Browse

You are looking at 51 - 60 of 1,471 items for

Peiwen Zheng School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Peiwen Zheng in
Google Scholar
PubMed
Close
,
Fan Wang Beijing Hui-Long-Guan Hospital, Peking University, Beijing, China

Search for other papers by Fan Wang in
Google Scholar
PubMed
Close
,
Hui Li Psychosomatic Medicine Research Division, Inner Mongolia Medical University, Huhhot, China

Search for other papers by Hui Li in
Google Scholar
PubMed
Close
,
Hanlu Chen School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Hanlu Chen in
Google Scholar
PubMed
Close
,
Mengtong Li School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Mengtong Li in
Google Scholar
PubMed
Close
,
Haozheng Ma School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Haozheng Ma in
Google Scholar
PubMed
Close
,
Jue He School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Jue He in
Google Scholar
PubMed
Close
,
Li Chen School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Li Chen in
Google Scholar
PubMed
Close
,
Yanlong Liu School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Yanlong Liu in
Google Scholar
PubMed
Close
, and
Haiyun Xu School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

Search for other papers by Haiyun Xu in
Google Scholar
PubMed
Close

Objective

This study aimed to reveal associations between metabolic hormones in cerebral spinal fluid (CSF) and cigarette smoking-induced weight gain and to explore the underlying mechanism.

Methods

A total of 156 adult men were included, comprising active smokers and nonsmokers. In addition to demographic information and body mass index (BMI), plasma levels of ApoA1 and ApoB, high-density lipoprotein, low-density lipoprotein, cholesterol, triglyceride, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase in the participants were measured. Moreover, the metabolic hormones adiponectin, fibroblast growth factor 21 (FGF21), ghrelin, leptin, and orexin A, as well as the trace elements iron and zinc in CSF, were assessed.

Results

Compared to nonsmokers, active smokers showed higher BMI, and elevated CSF levels of FGF21, Zn, and Fe, but decreased levels of metabolic hormones adiponectin, ghrelin, leptin, and orexin A. Negative correlations existed between CSF FGF21 and ghrelin, between CSF Zn and ghrelin, as well as between CSF Fe and orexin A in active smokers. Furthermore, elevated CSF FGF21 and Zn predicted ghrelin level decrease in the smokers.

Conclusion

These data relate smoking-induced weight gain to its neurotoxic effect on the neurons that synthesize metabolic hormones such as adiponectin, ghrelin, leptin, or orexin A in the brain, by disrupting mitochondrial function and causing oxidative stress in the neurons.

Open access
Weiwei Liang Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

Search for other papers by Weiwei Liang in
Google Scholar
PubMed
Close
,
Yilin Zhang Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China

Search for other papers by Yilin Zhang in
Google Scholar
PubMed
Close
,
Yan Guo Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

Search for other papers by Yan Guo in
Google Scholar
PubMed
Close
,
Pengyuan Zhang Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

Search for other papers by Pengyuan Zhang in
Google Scholar
PubMed
Close
,
Jiewen Jin Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

Search for other papers by Jiewen Jin in
Google Scholar
PubMed
Close
,
Hongyu Guan Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

Search for other papers by Hongyu Guan in
Google Scholar
PubMed
Close
, and
Yanbing Li Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

Search for other papers by Yanbing Li in
Google Scholar
PubMed
Close

Background

Filamin A (FLNA) is a member of the filamin family and has been found to be critical for the progression of several cancers. However, its biological function in papillary thyroid cancer (PTC) remains largely unexplored.

Methods

Data from The Cancer Genome Atlas (TCGA) databases were utilized to analyze the FLNA expression level and its influence on the clinical implications of patients with PTC. Gene Expression Omnibus (GEO) and qRT-PCR was used to verify the expression levels of FLNA in PTC. Kaplan–Meier survival analysis was conducted to evaluate the prognostic value of FLNA in PTC. Transwell assays and wound healing were performed to examine the biological function of FLNA knockdown in PTC cells. Gene set enrichment analysis (GSEA) and Western blotting were conducted to investigate the potential mechanisms underlying the role of FLNA in PTC progression. In addition, the relationship between FLNA expression and the tumor immune microenvironment (TME) in PTC was explored.

