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Tsung-Hui Wu Section of Endocrinology and Metabolism, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan

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Guan-Yu Su Section of Endocrinology and Metabolism, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan

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Tsung-Yun Liu Institute of Food Safety and Health Risk Assessment, College of Pharmaceutical Sciences, National Yang Ming Chiao Tung University, Taipei, Taiwan

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Hsiang-Tsui Wang Institute of Food Safety and Health Risk Assessment, College of Pharmaceutical Sciences, National Yang Ming Chiao Tung University, Taipei, Taiwan
Institute of Pharmacology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
PhD Program in Toxicology, Kaohsiung Medical University, Kaohsiung, Taiwan

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Chii-Min Hwu Section of Endocrinology and Metabolism, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
Faculty of Medicine, National Yang Ming Chiao Tung University School of Medicine, Taipei, Taiwan

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Acrolein, an unsaturated aldehyde, plays a pathological role in neurodegenerative diseases. However, less is known about its effects on peripheral neuropathy. The aim of this study was to investigate the association of acrolein and diabetic peripheral neuropathy in patients with type 2 diabetes. We recruited 148 ambulatory patients with type 2 diabetes. Each participant underwent an assessment of the Michigan Neuropathy Screening Instrument Physical Examination. Diabetic peripheral neuropathy was defined as Michigan Neuropathy Screening Instrument Physical Examination score ≥ 2.5. Serum levels and urinary levels of acrolein protein conjugates were measured. Urinary acrolein protein conjugates-to-creatinine ratios were determined. Patients with diabetic peripheral neuropathy had significantly higher urinary acrolein protein conjugates-to-creatinine ratios than those without diabetic peripheral neuropathy (7.91, 95% CI: 5.96–10.50 vs 5.31, 95% CI: 4.21–6.68, P = 0.029). Logarithmic transformation of urinary acrolein protein conjugates-to-creatinine ratios was positively associated with diabetic peripheral neuropathy in univariate logistic analysis, and the association remained significant in multivariate analysis (OR = 2.45, 95% CI: 1.12–5.34, P = 0.025). In conclusion, urinary acrolein protein conjugates-to-creatinine ratio may act as a new biomarker for diabetic peripheral neuropathy in type 2 diabetes. The involvement of acrolein in the pathogenesis of diabetic peripheral neuropathy warrants further investigation.

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I M A A van Roessel Department of Pediatric Endocrinology, Wilhelmina Children’s Hospital, University Medical Center Utrecht, Utrecht, The Netherlands

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J P de Graaf Dutch Pituitary Foundation, Nijkerk, The Netherlands
Department of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands
Endo-ERN European Reference Network on Rare endocrine conditions

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N R Biermasz Department of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands
Endo-ERN European Reference Network on Rare endocrine conditions

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E Charmandari Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, Aghia Sophia Children's Hospital, Athens, Greece
Division of Endocrinology and Metabolism, Center for Clinical, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece

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H M van Santen Department of Pediatric Endocrinology, Wilhelmina Children’s Hospital, University Medical Center Utrecht, Utrecht, The Netherlands

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Objective

Hypothalamic dysfunction is a rare condition and can be encountered in patients who have been diagnosed or treated for a suprasellar brain tumor. Due to its rarity, the signs and symptoms of hypothalamic dysfunction may be difficult to recognize, leading to delayed diagnosis of the suprasellar brain tumor or to difficulties in finding the health-care expertise for hypothalamic dysfunction after tumor treatment. To improve the care and outcome of patients with acquired hypothalamic dysfunction, professionals are required to understand the patient’s needs.

Design

A worldwide online survey was distributed from April 2022 to October 2022 to patients with childhood-onset hypothalamic dysfunction (as reported by the patient) following a brain tumor.

Methods

Patients were notified about the survey through patient advocacy groups, the SIOPe craniopharyngioma working group and the Endo-ERN platform.

Results

In total, 353 patients with hypothalamic dysfunction following craniopharyngioma (82.2%), low-grade glioma (3.1%) or a pituitary tumor (8.2%) or caregivers responded to the survey. Sixty-two percent had panhypopituitarism. Obesity (50.7%) and fatigue (48.2%) were considered the most important health problems. Unmet needs were reported for help with diet, exercise and psychosocial issues. Patients’ suggestions for future research include new treatments for hypothalamic obesity and alternative ways for hormone administration.

