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  • Abstract: Cushings x
  • Abstract: Glucocorticoids x
  • Abstract: Medulla x
  • Abstract: Noradrenaline x
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Boni Xiang Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Ran Tao Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Xinhua Liu Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Xiaoming Zhu Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Min He Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Zengyi Ma Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China

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Yehong Yang Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Zhaoyun Zhang Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Yiming Li Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Zhenwei Yao Department of Radiology, Huashan Hospital, Fudan University, Shanghai, China

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Yongfei Wang Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China

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Hongying Ye Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China

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Objective

The aim of this study was to evaluate thyroid functions in Cushing’s syndrome (CS), the dynamic changes of thyroid hormones and antithyroid antibodies in Cushing’s disease (CD) pre- and postoperatively.

Design and methods

This is a retrospective study enrolling 118 patients with CS (102 CD, 10 adrenal CS and 6 ectopic adrenocorticotropic syndrome (EAS)). Thyroid functions (thyroid-stimulation hormone (TSH), T3, free T3 (FT3), T4 and free T4 (FT4)) were measured in all CS at the time of diagnosis and in all CD 3 months after transsphenoidal pituitary tumor resection. Postoperative hormone monitoring within 3 months was conducted in 9 CD patients completing remission. Twenty-eight remitted CD patients experienced hormone and antithyroid antibody evaluation preoperatively and on the 3rd, 6th and 12th month after surgery.

Results

TSH, T3 and FT3 were below the reference range in 31%, 69% and 44% of the 118 CS patients. Remitted CD patients (81/102) had significantly higher TSH (P = 0.000), T3 (P = 0.000) and FT3 (P = 0.000) than those in the non-remission group (21/102). After remission of CD, TSH, T3 and FT3 showed a significant increase, with a few cases above the reference range. By 12 months, most CD patients’ thyroid functions returned to normal. Thyroid hormones (including TSH, T3 and FT3) were negatively associated with serum cortisol levels both before and after surgery. No significant changes of antithyroid autoantibodies were observed.

Conclusions

TSH, T3 and FT3 are suppressed in endogenous hypercortisolemia. After remission of CD, TSH, T3 and FT3 increased significantly, even above the reference range, but returned to normal 1 year after surgery in most cases. Antithyroid antibodies did not change significantly after remission of CD.

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Margret J Einarsdottir Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Penelope Trimpou Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Gudmundur Johannsson Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Oskar Ragnarsson Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden
Wallenberg Center for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden

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Objective

It is unknown whether glucocorticoid (GC)-induced adrenal insufficiency may cause premature mortality in GC users. We conducted a retrospective cohort study to investigate if undiagnosed and undertreated GC-induced adrenal insufficiency is a contributor to premature death in GC users.

Methods

Information on dispensed prescriptions in West Sweden from 2007 to 2014 was obtained from the Swedish Prescribed Drug Register. Cause of death was collected from the Swedish Cause of Death Register. Of 223,211 patients who received oral GC prescriptions, 665 died from sepsis within 6 months of their last prescription. Three hundred of these patients who had died in hospital were randomly selected for further investigation. Medical records were initially reviewed by one investigator. Furthermore, two additional investigators reviewed the medical records of patients whose deaths were suspected to be caused by GC-induced adrenal insufficiency.

Results

Of 300 patients (121 females, 40%), 212 (75%) were prescribed GC treatment at admission. The mean age was 76 ± 11 years (range 30–99). Undiagnosed or undertreated GC-induced adrenal insufficiency was considered a probable contributor to death by at least two investigators in 11 (3.7%) patients. In five of these 11 cases, long-term GC therapy was abruptly discontinued during hospitalization. Undiagnosed or undertreated GC-induced adrenal insufficiency was considered a possible contributing factor to death in a further 36 (12%) patients.

Conclusion

GC-induced adrenal insufficiency is an important contributor to premature death in GC users. Awareness of the disorder during intercurrent illness and following cessation of GC treatment is essential.