Results

FLNA was significantly upregulated in PTC tissues. High expression levels of FLNA was correlated with advanced TNM stage, T stage, and N stage, as well as poor disease-free interval (DFI) and progression-free interval (PFI) time in PTC patients. Moreover, we found that FLNA knockdown inhibited the migration and invasion of PTC cells. Mechanistically, FLNA knockdown inhibited epithelial–mesenchymal transition (EMT) in PTC and affected the activation of the FAK/AKT signaling pathway. In addition, FLNA expression was associated with TME in PTC.

Conclusion

FLNA may be regarded as a new therapeutic target for PTC patients.

Open access
Ayse Nurcan Cebeci Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

Search for other papers by Ayse Nurcan Cebeci in
Google Scholar
PubMed
Close
,
Vera Schempp Paediatric Endocrinology, University Hospital, Bonn, Germany

Search for other papers by Vera Schempp in
Google Scholar
PubMed
Close
,
Katharina Förtsch Paediatric Endocrinology, University Hospital, Düsseldorf, Germany

Search for other papers by Katharina Förtsch in
Google Scholar
PubMed
Close
,
Bettina Gohlke Paediatric Endocrinology, University Hospital, Bonn, Germany

Search for other papers by Bettina Gohlke in
Google Scholar
PubMed
Close
,
Michaela Marx Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

Search for other papers by Michaela Marx in
Google Scholar
PubMed
Close
,
Helmuth-Guenther Dörr Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

Search for other papers by Helmuth-Guenther Dörr in
Google Scholar
PubMed
Close
, and
Joachim Woelfle Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

Search for other papers by Joachim Woelfle in
Google Scholar
PubMed
Close

While subclinical or overt hypothyroidism are common in Down syndrome (DS); Graves’ disease (GD) is rare (ranges 0.6–3%). We aimed to evaluate the clinical features, course, and treatment of GD in children with DS and compare them with those without DS. Among 161 children with GD, 13 (8 female, 5 male) had DS (8%). Data were collected retrospectively from patients’ medical records. The mean age at diagnosis was 10.6 ± 4.5 years, with a female-to-male ratio 1.6:1. The main symptoms were weight loss (n = 6), increased irritability (n = 3), and increased sweating (n = 3). None had orbitopathy. Seven of 11 patients with a thyroid ultrasound at diagnosis had a goitre. On admission, all had thyroid-stimulating hormone (TSH) <0.01 mU/L (normal range (NR): 0.51–4.30), free triiodothyronine, free thyroxine (mean ± s.d .), and thyrotrophin receptor antibodies (median, range) were 22.2 ± 10.2 pmol/L (NR: 3.5–8.1), 50.2 ± 18.7 pmol/L (NR 12.6–20.9), and 17.0 (2.89–159.0) U/L (NR <1), respectively. Patients were treated either with methimazole (n = 10) or carbimazole (n = 3), a dose of 0.54 ± 0.36 mg/kg/day. The treatment was ‘block and replace’ in ten patients and ‘dose titration’ in three patients, with a mean duration of 43.4 ± 11.0 months. Of 13 patients, four are still receiving primary treatment, three are in remission, one patient had two medically treated recurrences, three underwent surgery without complications, and two patients were lost to follow-up. Our data show that the clinical course of GD in patients with DS was similar to those without DS and suggest that a prolonged medical therapy should be the preferred option.

