, pheochromocytoma, aldosteronism, or overt cortisol excess due to hyperfunction may be observed in patients with adrenal incidentaloma. It has been shown that cortical adenoma is the most frequent tumour type among adrenal incidentalomas ( 5 ), whereas adrenal
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Agnieszka Adamska, Vitalii Ulychnyi, Katarzyna Siewko, Anna Popławska-Kita, Małgorzata Szelachowska, Marcin Adamski, Angelika Buczyńska, and Adam Jacek Krętowski
Ermina Bach, Niels Møller, Jens Otto L Jørgensen, Mads Buhl, and Holger Jon Møller
Introduction CD163 is a cortisol-regulated monocyte and macrophage-specific surface glycoprotein and the extracellular portion of CD163 circulates in blood as a soluble protein (sCD163) ( 1 ). sCD163 is highly elevated in acute infections
Filippo Ceccato, Elisa Selmin, Giorgia Antonelli, Mattia Barbot, Andrea Daniele, Marco Boscaro, Mario Plebani, and Carla Scaroni
). Signs and symptoms of AI are often non-specific (fatigue, orthostatic hypotension, nausea, vomiting), and a clinical suspicion needs to be confirmed by biochemical testing. Baseline morning unstimulated serum cortisol (F) levels are measured in
Patricia Arroyo Tardio, Gabriela Baldini, and Eleonora Seelig
Objective: Hypercortisolism is a risk factor for obesity. Cortisol increases in response to food intake in lean subjects. In obese subjects, disturbances of the food-induced cortisol peak were reported, but data from sufficiently powered and well-controlled trials are lacking. Understanding the cortisol response to food is essential as amplified, or recurrent cortisol surges could lead to hypercortisolism and contribute to obesity. Therefore, we investigate the cortisol response to food in lean and obese subjects.
Design: This is a non-randomized, open-label study.
Methods: We assessed serum cortisol values after a high-calorie meal in lean and obese male subjects. Cortisol levels were frequently assessed before and for 3 hours after food intake.
Results: 36 subjects (18 lean, 18 obese) were included. There was no difference in overall cortisol levels between both groups during the study (area under the curve (AUC) obese: 55409 ±16994, lean: 60334 ±18001, p=0.4). Total cortisol levels reached peak concentrations 20 minutes after food intake in both groups; the maximum cortisol increase was similar in both groups (cortisol increase obese: 69.6 ±135.5 nmol/l, lean: 134.7 ±99.7 nmol/l; p=0.1). There was no correlation between body mass index (BMI) and baseline cortisol values (R2=0.001, p=0.83), cortisol increase (R2= 0.05, p=0.17), or cortisol AUC (R2= 0.03, p=0.28).
Conclusions: This study demonstrates that high-calorie food intake causes an immediate and substantial cortisol response in lean and obese subjects and is independent of body weight.
Martijn J J Finken, Aleid J G Wirix, Ines A von Rosenstiel-Jadoul, Bibian van der Voorn, Mai J M Chinapaw, Michaela F Hartmann, Joana E Kist-van Holthe, Stefan A Wudy, and Joost Rotteveel
effects on body fat disposition and vascular reactivity. Indeed, childhood obesity has been associated with alterations in hypothalamus–pituitary–adrenal (HPA) axis activity, including increased cortisol production and flattening of early-morning peak
Britt J van Keulen, Michelle Romijn, Bibian van der Voorn, Marita de Waard, Michaela F Hartmann, Johannes B van Goudoever, Stefan A Wudy, Joost Rotteveel, and Martijn J J Finken
essential for blood pressure maintenance ( 7 ) and has been presumed to play a role in the dampening of the immune response ( 8 ). During their first weeks of life, many preterm infants fail to mount an adequate cortisol response for the degree of stress or
Yiyan Wang, Yaoyao Dong, Yinghui Fang, Yao Lv, Qiqi Zhu, Xiaoheng Li, Qingquan Lian, and Ren-Shan Ge
DES induced an intrauterine growth restriction of pups in the placentas ( 6 ). However, the mechanism has not been fully elucidated. Figure 1 Chemical structure of cortisol and diethylstilbestrol. Glucocorticoid hormone is an inducing
Giovanni Fanni, Petros Katsogiannos, Bipasha Nandi Jui, Magnus Sundbom, Susanne Hetty, Maria J Pereira, and Jan W Eriksson
and pancreatic islets but also of others produced by the pituitary and adrenal glands. Therefore, in this study, we assess growth hormone (GH), ACTH, and cortisol levels, which are largely unexplored in this context. Herein, we report exploratory post
Gamze Akkuş, Isa Burak Güney, Fesih Ok, Mehtap Evran, Volkan Izol, Şeyda Erdoğan, Yıldırım Bayazıt, Murat Sert, and Tamer Tetiker
hyperaldosteronism, hypercortisolism and pheochromocytoma. Plasma renin/aldosterone ratios, plasma normetanephrine, metanephrines and urinary free cortisol (UFC) were also studied. Autonomous cortisol secretion was described as serum cortisol >1.8 µg/dL following 1
Sirazum Choudhury, Tricia Tan, Katharine Lazarus, and Karim Meeran
cortisol leading to steroid exposure at detrimental times in the day and finally, differences in the biological actions of oral synthetic glucocorticoids versus endogenous cortisol. Interrogation of the EU-AIR registry demonstrated a higher mortality of 1