Conclusions

According to the patient’s perspective, care for acquired hypothalamic dysfunction can be improved if delivered by experts with a holistic view of the patient in a multidisciplinary setting with a focus on quality of life. Future care and research on hypothalamic dysfunction must integrate the patients’ unmet needs.

Significance statement

Patients with hypothalamic dysfunction may experience a variety of symptoms, which are not always adequately recognized or addressed. In previous papers, the perspective of caregivers of children with craniopharyngioma has been reported (Klages et al. 2022, Craven et al. 2022). Now we address the patients’ perspective on acquired hypothalamic dysfunction using an Endo-ERN global survey. According to the patients’ perspective, care can be improved, with needs for improvement in the domains of obesity, fatigue and lifestyle. Research may focus on ways to improve hypothalamic obesity and alternative ways for hormone administration. Ideally, care should be delivered by doctors who have a holistic view of the patient in a multidisciplinary expert team. The results of this study can be used to formulate best practices for clinical care and to design future research proposals.

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Lukas Plachy Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Lenka Petruzelkova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Petra Dusatkova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Klara Maratova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Dana Zemkova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Lenka Elblova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Vit Neuman Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Stanislava Kolouskova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Barbora Obermannova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Marta Snajderova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Zdenek Sumnik Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Jan Lebl Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Stepanka Pruhova Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic

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Familial short stature (FSS) describes vertically transmitted growth disorders. Traditionally, polygenic inheritance is presumed, but monogenic inheritance seems to occur more frequently than expected. Clinical predictors of monogenic FSS have not been elucidated. The aim of the study was to identify the monogenic etiology and its clinical predictors in FSS children. Of 747 patients treated with growth hormone (GH) in our center, 95 with FSS met the inclusion criteria (pretreatment height ≤−2 SD in child and his/her shorter parent); secondary short stature and Turner/Prader–Willi syndrome were excluded criteria. Genetic etiology was known in 11/95 children before the study, remaining 84 were examined by next-generation sequencing. The results were evaluated by American College of Medical Genetics and Genomics (ACMG) guidelines. Nonparametric tests evaluated differences between monogenic and non-monogenic FSS, an ROC curve estimated quantitative cutoffs for the predictors. Monogenic FSS was confirmed in 36/95 (38%) children. Of these, 29 (81%) carried a causative genetic variant affecting the growth plate, 4 (11%) a variant affecting GH–insulin-like growth factor 1 (IGF1) axis and 3 (8%) a variant in miscellaneous genes. Lower shorter parent’s height (P = 0.015) and less delayed bone age (BA) before GH treatment (P = 0.026) predicted monogenic FSS. In children with BA delayed less than 0.4 years and with shorter parent’s heights ≤−2.4 SD, monogenic FSS was revealed in 13/16 (81%) cases. To conclude, in FSS children treated with GH, a monogenic etiology is frequent, and gene variants affecting the growth plate are the most common. Shorter parent’s height and BA are clinical predictors of monogenic FSS.

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Yijun Tang Department of Endocrinology and Metabolism, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Yao Chen Department of Endocrinology and Metabolism, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Jiayi Wang Department of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Qianwen Zhang Department of Endocrinology and Metabolism, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Yirou Wang Department of Endocrinology and Metabolism, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Yufei Xu Department of Medical Genetics and Molecular Diagnostic Laboratory, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Xin Li Department of Endocrinology and Metabolism, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Jian Wang International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Xiumin Wang Department of Endocrinology and Metabolism, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Diagnosis and management strategy of disorders of sex development (DSD) are difficult and various due to heterogeneous phenotype and genotype. Under widespread use of genomic sequencing technologies, multiple genes and mechanisms have been identified and proposed as genetic causes of 46,XY DSD. In this study, 178 46,XY DSD patients were enrolled and underwent gene sequencing (either whole-exome sequencing or targeted panel gene sequencing). Detailed clinical phenotype and genotype information were summarized which showed that the most common clinical manifestations were micropenis (56.74%, 101/178), cryptorchidism (34.27%, 61/178), and hypospadias (17.42%, 31/178). Androgen synthesis/action disorders and idiopathic hypogonadotropic hypogonadism were the most frequent clinical diagnoses, accounting, respectively, for 40.90 and 21.59%. From all next-generation sequencing results, 103 candidate variants distributed across 32 genes were identified in 88 patients. The overall molecular detection rate was 49.44% (88/178), including 35.96% (64/178) pathogenic/likely pathogenic variants and 13.48% (24/178) variants of uncertain significance. Of all, 19.42% (20/103) variants were first reported in 46,XY DSD patients. Mutation c.680G>A (p.R227Q) on SRD5A2 (steroid 5-alpha-reductase 2) (36.67%, 11/30) was a hotspot mutation in the Chinese population. Novel candidate genes related to DSD (GHR (growth hormone receptor) and PHIP (pleckstrin homology domain-interacting protein)) were identified. Overall, this was a large cohort of 46,XY DSD patients with a common clinical classification and phenotype spectrum of Chinese patients. Targeted gene panel sequencing covered most of the genes contributing to DSD, whereas whole-exome sequencing detected more candidate genes.