Open access
Zhenyu Liu Department of Clinical Medicine, Beijing Luhe Hospital, Capital Medical University, Tongzhou District, Beijing, China

Search for other papers by Zhenyu Liu in
Google Scholar
PubMed
Close
,
Huixi Kong Department of Clinical Medicine, Beijing Shijitan Hospital, Capital Medical University, Haidian District, Beijing, China

Search for other papers by Huixi Kong in
Google Scholar
PubMed
Close
, and
Baoyu Zhang Center for Endocrine Metabolism and Immune Diseases, Beijing Luhe Hospital, Capital Medical University, Tongzhou District, Beijing, China

Search for other papers by Baoyu Zhang in
Google Scholar
PubMed
Close

To optimize the treatment plan for patients with type 2 diabetes mellitus (T2DM) and hyperuricemia, this narrative literature review summarizes the effect of antidiabetic drugs on serum uric acid (SUA) levels using data from observational studies, prospective clinical trials, post hoc analyses, and meta-analyses. SUA is an independent risk factor for T2DM, and evidence has shown that patients with both gout and T2DM exhibit a mutually interdependent effect on higher incidences. We find that insulin and dipeptidyl peptidase 4 inhibitor (DPP-4i) except linagliptin could increase the SUA and other drugs including metformin, thiazolidinediones (TZDs), glucagon-like peptide-1 receptor agonists (GLP-1 RAs), linagliptin, sodium–glucose cotransporter 2 inhibitors (SGLT2i), and α-glucosidase inhibitors have a reduction effect on SUA. We explain the mechanisms of different antidiabetic drugs above on SUA and analyze them compared with actual data. For sulfonylureas, meglitinides, and amylin analogs, the underlying mechanism remains unclear. We think the usage of linagliptin and SGLT2i is the most potentially effective treatment of patients with T2DM and hyperuricemia currently. Our review is a comprehensive summary of the effects of antidiabetic drugs on SUA, which includes actual data, the mechanisms of SUA regulation, and the usage rate of drugs.

Open access
Yueyuan Yang Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Yueyuan Yang in
Google Scholar
PubMed
Close
,
Tingting Yu Department of Radiology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Tingting Yu in
Google Scholar
PubMed
Close
,
Zhili Niu Department of Clinical Laboratory, Institute of translational medicine, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Zhili Niu in
Google Scholar
PubMed
Close
, and
Ling Gao Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Ling Gao in
Google Scholar
PubMed
Close

Objective

Uridine might be a common link between pathological pathways in diabetes and cardiovascular diseases. This study aimed to investigate the predictive value of plasma uridine for type 2 diabetes (T2D) and T2D with atherosclerosis.

Methods

Individuals with T2D and healthy controls (n = 218) were randomly enrolled in a cross-sectional study. Patients with T2D were divided into two groups based on carotid ultrasound: patients with carotid atherosclerosis (CA) (group DCA) and patients without CA (group D). Plasma uridine was determined using HPLC-MS/MS. Correlation and logistic regression analyses were used to analyze the results.

Results

Fasting and postprandial uridine were significantly increased in patients with T2D compared with healthy individuals. Logistic regression suggested that fasting and postprandial uridine were independent risk factors for T2D. The receiver operating characteristic (ROC) curve showed that fasting uridine had a predictive value on T2D (95% CI, 0.686–0.863, sensitivity 74.3%, specificity 71.8%). Fasting uridine was positively correlated with LDL-c, FBG, and PBG and negatively correlated with fasting C-peptide (CP-0h) and HOMA-IS. The change in postprandial uridine from fasting baseline (Δuridine) was smaller in T2D patients with CA compared with those without (0.80 (0.04–2.46) vs 2.01 (0.49–3.15), P = 0.010). Δuridine was also associated with T2D with CA and negatively correlated with BMI, CP-0h, and HOMA-IR.

Conclusion

Fasting uridine has potential as a predictor of diabetes. Δuridine is closely associated with carotid atherosclerosis in patients with T2D.

Open access
Arno Téblick Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by Arno Téblick in
Google Scholar
PubMed
Close
,
Ilse Vanhorebeek Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by Ilse Vanhorebeek in
Google Scholar
PubMed
Close
,
Inge Derese Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by Inge Derese in
Google Scholar
PubMed
Close
,
An Jacobs Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by An Jacobs in
Google Scholar
PubMed
Close
,
Renata Haghedooren Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by Renata Haghedooren in
Google Scholar
PubMed
Close
,
Sofie Maebe Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by Sofie Maebe in
Google Scholar
PubMed
Close
,
Gerdien A Zeilmaker-Roest Department of Neonatal & Pediatric Intensive Care, Division of Pediatric Intensive Care, Erasmus MC – Sophia Children’s Hospital, Rotterdam, the Netherlands

