Endocrine dysfunction in sepsis: a beneficial or deleterious host response?

Abstract

Sepsis is a systemic, deleterious inflammatory host response triggered by an infective agent leading to severe sepsis, septic shock and multi-organ failure. The host response to infection involves a complex, organized and coherent interaction between immune, autonomic, neuroendocrine and behavioral systems. Recent data have confirmed that disturbances of the autonomic nervous and neuroendocrine systems could contribute to sepsis-induced organ dysfunction.Through this review, we aimed to summarize the current knowledge about the endocrine dysfunction as response to sepsis, specifically addressed to vasopressin, copeptin, cortisol, insulin and leptin. We searched the following readily accessible, clinically relevant databases: PubMed, UpToDate, BioMed Central.The immune system could be regarded as a "diffuse sensory organ" that signals the presence of pathogens to the brain through different pathways, such as the vagus nerve, endothelial activation/dysfunction, cytokines and neurotoxic mediators and the circumventricular organs, especially the neurohypophysis. The hormonal profile changes substantially as a consequence of inflammatory mediators and microorganism products leading to inappropriately low levels of vasopressin, sick euthyroid syndrome, reduced adrenal responsiveness to ACTH, insulin resistance, hyperglycemia as well as hyperleptinemia.In conclusion, clinical diagnosis of this "pan-endocrine illness" is frequently challenging due to the many limiting factors. The most important benefits of endocrine markers in the management of sepsis may be reflected by their potential to be used as biomarkers in different scoring systems to estimate the severity of the disease and the risk of death.

Catecholamine Vasopressor Support Sparing Strategies in Vasodilatory Shock

“…Adrenocorticotrophic hormone release is activated by the V1b receptor, whereas the V2 receptor, primarily located in the kidney, is associated with maintaining fluid balance as well as osmotic effects. 14 Vasopressin serum concentrations are increased in the setting of hypotension; however, a biphasic pattern, with an initial increase in vasopressin secretion from the posterior pituitary followed by AVP deficiency, was observed during a 48-to 96-hour period following the development of septic shock. 15 The resulting deficiency of serum vasopressin concentrations is thought to contribute to vasodilation and vascular hyperresponsiveness that may contribute to the development of vasopressordependent septic shock.…”

“…The V1a receptor is of particular interest in the elevation of arterial pressure in septic shock. Adrenocorticotrophic hormone release is activated by the V1b receptor, whereas the V2 receptor, primarily located in the kidney, is associated with maintaining fluid balance as well as osmotic effects . Vasopressin serum concentrations are increased in the setting of hypotension; however, a biphasic pattern, with an initial increase in vasopressin secretion from the posterior pituitary followed by AVP deficiency, was observed during a 48‐ to 96‐hour period following the development of septic shock .…”

Usefulness of the Geriatric Nutritional Risk Index to predict the severity of cholecystitis among older patients in the emergency department

“…These results support the opinion that the presence of SOD is not attributable to a localized inflammation alone. A dysregulated host response to pathogenic agents can be affected by interactions between the autonomic, neuroendocrine, metabolic, and immune systems . Malnutrition has been thought to alter the homeostatic response and impair cellular immunity .…”

Letter to the Editor: Early serum procalcitonin, but not C reactive protein, might improve the prediction of sepsis in multiple trauma patients. A prospective observational study

“…The use of PCT serum concentration in the first 24 hours after the traumatic event might improve the prognostic information that currently available scores offer to the intensive care unit physician, as it reflects the severity of the initial inflammatory response. The study of altered neuroendocrine responses and autonomic nervous system imbalance, both linked to immune suppression in response to trauma and sepsis, might reveal other valuable biomarkers to estimate the severity of the disease and the risk of death [8,9].…”