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Hanna F Nowotny Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Jillian Bryce Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Salma R Ali Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Roberta Giordano Department of Clinical and Biological Sciences, University of Turin, Turin, Italy
Division of Endocrinology, Diabetes and Metabolism, Department of Medical Sciences, University of Turin, Turin, Italy

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Federico Baronio Pediatric Unit, Department Hospital of Woman and Child, Endo-ERN Centre IT11, IRCSS AOU S.Orsola-Malpighi University Hospital, Bologna, Italy

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Irina Chifu Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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Lea Tschaidse Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Martine Cools Department of Paediatric Endocrinology, Ghent University Hospital, University of Ghent, Ghent, Belgium

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Erica LT van den Akker Department of Pediatrics, Division of Pediatric Endocrinology, Erasmus MC - Sophia Children’s Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands

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Henrik Falhammar Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Department of Endocrinology, Karolinska University Hospital, Stockholm, Sweden

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Natasha M Appelman-Dijkstra Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Luca Persani Department of Endocrine and Metabolic Diseases, Istituto Auxologico Italiano IRCCS, Milan, Italy
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan Italy

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Guglielmo Beccuti Department of Clinical and Biological Sciences, University of Turin, Turin, Italy

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Ian L Ross Division of Endocrinology, Department of Medicine, University of Cape Town, Cape Town, South Africa

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Simona Grozinsky-Glasberg Neuroendocrine Tumor Unit, ENETS Center of Excellence, Department of Endocrinology and Metabolism, Hadassah Medical Organisation and Faculty of Medicine, the Hebrew University, Jerusalem, Israel

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Alberto M Pereira Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Eystein S Husebye Department of Clinical Science and KG Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Department of Medicine, Karolinska Institutet, Stockholm, Sweden

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Stefanie Hahner Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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S Faisal Ahmed Office for Rare Conditions, University of Glasgow, Glasgow, UK
Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands
Developmental Endocrinology Research Group, University of Glasgow, Glasgow, United Kingdom

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Nicole Reisch Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Background

Information on clinical outcomes of coronavirus disease 19 (COVID-19) infection in patients with adrenal disorders is scarce.

Methods

A collaboration between the European Society of Endocrinology (ESE) Rare Disease Committee and European Reference Network on Rare Endocrine Conditions via the European Registries for Rare Endocrine Conditions allowed the collection of data on 64 cases (57 adrenal insufficiency (AI), 7 Cushing’s syndrome) that had been reported by 12 centres in 8 European countries between January 2020 and December 2021.

Results

Of all 64 patients, 23 were males and 41 females (13 of those children) with a median age of 37 and 51 years. In 45/57 (95%) AI cases, COVID-19 infection was confirmed by testing. Primary insufficiency was present in 45/57 patients; 19 were affected by Addison’s disease, 19 by congenital adrenal hyperplasia and 7 by primary AI (PAI) due to other causes. The most relevant comorbidities were hypertension (12%), obesity (n = 14%) and diabetes mellitus (9%). An increase by a median of 2.0 (IQR 1.4) times the daily replacement dose was reported in 42 (74%) patients. Two patients were administered i.m. injection of 100 mg hydrocortisone, and 11/64 were admitted to the hospital. Two patients had to be transferred to the intensive care unit, one with a fatal outcome. Four patients reported persistent SARS-CoV-2 infection, all others complete remission.

Conclusion

This European multicentre questionnaire is the first to collect data on the outcome of COVID-19 infection in patients with adrenal gland disorders. It suggests good clinical outcomes in case of duly dose adjustments and emphasizes the importance of patient education on sick day rules.

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Fiona Broughton Pipkin Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Hiten D Mistry Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Chandrima Roy Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Bernhard Dick Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Jason Waugh Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Rebecca Chikhi Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Lesia O Kurlak Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Markus G Mohaupt Department of Obstetrics and Gynaecology, Department of Nephrology, Leicester Royal Infirmary, School of Medicine, University of Nottingham, Nottingham, NG5 1PB, UK

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Pre-eclampsia leads to disturbed fetal organ development, including metabolic syndrome, attributed to altered pituitary-adrenal feedback loop. We measured cortisol metabolites in infants born from pre-eclamptic and normotensive women and hypothesised that glucocorticoid exposure would be exaggerated in the former. Twenty-four hour urine was collected from infants at months 3 and 12. Cortisol metabolites and apparent enzyme activities were analysed by gas chromatography-mass spectrometry. From 3 to 12 months, excretion of THS, THF and pregnandiol had risen in both groups; THF also rose in the pre-eclamptic group. No difference was observed with respect to timing of the visit or to hypertensive status for THE or total F metabolites (P>0.05). All apparent enzymes activities, except 17α-hydroxylase, were lower in infants at 12 compared to 3 months in the normotensive group. In the pre-eclamptic group, only 11β-HSD activities were lower at 12 months.17α-hydroxylase and 11β-HSD activities of tetrahydro metabolites were higher in the pre-eclamptic group at 3 months (P<0.05). 11β-hydroxylase activity increased in the pre-eclamptic group at 12 months. Cortisol excretion, determined by increased 11β-hydroxylase, compensates for high 11β-HSD-dependent cortisol degradation at 3 months and at 12 months counterbalances the reduced cortisol substrate availability in infants born from pre-eclamptic mothers.