Search for other papers by Gerdien A Zeilmaker-Roest in
Google Scholar
PubMed
Close
,
Enno D Wildschut Department of Neonatal & Pediatric Intensive Care, Division of Pediatric Intensive Care, Erasmus MC – Sophia Children’s Hospital, Rotterdam, the Netherlands

Search for other papers by Enno D Wildschut in
Google Scholar
PubMed
Close
,
Lies Langouche Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by Lies Langouche in
Google Scholar
PubMed
Close
, and
Greet Van den Berghe Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

Search for other papers by Greet Van den Berghe in
Google Scholar
PubMed
Close

In critically ill adults, high plasma cortisol in the face of low ACTH coincides with high pro-opiomelanocortin (POMC) levels. Glucocorticoids further lower ACTH without affecting POMC. We hypothesized that in pediatric cardiac surgery-induced critical illness, plasma POMC is elevated, plasma ACTH transiently rises intraoperatively but becomes suppressed post-operatively, and glucocorticoid administration amplifies this phenotype. From 53 patients (0–36 months), plasma was obtained pre-operatively, intraoperatively, and on post-operative days 1 and 2. Plasma was also collected from 24 healthy children. In patients, POMC was supra-normal pre-operatively (P < 0.0001) but no longer thereafter (P > 0.05). ACTH was never high in patients. While in glucocorticoid-naive patients ACTH became suppressed by post-operative day 1 (P < 0.0001), glucocorticoid-treated patients had already suppressed ACTH intraoperatively (P ≤ 0.0001). Pre-operatively high POMC, not accompanied by increased plasma ACTH, suggests a centrally activated HPA axis with reduced pituitary processing of POMC into ACTH. Increasing systemic glucocorticoid availability with glucocorticoid treatment accelerated the suppression of plasma ACTH.

Significance statement

Glucocorticoids are often administered during pediatric cardiac surgery. In critically ill children, endogenous systemic glucocorticoid availability is elevated already upon ICU admission while ACTH levels are normal. This hormonal constellation suggests the presence of active feedback inhibition of ACTH. In this study, we have documented that intraoperative administration of glucocorticoids accelerates the suppression of ACTH, resulting in low plasma ACTH already upon ICU admission. Pre-operative plasma POMC, the ACTH precursor, but not ACTH, was increased. This is compatible with a centrally activated HPA axis prior to surgery in young children but reduced processing of POMC into ACTH within the pituitary. These findings suggest that glucocorticoid treatment in the context of pediatric cardiac surgery may amplify pre-existing impaired pituitary processing of the prohormone POMC.

Open access
Bushra Shahida Department of Clinical Sciences, Genomics, Diabetes and Endocrinology, Lund University, Malmö, Sweden
Department of Diabetes & Endocrinology, Skåne University Hospital, Malmö, Sweden

Search for other papers by Bushra Shahida in
Google Scholar
PubMed
Close
,
Tereza Planck Department of Clinical Sciences, Genomics, Diabetes and Endocrinology, Lund University, Malmö, Sweden
Department of Diabetes & Endocrinology, Skåne University Hospital, Malmö, Sweden

Search for other papers by Tereza Planck in
Google Scholar
PubMed
Close
,
Tania Singh Department of Clinical Sciences, Genomics, Diabetes and Endocrinology, Lund University, Malmö, Sweden

Search for other papers by Tania Singh in
Google Scholar
PubMed
Close
,
Peter Åsman Department of Clinical Sciences Malmö, Ophthalmology, Lund University, Malmö, Sweden
Department of Ophthalmology, Skåne University Hospital, Malmö, Sweden

Search for other papers by Peter Åsman in
Google Scholar
PubMed
Close
, and
Mikael Lantz Department of Clinical Sciences, Genomics, Diabetes and Endocrinology, Lund University, Malmö, Sweden
Department of Diabetes & Endocrinology, Skåne University Hospital, Malmö, Sweden