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Henry Zelada Division of Endocrinology, Diabetes and Metabolism, University of Alabama at Birmingham Heersink School of Medicine, Birmingham, Alabama, USA

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M Citlalli Perez-Guzman Internal Medicine Division of Endocrinology, Centro Médico ABC, Mexico City, Mexico

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Daniel R Chernavvsky Center for Diabetes Technology, University of Virginia, Charlottesville, Virginia, USA

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Rodolfo J Galindo Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine. Miami, Florida, USA

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Over the last few years, several exciting changes in continuous glucose monitoring (CGM) technology have expanded its use and made CGM the standard of care for patients with type 1 and type 2 diabetes using insulin therapy. Consequently, hospitals started to notice increased use of these devices in their hospitalized patients. Furthermore during the coronavirus disease 2019 (COVID) pandemic, there was a critical need for innovative approaches to glycemic monitoring, and several hospitals started to implement CGM protocols in their daily practice. Subsequently, a plethora of studies have demonstrated the efficacy and safety of CGM use in the hospital, leading to clinical practice guideline recommendations. Several studies have also suggested that CGM has the potential to become the standard of care for some hospitalized patients, overcoming the limitations of current capillary glucose testing. Albeit, there is a need for more studies and particularly regulatory approval. In this review, we provide a historical overview of the evolution of glycemic monitoring in the hospital and review the current evidence, implementation protocols, and guidance for the use of CGM in hospitalized patients.

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Yee-Ming M Cheung Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia
Division of Endocrinology, Diabetes and Metabolism, Northwell, Great Neck, New York, USA

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Rudolf Hoermann Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

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Karen Van Department of Endocrinology, Austin Health, Melbourne, Australia

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Damian Wu Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

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Jenny Healy Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia

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Bella Halim Department of Endocrinology, Austin Health, Melbourne, Australia

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Manjri Raval Department of Endocrinology, Austin Health, Melbourne, Australia

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Maria McGill Department of Radiology, Austin Health, Melbourne, Australia

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Ali Al-Fiadh Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Cardiology, Austin Health, Melbourne Australia

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Michael Chao Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia

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Shane White Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia

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Belinda Yeo Olivia Newton-John Cancer Research and Wellness Centre, Austin Health, Melbourne, Australia
Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Australia

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Jeffrey D Zajac Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia

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Mathis Grossmann Department of Medicine, The University of Melbourne, Austin Health, Melbourne, Australia
Department of Endocrinology, Austin Health, Melbourne, Australia

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Purpose

We previously demonstrated that 12 months of aromatase inhibitor (AI) treatment was not associated with a difference in body composition or other markers of cardiometabolic health when compared to controls. Here we report on the pre-planned extension of the study. The pre-specified primary hypothesis was that AI therapy for 24 months would lead to increased visceral adipose tissue (VAT) area when compared to controls.

Methods

We completed a 12-month extension to our prospective 12-month cohort study of 52 women commencing AI treatment (median age 64.5 years) and 52 women with breast pathology not requiring endocrine therapy (63.5 years). Our primary outcome of interest was VAT area. Secondary and exploratory outcomes included other measures of body composition, hepatic steatosis, measures of atherosclerosis and vascular reactivity. Using mixed models and the addition of a fourth time point, we increased the number of study observations by 79 and were able to rigorously determine the treatment effect.

Results

Among study completers (AI = 39, controls = 40), VAT area was comparable between groups over 24 months, the mean-adjusted difference was −1.54 cm2 (95% CI: −14.9; 11.9, P = 0.79). Both groups demonstrated parallel and continuous increases in VAT area over the observation period that did not diverge or change between groups. No statistically significant difference in our secondary and exploratory outcomes was observed between groups.