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Grethe Å Ueland Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Thea Grinde Department of Clinical Science, University of Bergen, Bergen, Norway

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Paal Methlie Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
K. G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway

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Oskar Kelp Department of Medicine, Akershus University Hospital, Nordbyhagen, Norway

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Kristian Løvås Department of Medicine, Haukeland University Hospital, Bergen, Norway
K. G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway

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Eystein S Husebye Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
K. G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway

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Objective:

Autonomous cortisol secretion (ACS) is a condition with ACTH-independent cortisol overproduction from adrenal incidentalomas (AI) or adrenal hyperplasia. The hypercortisolism is often mild, and most patients lack typical clinical features of overt Cushing’s syndrome (CS). ACS is not well defined and diagnostic tests lack validation.

Methods:

Retrospective study of 165 patients with AI evaluated clinically and by assay of morning plasma ACTH, late-night saliva cortisol, serum DHEA sulphate (DHEAS), 24-h urine-free cortisol, and cortisol after dexamethasone suppression.

Results:

Patients with AI (n = 165) were diagnosed as non-functioning incidentalomas (NFI) (n = 82) or ACS (n = 83) according to current European guidelines. Late-night saliva cortisol discriminated poorly between NFI and ACS, showing a high rate of false-positive (23/63) and false-negative (38/69) results. The conventional low-dose dexamethasone suppression test (LDDST) did not improve the diagnostic specificity, compared with the 1 mg overnight DST. Receiver operating characteristic curve analysis of DHEAS in the two cohorts demonstrated an area under the curve of 0.76 (P < 0.01) with a sensitivity for ACS of 58% and a specificity of 80% using the recommended cutoff at 1.04 µmol/L (40 µg/dL).

Conclusion:

We here demonstrate in a large retrospective cohort of incidentaloma patients, that neither DHEAS, late-night saliva cortisol nor 24-h urine free cortisol are useful to discriminate between non-functioning adrenal incidentalomas and ACS. The conventional LDDST do not add further information compared with the 1 mg overnight DST. Alternative biomarkers are needed to improve the diagnostic workup of ACS.

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Yiyan Wang Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Yaoyao Dong Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Yinghui Fang Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Yao Lv Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Qiqi Zhu Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Xiaoheng Li Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Qingquan Lian Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Ren-Shan Ge Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Glucocorticoid hormone might cause intrauterine growth restriction. The glucocorticoid-metabolizing enzyme 11β-hydroxysteroid dehydrogenase 2 (HSD11B2) in the placenta eliminates excess levels of glucocorticoids during pregnancy. The aim of the current study was to define the effects of diethylstilbestrol (DES) on HSD11B2 activity in the mammalian placentas and identify its mode of action. Rat and human placental microsomal HSD11B2 were incubated with different concentrations of DES, and IC50 values were determined. The mode of action was analyzed by incubation of DES together with substrates, glucocorticoid and NAD+. DES suppressed rat and human HSD11B2 with IC50 values of 5.33 and 12.62 μM, respectively. DES was a competitive inhibitor of rat and human HSD11B2 when steroid substrates were added, while it was an uncompetitive inhibitor when cofactor NAD+ was exposed. Oral administration of DES (0.5 mg/kg) to the rat delayed the cortisol metabolism in adult female Sprague–Dawley rats, as indicated by the increases in cortisol’s elimination half-life, maximum concentration and area under the curve. In conclusion, DES is a potent HSD11B2 inhibitor, possibly contributing to the intrauterine growth restriction.

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Jingya Zhou Department of Medical Records, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
Collaborating Center for the WHO Family of International Classifications in China, Beijing, China

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Meng Zhang Department of Medical Records, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
Collaborating Center for the WHO Family of International Classifications in China, Beijing, China

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Lin Lu Department of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
Key Laboratory of Endocrinology of National Health Commission of People’s Republic of China, Beijing, China

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Xiaopeng Guo Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
China Pituitary Disease Registry Center, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China

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Lu Gao Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
China Pituitary Disease Registry Center, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China

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Weigang Yan Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

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Haiyu Pang Central Research Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
Clinical Epidemiology Unit, International Epidemiology Network, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

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Yi Wang Department of Medical Records, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
Collaborating Center for the WHO Family of International Classifications in China, Beijing, China

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Bing Xing Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
China Pituitary Disease Registry Center, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China

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Objective

To investigate the validity of discharge ICD-10 codes in detecting the etiology of endogenous Cushing’s syndrome (CS) in hospitalized patients.