Search for other papers by Mikael Lantz in
Google Scholar
PubMed
Close

Graves’ disease (GD) and Graves’ ophthalmopathy (GO) are complex autoimmune diseases. This study delved into the impact of cigarette smoke extract (CSE), simvastatin, and/or diclofenac on peripheral blood mononuclear cells (PBMCs). Specifically, we explored alterations in IL-1B, IL-6, PTGS2 expression, B- and T-lymphocyte proliferation, and Immunoglobulin G (IgG) production. We also assessed IGF1’s influence on B- and T-lymphocyte proliferation. PBMCs from Graves’ patients were exposed to CSE with/without simvastatin and/or diclofenac. Gene and protein expression was compared with untreated PBMCs. B- and T-lymphocyte proliferation was assessed following IGF1 treatment. PBMCs exposed to CSE exhibited increased expression of IL-1B (6-fold), IL-6 (10-fold), and PTGS2 (5.6-fold), and protein levels of IL-1B (4-fold), IL-6 (16-fold) and PGE2 (3.7-fold) compared with untreated PBMCs. Simvastatin and/or diclofenac downregulated the expression of PTGS2 (0.5-fold), IL-6 (0.4-fold), and IL-1B (0.6-fold), and the protein levels of IL-1B (0.6-fold), IL-6 (0.6-fold), and PGE2 (0.6-fold) compared with untreated PBMCs. CSE exposure in PBMCs increased the proliferation of B and T lymphocytes by 1.3-fold and 1.4-fold, respectively, compared with untreated. CSE exposure increased IgG (1.5-fold) in supernatant from PBMCs isolated from Graves’ patients. IGF1 treatment increased the proliferation of B and T lymphocytes by 1.6-fold. Simvastatin downregulated the proliferation of B and T lymphocytes by 0.7-fold. Our study shows that CSE significantly upregulated the expression and release of the inflammatory markers PTGS2, IL-6 and IL-1B,the IgG levels, and the proliferation of B and T lymphocytes. Additionally, IGF1 increased the proliferation of B and T lymphocytes. Finally, these effects were decreased by diclofenac and/or simvastatin treatment.

Open access
Ayana Suzuki Department of Diagnostic Pathology and Cytology, Kuma Hospital, Kobe, Japan

Search for other papers by Ayana Suzuki in
Google Scholar
PubMed
Close
,
Mitsuyoshi Hirokawa Department of Diagnostic Pathology and Cytology, Kuma Hospital, Kobe, Japan

Search for other papers by Mitsuyoshi Hirokawa in
Google Scholar
PubMed
Close
,
Izumi Otsuka Secretary Section, Kuma Hospital, Kobe, Japan

Search for other papers by Izumi Otsuka in
Google Scholar
PubMed
Close
,
Akihiro Miya Department of Surgery, Kuma Hospital, Kobe, Japan

Search for other papers by Akihiro Miya in
Google Scholar
PubMed
Close
,
Akira Miyauchi Department of Surgery, Kuma Hospital, Kobe, Japan

Search for other papers by Akira Miyauchi in
Google Scholar
PubMed
Close
, and
Takashi Akamizu Department of Internal Medicine, Kuma Hospital, Kobe, Japan