Conclusions

While these findings provide reassurance that short-to-medium-term exposure to AI therapy is not associated with metabolically adverse changes when compared to controls, risk evolution should be less focussed on the AI-associated effect and more on the general development of cardiovascular risk over time.

Open access
Bjarke R Medici Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark

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Birte Nygaard Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Jeppe L la Cour Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark

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Martin Krakauer Department of Clinical Physiology and Nuclear Medicine, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Physiology and Nuclear Medicine, Bispebjerg and Frederiksberg Hospital, University of Copenhagen, Copenhagen, Denmark

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Andreas Brønden Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Pharmacology, Bispebjerg and Frederiksberg Hospital, University of Copenhagen, Copenhagen, Denmark

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Mette P Sonne Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark

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Jens J Holst Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Jens F Rehfeld Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Tina Vilsbøll Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Herlev, Denmark

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Jens Faber Department of Medicine, Herlev Hospital, University of Copenhagen, Herlev, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Filip K Knop Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Herlev, Denmark

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Context

In individuals with hypothyroidism and overweight, levothyroxine substitution therapy is often expected to cause weight loss due to its effect on resting energy expenditure. However, despite levothyroxine-induced enhancement of resting energy expenditure, fat mass loss is rarely seen after levothyroxine substitution therapy. The mechanism behind this conundrum is unknown.

Aim

The aim of the study was to assess the effect of levothyroxine therapy on hunger sensations and ad libitum food intake in individuals with hypothyroidism.

Design and setting

Prospective cohort study of 18 newly diagnosed hypothyroid women (thyroid-stimulating hormone (TSH) >10 mU/L). Participants were investigated at diagnosis, after normalization of TSH (<4.0 mU/L), and after 6 months of successful treatment. Eighteen age and body mass index-matched healthy controls were also included.

Intervention

Hypothyroid individuals were treated with levothyroxine according to European Thyroid Association guidelines.

Main outcomes

Changes in hunger sensation were assessed using visual analog scales (cm) before and during a standardized mixed meal test, and food intake was measured during a subsequent ad libitum meal (g).

Results

After 6 months of levothyroxine therapy, mean resting energy expenditure was increased by 144 kcal/day (10%) (P < 0.001). Weight loss was comprised of 0.8 kg fat-free mass while fat mass remained unchanged. Fasting hunger sensation increased from a mean of 4.5 (s.d. 2.2) cm to 5.5 (s.d. 2.2) cm (P = 0.047). The numerical increase in ad libitum meal intake did not reach statistical significance.

Conclusion

Our data suggest that levothyroxine-induced hunger may be a culprit in the lack of fat mass loss from levothyroxine therapy.

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Molly L Tanenbaum Division of Endocrinology, Gerontology, and Metabolism, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA

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Persis V Commissariat Section on Clinical, Behavioral, and Outcomes Research, Joslin Diabetes Center, Boston, Massachusetts, USA

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Diabetes technology continues to advance, with more individuals with type 1 diabetes (T1D) adopting insulin pumps, continuous glucose monitoring (CGM), and automated insulin delivery (AID) systems that integrate real-time glucose data with an algorithm to assist with insulin dosing decisions. These technologies are linked with benefits to glycemic outcomes (e.g. increased time in target range), diabetes management behaviors, and quality of life. However, current devices and systems are not without barriers and hassles for the user. The intent of this review is to describe the personal challenges and reactions that users experience when interacting with current diabetes technologies, which can affect their acceptance and motivation to engage with their devices. This review will discuss user experiences and strategies to address three main areas: (i) the emotional burden of utilizing a wearable device; (ii) the perceived and experienced negative social consequences of device use; and (iii) the practical challenges of wearing devices.

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Heng Yeh Department of Emergency Medicine, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan
College of Medicine, Chang Gung University, Taoyuan, Taiwan

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Hsuan Yeh College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Chun-Cheng Chiang College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Ju-Ching Yen College of Medicine, China Medical University, Taichung, Taiwan

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I-Kuan Wang College of Medicine, China Medical University, Taichung, Taiwan
Department of Nephrology, China Medical University Hospital, Taichung, Taiwan

