High prevalence of decreased cortisol reserve in brain-dead potential organ donors

Dimopoulou, Ioanna; Tsagarakis, Stylianos; Anthi, Anastasia; Milou, E; Ilias, Ιoannis; Stavrakaki, Krystallia; Charalambidis, Charalambos; Tzanela, Marinella; Orfanos, Stylianos E.; Mandragos, Konstantinos; Thalassinos, Nikolaos; Roussos, Charis

doi:10.1097/01.ccm.0000059644.54819.67

Cited by 88 publications

(51 citation statements)

References 25 publications

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“…Patients' diagnoses were evenly distributed among groups. Even though it has been reported that in patients who had severe life-threatening illnesses at the time of death (24,25) or in brain-dead potential organ donors (26,27) serum ACTH and cortisol levels are controversial, ACTH overstimulation in vivo could not be discarded. In a previous study of 3␤-HSD mRNA expression in human adrenal tissues that we have published (4), tissue samples were obtained from similar sources.…”

Section: Discussionmentioning

confidence: 99%

Expression of the IGF System in Human Adrenal Tissues from Early Infancy to Late Puberty: Implications for the Development of Adrenarche

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Expression of the IGF System in Human Adrenal Tissues from Early Infancy to Late Puberty: Implications for the Development of Adrenarche

et al. 2005

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“…After brain death plasma levels of cortisol were significantly lower than in the patients who did not deteriorate to brain death, and 76% of the brain-dead patients did not respond to ACTH stimulation compared with 10% in the non-brain-dead group. 45 Thus, the prevalence of an attenuated adrenocortical response to physiologic concentrations of ACTH seems to be high in braindead patients, but its clinical implications are not settled. Corticoid treatment of brain-dead donors is routinely used by many centers, not to substitute adrenocortical failure, but to attenuate immune responses.…”

Section: Pulmonary Changesmentioning

confidence: 99%

“…44 Although plasma cortisol values remain within normal levels in most brain-dead donors, 34,35 the capacity to increase secretion upon ACTH stimulation seems to be reduced. 45 In a group of 37 patients with serious brain injury, 17 patients progressed to brain death. After brain death plasma levels of cortisol were significantly lower than in the patients who did not deteriorate to brain death, and 76% of the brain-dead patients did not respond to ACTH stimulation compared with 10% in the non-brain-dead group.…”

Section: Pulmonary Changesmentioning

confidence: 99%

Brain death and its implications for management of the potential organ donor

Bugge

2009

Acta Anaesthesiol Scand

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The systemic physiologic changes that occur during and after brain death affect all organs suitable for transplantation. Major changes occur in the cardiovascular, pulmonary, endocrine, and immunological systems, and, if untreated may soon result in cardiovascular collapse and somatic death. Understanding these complex physiologic changes is mandatory for developing effective strategies for donor resuscitation and management in such a way that the functional integrity of potentially transplantable organs is maintained. This review elucidates these physiological changes and their consequences, and based on these consequences the rationale behind current medical management of brain-dead organ donors is discussed.

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“…However, neural influences or effects exerted by other circulating mediators cannot be excluded. Of interest, acute ACTH administration in brain-dead potential organ donors induced impaired cortisol release [40] . These results are consistent with downregulation of the ACTH receptor MC2R in the adrenal glands, i.e another peripheral melanocortin receptor.…”

Section: Discussionmentioning

confidence: 99%

Reduced Expression of the Melanocortin-1 Receptor in Human Liver during Brain Death

Gatti

Colombo

Turcatti

et al. 2006

Neuroimmunomodulation

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Objective: There is evidence that brain death has detrimental effects on peripheral organs. Clinical and experimental studies on organ donors showed marked inflammation in tissue samples of livers and kidneys collected during brain death. The inflammatory reaction is characterized by release of cytokines and inflammatory cell infiltration. Because melanocortins and their receptors are significant modulators of inflammation, we hypothesized that downregulation of melanocortin receptors during brain death could contribute to enhance inflammation. Methods: Using real-time polymerase chain reaction (PCR) analysis, we determined expression of melanocortin receptors in liver biopsies obtained from brain-dead organ donors before cold ischemia and in normal liver tissue during resection of benign focal lesions of the liver. Tissue biopsies were also analyzed for expression of intercellular adhesion molecule-1 (ICAM-1), which has a central function in inflammatory cell migration. Results: Expression of melanocortin-1 receptor (MC1R) mRNA was markedly reduced in liver samples obtained from brain-dead organ donors compared to hepatic tissue collected during resection of benign focal lesions of the liver. Conversely, expression of the adhesion molecule ICAM-1 was significantly increased in livers of brain-dead organ donors. Conclusions: Disruption of the endogenous anti-inflammatory circuit based on MC1R could contribute to tissue damage during brain death.

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High prevalence of decreased cortisol reserve in brain-dead potential organ donors

Abstract: Adrenal cortisol secretion after dynamic stimulation is deficient in a substantial proportion of brain-dead potential organ donors.

Cited by 88 publications

References 25 publications

Expression of the IGF System in Human Adrenal Tissues from Early Infancy to Late Puberty: Implications for the Development of Adrenarche

Expression of the IGF System in Human Adrenal Tissues from Early Infancy to Late Puberty: Implications for the Development of Adrenarche

Brain death and its implications for management of the potential organ donor

Reduced Expression of the Melanocortin-1 Receptor in Human Liver during Brain Death

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