Methods

We evaluated the sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of CS etiology-related ICD-10 codes or code combinations by comparing hospital discharge administrative data (DAD) with established diagnoses from medical records.

Results

Coding for patients with adrenocortical adenoma (ACA) and those with bilateral macronodular adrenal hyperplasia (BMAH) demonstrated disappointingly low sensitivity at 78.8% (95% CI: 70.1–85.6%) and 83.9% (95% CI: 65.5–93.9%), respectively. BMAH had the lowest PPV of 74.3% (95% CI: 56.4–86.9%). In confirmed ACA patients, the sensitivity for ACA code combinations was higher in patients initially admitted to the Department of Endocrinology before surgery than that in patients directly admitted to the Department of Urology (90.0 vs 73.1%, P = 0.033). The same phenomenon was observed in the PPV for the BMAH code (100.0 vs 60.9%, P = 0.012). Misinterpreted or confusing situations caused by coders (68.1%) and by the omission or denormalized documentation of symptomatic diagnosis by clinicians (26.1%) accounted for the main source of coding errors.

Conclusions

Hospital DAD is an effective data source for evaluating the etiology of CS but not ACA and BMAH. Improving surgeons’ documentation, especially in the delineation of symptomatic and locative diagnoses in discharge abstracts; department- or disease-specific training for coders and more multidisciplinary collaboration are ways to enhance the applicability of administrative data for CS etiologies.

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Clara Lundetoft Clausen Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark

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Trine Holm Johannsen Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Niels Erik Skakkebæk Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Hanne Frederiksen Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Anders Juul Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Thomas Benfield Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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In the context of severe coronavirus disease 2019 (COVID-19) illness, we examined endogenous glucocorticoid concentrations, steroidogenic enzyme activity, and their correlation with inflammation and patient outcomes. This observational study included 125 hospitalized COVID-19 patients and 101 healthy individuals as a reference group. We utilized LC-MS to assess serum concentrations of 11-deoxycortisol, cortisol, and cortisone, as well as activities of steroidogenic enzymes (11β-hydroxylase and 11β-hydroxysteroid-dehydrogenase type 1). Cox proportional hazards regression analysis and competing risk analysis were employed to analyze associations between glucocorticoid concentrations and outcomes, adjusting for relevant factors. In patients with COVID-19, cortisol concentrations were higher and cortisone concentrations were lower compared to the reference group, while 11-deoxycortisol concentrations were similar. Steroidogenic enzyme activity favored cortisol production. Correlations between glucocorticoid concentrations and inflammatory markers were low. A doubling in concentrations cortisol, was associated with increased 90-day mortality and mechanical ventilation (HR: 2.40 95% CI: (1.03–5.59) , P = 0.042 and HR: 3.83 (1.19–12.31), P = 0.024). A doubling in concentrations of 11-deoxycortisol was also associated to mortality (HR: 1.32 (1.05–1.67), P = 0.018), whereas concentrations of cortisone were associated with mechanical ventilation (HR: 5.09 (1.49–17.40), P = 0.009). In conclusion, serum concentrations of glucocorticoid metabolites were altered in patients hospitalized with severe COVID-19, and steroidogenic enzyme activity resulting in the conversion of cortisone to biologically active cortisol was preserved, thus not favoring critical-illness-related corticosteroid insufficiency at the enzymatic level. Glucocorticoid release did not counterbalance the hyperinflammatory state in patients with severe COVID-19. High serum concentrations of 11-deoxycortisol and cortisol were associated with 90-day mortality, and high serum concentrations of cortisol and cortisone were associated with mechanical ventilation.

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Paal Methlie Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Steinar Hustad Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Ralf Kellman Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Bjørg Almås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Martina M Erichsen Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Eystein S Husebye Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Kristian Løvås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Objective

Liquid chromatography–tandem mass spectrometry (LC–MS/MS) offers superior analytical specificity compared with immunoassays, but it is not available in many regions and hospitals due to expensive instrumentation and tedious sample preparation. Thus, we developed an automated, high-throughput LC–MS/MS assay for simultaneous quantification of ten endogenous and synthetic steroids targeting diseases of the hypothalamic–pituitary–adrenal axis and gonads.