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Shou-Hsuan Liu College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Cheng-Chia Lee College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Cheng-Hao Weng College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Wen-Hung Huang College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Ching-Wei Hsu College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Tzung-Hai Yen College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Secondary hyperparathyroidism (SHPT) is a common complication of end-stage kidney disease (ESKD). Hungry bone syndrome (HBS) occurs frequently in patients on maintenance dialysis receiving parathyroidectomy for refractory SHPT. However, there is scanty study investigating the clinical risk factors that predict postoperative HBS, and its outcome in peritoneal dialysis (PD) patients. We conducted a single-center retrospective study to analyze 66 PD patients who had undergone parathyroidectomy for secondary hyperparathyroidism at Chang Gung Memorial Hospital between 2009 and 2019. The patients were stratified into two groups based on the presence (n=47) or absence (n=19) of HBS after parathyroidectomy. Subtotal parathyroidectomy was the most common surgery performed (74.2%), followed by total parathyroidectomy with autoimplantation (25.8%). Pathological examination of all surgical specimens revealed parathyroid hyperplasia (100%). Patients with HBS had lower levels of postoperative nadir corrected calcium, higher alkaline phosphate (ALP), and higher potassium levels compared with patients without HBS (all P<0.05). A multivariate logistic regression model confirmed that lower preoperative serum calcium level (OR 0.354, 95% CI 0.133–0.940, P=0.037), higher ALP (OR 1.026, 95% CI 1.008–1.044, P=0.004), and higher potassium level (OR 6.894, 95% CI 1.806–26.317, P=0.005) were associated with HBS after parathyroidectomy. Patients were followed for 58.2±30.8 months after the surgery. There was no significant difference between HBS and non-HBS groups in persistence (P=0.496) or recurrence (P=1.000) of hyperparathyroidism. The overall mortality rate was 10.6% with no significant difference found between both groups (P=0.099). We concluded that HBS is a common complication (71.2%) of parathyroidectomy for SHPT and should be managed appropriately.

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Alexandra Kiess Department of Pediatric Cardiology, Faculty of Medicine, Heart Center Leipzig, University of Leipzig, Strümpellstraße, Leipzig, Germany
Department of Child and Adolescent Medicine, Section of Pediatric Cardiology, University Hospital Jena, Am Klinikum, Jena, Germany

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Jessica Green Alder Hey Children's NHS Foundation Trust, Pediatric Intensive Care Unit, Eaton Road Liverpool, Great Britain

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Anja Willenberg Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics (ILM), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Uta Ceglarek Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics (ILM), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Ingo Dähnert Department of Pediatric Cardiology, Faculty of Medicine, Heart Center Leipzig, University of Leipzig, Strümpellstraße, Leipzig, Germany

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Wieland Kiess LIFE Leipzig Research Center for Civilization Diseases, University of Leipzig, Philipp-Rosenthal-Strasse, Leipzig, Germany
Department of Women and Child Health, Hospital for Children and Adolescents and Center for Pediatric Research (CPL), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Mandy Vogel LIFE Leipzig Research Center for Civilization Diseases, University of Leipzig, Philipp-Rosenthal-Strasse, Leipzig, Germany
Department of Women and Child Health, Hospital for Children and Adolescents and Center for Pediatric Research (CPL), University of Leipzig, Liebigstrasse, Leipzig, Germany

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Background and objectives

As part of the LIFE Child study, we previously described the associations between N-terminal-pro-hormone brain natriuretic peptide (NT-proBNP) and hs-troponin T (hs-TnT) levels and an individual’s sex, age and pubertal status, as well as with body mass index (BMI) and serum lipid levels. For NT-proBNP, we found inverse associations with advancing puberty, increasing BMI and serum lipid levels. These findings led us to further question the putative influences of the developing individual’s metabolic and growth status as represented by levels of insulin-like growth factor-1 (IGF-1) and IGF-1-binding protein-3 (IGF-BP3) as well as hemoglobin A1c (HbA1c) and Cystatin C (CysC).

Material and methods

Serum values, medical history and anthropometric data provided by 2522 children aged 0.25–18 years were collected and analyzed as per study protocol.

Results

A strong negative association between NT-proBNP values and IGF-1, IGF-BP3 and HbA1c levels was identified. For IGF-BP3, this interaction was modulated by sex and age, for HbA1c only by age. For hs-TnT, a positive association was found with IGF-BP3, IGF-1 and CysC. The association between hs-TnT and IGF-1 was sex dependent. The association between CysC and hs-TnT was stronger in girls, but the interaction with age was only seen in boys. Between hs-TnT and HbA1c, the association was significantly negative and modulated by age.

Conclusion

Based on our large pediatric cohort, we could identify age- and sex-dependent interactions between the metabolic status represented by IGF-1, IGF-BP3, CysC and HbA1c levels and the cardiac markers NT-proBNP and hs-TnT.

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