Search for other papers by Takashi Akamizu in
Google Scholar
PubMed
Close

Papillary thyroid carcinoma (PTC) with marked cystic formation (CPTC) is not a subtype of PTC, and its clinical characteristics have not been fully investigated. This study aimed to clarify the clinical and pathological characteristics of CPTC and propose important indicators for its clinical management. Thirty-three CPTC nodules with cystic areas occupying >50% of their volume were examined. Two matched controls (MCs) were prepared, one with tumor diameter matched for whole tumor diameter (WTD) of CPTCs and the other with tumor diameter matched for solid area diameter (SAD) of CPTCs. The mean age of patients with CPTC was 55.2 years significantly older than that in SAD-MCs. Of the CPTCs, 69.7% were classified as highly suspicious by ultrasonography, and the prevalence was lower than that in WTD-MCs (88.9%) and SAD-MCs (91.5%). Total thyroidectomy was performed in 69.7% of CPTC cases, which was significantly less frequent than that in WDT-MCs (91.7%) and similar to that in SAD-MCs (76.1%). Histologically, CPTCs exhibited two characteristic findings: invasion from the solid area into the surrounding normal thyroid tissue and granulation tissue around the cystic wall. The frequencies of the cases with pathological lateral node metastasis, extrathyroidal extension, and Ki-67 labeling index ≥5% in CPTCs were significantly lower than those in WTD-MCs and relatively similar to those in SAD-MCs. In the surgical strategy and prognosis of CPTC, the evaluation of tumor size should be based on SAD rather than on WTD. We advocate measuring not only WTD but also SAD in CPTC.

Open access
M Cherenko Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

Search for other papers by M Cherenko in
Google Scholar
PubMed
Close
,
N M Appelman-Dijkstra Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

Search for other papers by N M Appelman-Dijkstra in
Google Scholar
PubMed
Close
,
A L Priego Zurita Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

Search for other papers by A L Priego Zurita in
Google Scholar
PubMed
Close
,
N R Biermasz Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

Search for other papers by N R Biermasz in
Google Scholar
PubMed
Close
,
O M Dekkers Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

Search for other papers by O M Dekkers in
Google Scholar
PubMed
Close
,
,
F A Klok Department of Medicine, Division of Thrombosis and Haemostasis, Leiden University Medical Centre, Leiden, Netherlands

Search for other papers by F A Klok in
Google Scholar
PubMed
Close
,
N Reisch Department of Medicine IV, LMU University Hospital, LMU Munich, Munich, Germany

Search for other papers by N Reisch in
Google Scholar
PubMed
Close
,
A Aulinas Department of Endocrinology, Fundacio de Gestio Sanitaria Hospital de la Santa Creu i Sant Pau, IR-SantPau and CIBERER Unit 747 (ISCIII), Barcelona, Spain

Search for other papers by A Aulinas in
Google Scholar
PubMed
Close
,
B Biagetti Department of Endocrinology, Hospital Universitari Vall d’Hebron, Barcelona, Spain

Search for other papers by B Biagetti in
Google Scholar
PubMed
Close
,
S Cannavo Endocrine Unit, University Hospital AOU Policlinico G. Martino, Messina, Italy

Search for other papers by S Cannavo in
Google Scholar
PubMed
Close
,
L Canu University Hospital Florence Careggi, Florence, Italy

Search for other papers by L Canu in
Google Scholar
PubMed
Close
,
M Detomas Department of Internal Medicine, University Hospital Würzburg, Wuerzburg, Germany

Search for other papers by M Detomas in
Google Scholar
PubMed
Close
,
F Devuyst Department of Endocrinology, Hôpital Universitaire de Bruxelles, Hôpital Erasme, Brussels, Belgium

Search for other papers by F Devuyst in
Google Scholar
PubMed
Close
,
H Falhammar Department of Endocrinology, Karolinska University Hospital and Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

Search for other papers by H Falhammar in
Google Scholar
PubMed
Close
,
R A Feelders Department of Internal Medicine, Division of Endocrinology, Erasmus MC, Rotterdam, Netherlands

Search for other papers by R A Feelders in
Google Scholar
PubMed
Close
,
F Ferrau Endocrine Unit, University Hospital AOU Policlinico G. Martino, Messina, Italy

Search for other papers by F Ferrau in
Google Scholar
PubMed
Close
,
F Gatto IRCCS Ospedale Policlinico San Martino, Genova, Genoa, Italy

Search for other papers by F Gatto in
Google Scholar
PubMed
Close
,
C Grasselli Cardiovascular Medicine Unit, AUSL-IRCCS, Reggio Emilia, Italy

Search for other papers by C Grasselli in
Google Scholar
PubMed
Close
,
P van Houten Department of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, Netherlands

Search for other papers by P van Houten in
Google Scholar
PubMed
Close
,
C Hoybye Department of Endocrinology, Karolinska University Hospital and Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