Methods

Deuterated internal standards were added to 85 μl serum and processed by liquid–liquid extraction. Cortisol, cortisone, prednisolone, prednisone, 11-deoxycortisol, dexamethasone, testosterone, androstenedione and progesterone were resolved by ultra-high-pressure chromatography on a reversed-phase column in 6.1 min and detected by triple-quadrupole mass spectrometry. The method was used to assess steroid profiles in women with Addison's disease (AD, n=156) and blood donors (BDs, n=102).

Results

Precisions ranged from 4.5 to 10.1% relative standard deviations (RSD), accuracies from 95 to 108% and extraction recoveries from 60 to 84%. The method was practically free of matrix effects and robust to individual differences in serum composition. Most postmenopausal AD women had extremely low androstenedione concentrations, below 0.14 nmol/l, and median testosterone concentrations of 0.15 nmol/l (interquartile range 0.00–0.41), considerably lower than those of postmenopausal BDs (1.28 nmol/l (0.96–1.64) and 0.65 nmol/l (0.56–1.10) respectively). AD women in fertile years had androstenedione concentrations of 1.18 nmol/l (0.71–1.76) and testosterone concentrations of 0.44 nmol/l (0.22–0.63), approximately half of those found in BDs of corresponding age.

Conclusion

This LC–MS/MS assay provides highly sensitive and specific assessments of glucocorticoids and androgens with low sample volumes and is suitable for endocrine laboratories and research. Its utility has been demonstrated in a large cohort of women with AD, and the data suggest that women with AD are particularly androgen deficient after menopause.

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

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N M Appelman-Dijkstra Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

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A L Priego Zurita Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

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N R Biermasz Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

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O M Dekkers Department of Medicine, Division of Endocrinology, Leiden University Medical Centre, Leiden, Netherlands

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F A Klok Department of Medicine, Division of Thrombosis and Haemostasis, Leiden University Medical Centre, Leiden, Netherlands

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N Reisch Department of Medicine IV, LMU University Hospital, LMU Munich, Munich, Germany

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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

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B Biagetti Department of Endocrinology, Hospital Universitari Vall d’Hebron, Barcelona, Spain

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S Cannavo Endocrine Unit, University Hospital AOU Policlinico G. Martino, Messina, Italy

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L Canu University Hospital Florence Careggi, Florence, Italy

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M Detomas Department of Internal Medicine, University Hospital Würzburg, Wuerzburg, Germany

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F Devuyst Department of Endocrinology, Hôpital Universitaire de Bruxelles, Hôpital Erasme, Brussels, Belgium

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H Falhammar Department of Endocrinology, Karolinska University Hospital and Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

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R A Feelders Department of Internal Medicine, Division of Endocrinology, Erasmus MC, Rotterdam, Netherlands

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F Ferrau Endocrine Unit, University Hospital AOU Policlinico G. Martino, Messina, Italy

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F Gatto IRCCS Ospedale Policlinico San Martino, Genova, Genoa, Italy

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C Grasselli Cardiovascular Medicine Unit, AUSL-IRCCS, Reggio Emilia, Italy

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P van Houten Department of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, Netherlands

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C Hoybye Department of Endocrinology, Karolinska University Hospital and Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

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A M Isidori Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy

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A Kyrilli Department of Endocrinology, Hôpital Universitaire de Bruxelles, Hôpital Erasme, Brussels, Belgium

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P Loli Division of Endocrinology, San Raffaele Vita-Salute University, IRCCS San Raffaele Hospital Milan, Italy

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D Maiter Department of Endocrinology, Cliniques universitaires Saint-Luc – UCLouvain, Brussels, Belgium

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E Nowak Department of Medicine IV, LMU University Hospital, LMU Munich, Munich, Germany

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R Pivonello Dipartimento di Medicina Clinica e Chirurgia, Sezione di Endocrinologia, Diabetologia, Andrologia e Nutrizione, Università “Federico II” di Napoli, Naples, Italy

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O Ragnarsson Sahlgrenska Academy, Wallenberg Centre for Molecular and Translational Medicine, Institute of Medicine (O.R.), University of Gothenburg, Sweden

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R V Steenaard Department of Internal Medicine, Máxima MC, Veldhoven, Netherlands

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N Unger University Hospital Essen, Department of Endocrinology, Diabetes and Metabolism, Essen, Germany

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A van de Ven Department of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, Netherlands

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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

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D Yeste Pediatric Endocrinology Service, Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. CIBER Enfermedades Raras, Instituto Carlos III, Madrid, Spain

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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

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A M Pereira Department of Endocrinology & Metabolism, Amsterdam University Medical Centre, Amsterdam, Noord-Holland, Netherlands

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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.

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