China

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Muxin Zhai M Zhai, Anhui Medical University, Hefei, China

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Cao Yuhan C Yuhan, Anhui Medical University, Hefei, China

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Yajing Liu Y Liu, NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract (Anhui Medical University), Hefei, China

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Qiang Hong Q Hong, Department of Histology and Embryology, Anhui Medical University, Hefei, 230032, China

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Fenfen Xie F Xie, Department of Histology and Embryology, Anhui Medical University, Hefei, 230032, China

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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.

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