Search for other papers by C Hoybye in
Google Scholar
PubMed
Close
,
A M Isidori Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy

Search for other papers by A M Isidori in
Google Scholar
PubMed
Close
,
A Kyrilli Department of Endocrinology, Hôpital Universitaire de Bruxelles, Hôpital Erasme, Brussels, Belgium

Search for other papers by A Kyrilli in
Google Scholar
PubMed
Close
,
P Loli Division of Endocrinology, San Raffaele Vita-Salute University, IRCCS San Raffaele Hospital Milan, Italy

Search for other papers by P Loli in
Google Scholar
PubMed
Close
,
D Maiter Department of Endocrinology, Cliniques universitaires Saint-Luc – UCLouvain, Brussels, Belgium

Search for other papers by D Maiter in
Google Scholar
PubMed
Close
,
E Nowak Department of Medicine IV, LMU University Hospital, LMU Munich, Munich, Germany

Search for other papers by E Nowak in
Google Scholar
PubMed
Close
,
R Pivonello Dipartimento di Medicina Clinica e Chirurgia, Sezione di Endocrinologia, Diabetologia, Andrologia e Nutrizione, Università “Federico II” di Napoli, Naples, Italy

Search for other papers by R Pivonello in
Google Scholar
PubMed
Close
,
O Ragnarsson Sahlgrenska Academy, Wallenberg Centre for Molecular and Translational Medicine, Institute of Medicine (O.R.), University of Gothenburg, Sweden

Search for other papers by O Ragnarsson in
Google Scholar
PubMed
Close
,
R V Steenaard Department of Internal Medicine, Máxima MC, Veldhoven, Netherlands

Search for other papers by R V Steenaard in
Google Scholar
PubMed
Close
,
N Unger University Hospital Essen, Department of Endocrinology, Diabetes and Metabolism, Essen, Germany

Search for other papers by N Unger in
Google Scholar
PubMed
Close
,
A van de Ven Department of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, Netherlands

Search for other papers by A van de Ven in
Google Scholar
PubMed
Close
,
S M Webb Department of Endocrinology, Fundacio de Gestio Sanitaria Hospital de la Santa Creu i Sant Pau, IR-SantPau and CIBERER Unit 747 (ISCIII), Barcelona, Spain

Search for other papers by S M Webb in
Google Scholar
PubMed
Close
,
D Yeste Pediatric Endocrinology Service, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. CIBER Enfermedades Raras, Instituto Carlos III, Madrid, Spain

Search for other papers by D Yeste in
Google Scholar
PubMed
Close
,
S F Ahmed Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands
University of Glasgow, Office for Rare Conditions, Glasgow, UK
University of Glasgow, Developmental Endocrinology Research Group, Royal Hospital for Children, Glasgow, UK

Search for other papers by S F Ahmed in
Google Scholar
PubMed
Close
, and
A M Pereira Department of Endocrinology & Metabolism, Amsterdam University Medical Centre, Amsterdam, Noord-Holland, Netherlands

Search for other papers by A M Pereira in
Google Scholar
PubMed
Close

Background

Patients with Cushing syndrome (CS) are at increased risk of venous thromboembolism (VTE).

Objective

The aim was to evaluate the current management of new cases of CS with a focus on VTE and thromboprophylaxis.

Design and methods

A survey was conducted within those that report in the electronic reporting tool (e-REC) of the European Registries for Rare Endocrine Conditions (EuRRECa) and the involved main thematic groups (MTG’s) of the European Reference Networks for Rare Endocrine Disorders (Endo-ERN) on new patients with CS from January 2021 to July 2022.

Results

Of 222 patients (mean age 44 years, 165 females), 141 patients had Cushing disease (64%), 69 adrenal CS (31%), and 12 patients with ectopic CS (5.4%). The mean follow-up period post-CS diagnosis was 15 months (range 3–30). Cortisol-lowering medications were initiated in 38% of patients. One hundred fifty-four patients (69%) received thromboprophylaxis (including patients on chronic anticoagulant treatment), of which low-molecular-weight heparins were used in 96% of cases. VTE was reported in six patients (2.7%), of which one was fatal: two long before CS diagnosis, two between diagnosis and surgery, and two postoperatively. Three patients were using thromboprophylaxis at time of the VTE diagnosis. The incidence rate of VTE in patients after Cushing syndrome diagnosis in our study cohort was 14.6 (95% CI 5.5; 38.6) per 1000 person-years.

