Searchable abstracts of presentations at key conferences in endocrinology
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13th European Congress of Endocrinology

Symposia

Endocrine response to critical illness

ea0026s13.1 | Endocrine response to critical illness | ECE2011

The HPA axis in critical illness

Annane D

The role of the hypothalamic–pituitary adrenal axis in host response to an infection is crucial. The initial inflammatory response to sepsis activates the endogenous release of cortisol which in turn will modulate the synthesis and release of both pro- and anti-inflammatory mediators to restrict inflammation to the infected tissues. However, a number of factors including vascular or ischemic damage, inflammation and apoptosis within the hypothalamic–pituitary adrenal...

ea0026s13.2 | Endocrine response to critical illness | ECE2011

Thyroid hormone metabolism in inflammation and sepsis

Boelen A

During illness changes in thyroid hormone metabolism occur, collectively known as the non-thyroidal illness syndrome (NTIS). NTIS is characterized by low serum thyroid hormone levels, while TSH and TRH expression do not increase, indicating a disturbance of the normal thyroid hormone feedback regulation.Although the common view was that NTIS results in overall downregulation of metabolism in order to save energy, recent work has shown that genes involved...

ea0026s13.3 | Endocrine response to critical illness | ECE2011

Novel insights in endocrine and metabolic changes during critical illness

Van den Berghe G

Host responses to critical illness, such as excessive inflammation and hyperglycemia, trigger detrimental chain reactions that damage cellular proteins and organelles. Such responses to illness contribute to the risk of non-resolving multiple organ dysfunction and adverse outcome. Autophagy is a bulk degradation pathway able to remove toxic protein aggregates and damaged organelles. Morphologically, both liver and muscle of critically ill patients reveal an autophagy-deficienc...