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K Amrein, A Papinutti, E Mathew, G Vila and D Parekh

The prevalence of vitamin D deficiency in intensive care units ranges typically between 40 and 70%. There are many reasons for being or becoming deficient in the ICU. Hepatic, parathyroid and renal dysfunction additionally increases the risk for developing vitamin D deficiency. Moreover, therapeutic interventions like fluid resuscitation, dialysis, surgery, extracorporeal membrane oxygenation, cardiopulmonary bypass and plasma exchange may significantly reduce vitamin D levels. Many observational studies have consistently shown an association between low vitamin D levels and poor clinical outcomes in critically ill adults and children, including excess mortality and morbidity such as acute kidney injury, acute respiratory failure, duration of mechanical ventilation and sepsis. It is biologically plausible that vitamin D deficiency is an important and modifiable contributor to poor prognosis during and after critical illness. Although vitamin D supplementation is inexpensive, simple and has an excellent safety profile, testing for and treating vitamin D deficiency is currently not routinely performed. Overall, less than 800 patients have been included in RCTs worldwide, but the available data suggest that high-dose vitamin D supplementation could be beneficial. Two large RCTs in Europe and the United States, together aiming to recruit >5000 patients, have started in 2017, and will greatly improve our knowledge in this field. This review aims to summarize current knowledge in this interdisciplinary topic and give an outlook on its highly dynamic future.

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Greta B Raglan, Louis A Schmidt and Jay Schulkin

Introduction Stress reactions are by no means universal, and the activation of ‘stress hormones’, such as glucocorticoids or corticotropin-releasing hormone (CRH), is not necessarily the mark of a stress response ( 1 ). Some individuals have

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Trevor Lewis, Eva Zeisig and Jamie E Gaida

the context of the stress response, it is important to remember that the HPA axis is only one of many stress-responsive systems within the body ( 15 , 18 ). A stressor is a real or perceived threat to homeostasis or well-being. This definition

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Carolina Inda, Natalia G Armando, Paula A dos Santos Claro and Susana Silberstein

are essential to the stress response driving both basal and stress-induced hypothalamic–pituitary–adrenal axis (HPA) activation. Besides the hypothalamus, CRH is widely distributed in extrahypothalamic circuits of the brain where it functions as a

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I Azzam, S Gilad, R Limor, N Stern and Y Greenman

is also involved in the response to acute stressors such as major surgery ( 12 ) and stress-induced gastric mucosal injury ( 13 , 14 ). Ghrelin stimulates the secretion of hormones involved in the stress response, including vasopressin, ACTH

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S U Jayasinghe, S J Torres, C A Nowson, A J Tilbrook and A I Turner

pathways may play a role in mediating the stress response (14) . Therefore, it is possible that various factors that were not investigated in this experiment are involved in mediating the effects of stress in lean and overweight/obese men. Further research

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Xi Wang and Qi Yu

girls with MAS-associated PPP and may impair the adrenocortical stress response ( 9 ). A 36-month trial of the third-generation aromatase inhibitor letrozole in ten girls with MAS-associated PP found a significant decrease in the growth velocity standard

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Rachel K Rowe, Benjamin M Rumney, Hazel G May, Paska Permana, P David Adelson, S Mitchell Harman, Jonathan Lifshitz and Theresa C Thomas

increase in CORT released under acute restraint stress, indicating an altered neuroendocrine stress response. After treatment with DEX, the HPE response to restraint stress was suppressed in both brain-injured and uninjured sham rats, indicating an intact

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Arno Téblick, Lies Langouche and Greet Van den Berghe

hallmark of critical illness, is the immediate initiation of multiple physiologic processes in an attempt to rebalance the complex dynamic equilibrium, commonly known as homeostasis. This so-called ‘stress response’ comprises many tightly controlled neural

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Peter Ergang, Anna Mikulecká, Martin Vodicˇka, Karla Vagnerová, Ivan Mikšík and Jirˇí Pácha

( 22 ). To induce stress, the animals were submitted to repeated social defeat, which is the result of intraspecific confrontation between male rats. This model provides a relevant tool to study stress response features, as well as differences in the