Conclusion

Thirty percent of patients with CS did not receive preoperative thromboprophylaxis during their active disease stage, and half of the VTE cases even occurred during this stage despite thromboprophylaxis. Prospective trials to establish the optimal thromboprophylaxis strategy in CS patients are highly needed.

Significance statement

The incidence rate of venous thromboembolism in our study cohort was 14.6 (95% CI 5.5; 38.6) per 1000 person-years. Notably, this survey showed that there is great heterogeneity regarding time of initiation and duration of thromboprophylaxis in expert centers throughout Europe.

Open access
Sherwin Criseno Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
School of Nursing and Midwifery, Institute of Clinical Sciences, University of Birmingham, UK

Search for other papers by Sherwin Criseno in
Google Scholar
PubMed
Close
,
Helena Gleeson Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK

Search for other papers by Helena Gleeson in
Google Scholar
PubMed
Close
,
Andrew A Toogood Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK

Search for other papers by Andrew A Toogood in
Google Scholar
PubMed
Close
,
Neil Gittoes Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK

Search for other papers by Neil Gittoes in
Google Scholar
PubMed
Close
,
Anne Topping School of Nursing and Midwifery, Institute of Clinical Sciences, University of Birmingham, UK

Search for other papers by Anne Topping in
Google Scholar
PubMed
Close
, and
Niki Karavitaki Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK

Search for other papers by Niki Karavitaki in
Google Scholar
PubMed
Close

Objective

We conducted a survey of UK endocrine clinicians between June 2022 and August 2022 to understand current practices regarding GH treatment discontinuation in adults with growth hormone deficiency.

Design and methods

Using Survey Monkey®, a web-based multiple-choice questionnaire was disseminated to the UK Society for Endocrinology membership. It consisted of 15 questions on demographics, number of patients receiving GH and current practice on GH treatment discontinuation.

Results

In total, 102 endocrine clinicians completed the survey. Of these, 65 respondents (33 endocrinologists and 32 specialist nurses) indicated active involvement in managing patients with growth hormone deficiency. In total, 27.7% of clinicians were routinely offering a trial of GH discontinuation to adults receiving long-term GH therapy. Only 6% had a clinical guideline to direct such practice. In total, 29.2% stated that GH discontinuation should be routinely offered as an option to patients on long-term treatment, whilst 60% were not clearly in favour or against this approach but stated that it should probably be considered, and 9.2% were against. During the GH withdrawal period, most clinicians monitor signs and symptoms (75.4%), measure IGF-1 (84.6%), and complete a quality-of-life assessment (89.2%).

Conclusion

The practice of offering a trial of GH discontinuation in growth hormone deficiency adults on long-term GH therapy is highly variable, reflecting the lack of high-quality evidence. Around a quarter of clinicians offer GH withdrawal for a number of reasons, but only a few have a local clinical guidance. A further 60% of clinicians stated they would probably consider such an approach. Methodologically sound studies underpinning the development of safe and cost-effective guidance are needed.

Significance statement

In this UK survey of endocrine clinicians managing adults with growth hormone deficiency on long-term GH therapy, we explored for the first-time current practice and views on offering GH treatment discontinuation. In total, 27.7% of clinicians were routinely offering this option for a variety of reasons. Only 6% have local clinical guideline available to direct their practice on this. The majority of clinicians (60%), were not clearly in favour or against this approach but indicated it should probably be considered. In the absence of robust evidence on consequences of GH withdrawal, clinicians proposed monitoring of various clinical, biochemical and quality-of-life parameters during the period of discontinuation. Methodologically sound studies that will underpin the development of a safe, cost-effective guidance are needed.

Open access