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Review
, 8 (8), R131-R143

Anterior Pituitary Function in Critical Illness

Affiliations
Review

Anterior Pituitary Function in Critical Illness

Arno Téblick et al. Endocr Connect.

Abstract

Critical illness is hallmarked by major changes in all hypothalamic-pituitary-peripheral hormonal axes. Extensive animal and human studies have identified a biphasic pattern in circulating pituitary and peripheral hormone levels throughout critical illness by analogy with the fasting state. In the acute phase of critical illness, following a deleterious event, rapid neuroendocrine changes try to direct the human body toward a catabolic state to ensure provision of elementary energy sources, whereas costly anabolic processes are postponed. Thanks to new technologies and improvements in critical care, the majority of patients survive the acute insult and recover within a week. However, an important part of patients admitted to the ICU fail to recover sufficiently, and a prolonged phase of critical illness sets in. This prolonged phase of critical illness is characterized by a uniform suppression of the hypothalamic-pituitary-peripheral hormonal axes. Whereas the alterations in hormonal levels during the first hours and days after the onset of critical illness are evolutionary selected and are likely beneficial for survival, endocrine changes in prolonged critically ill patients could be harmful and may hamper recovery. Most studies investigating the substitution of peripheral hormones or strategies to overcome resistance to anabolic stimuli failed to show benefit for morbidity and mortality. Research on treatment with selected and combined hypothalamic hormones has shown promising results. Well-controlled RCTs to corroborate these findings are needed.

Keywords: CIRCI; NTI; critical illness; neuroendocrine axis; pituitary function.

Figures

Figure 1
Figure 1
Changes in GH during critical illness. During the acute phase of critical illness, the nocturnal secretion of growth hormone is augmented with an increase in pulse amplitude and pulse frequency. In prolonged critical illness this pulsatile pattern becomes blunted. Adapted, with permission, from (3).
Figure 2
Figure 2
Changes in TSH during critical illness. The typical nocturnal surge of TSH disappears during the entire course of critical illness, mean TSH levels in the acute phase are not dramatically altered. Conversely, TSH levels are distinct lowered during the chronic phase of critical illness. Adapted, with permission, from (3).
Figure 3
Figure 3
Changes in the ACTH and cortisol during critical illness. (A) The ACTH–cortisol dissociation, that is high levels of cortisol and low levels of ACTH, during the first week of ICU stay. Adapted, with permission, from (47). (B) The time course of HPA axis alteration beyond the first week of critical illness. The ACTH–cortisol dissociation appears to continue throughout the first month of ICU stay. In ‘very long stay’ patients (>4 weeks in ICU) cortisol and ACTH plasma concentrations gradually return to normal levels, despite their severity of illness. The blue areas indicate the range of healthy individuals. Adapted by permission from Springer Nature: Intensive Care Medicine; Adrenocortical function during prolonged critical illness and beyond: a prospective observational study, Peeters B, Meersseman P, Vander Perre S, Wouters PJ, Vanmarcke D, Debaveye Y, Billen J, Vermeersch P, Langouche L & Van den Berghe G; copyright 2018 (46).
Figure 4
Figure 4
Simplified cartoon depicting the biphasic neuroendocrine response to critical illness. Trends in plasma concentrations of the most important pituitary and peripheral hormones during critical illness are rendered over time and compared to the physiological ranges in healthy individuals (black line). A rise in growth hormone levels is seen in the first hours after the onset of critical illness (orange line). This rise in GH coincides with a decrease in IGF-I (yellow line). During the chronic phase of critical illness, IGF-I further decreases and GH plasma concentration start to normalize. Thyroid hormone T3 levels rapidly decreases after the onset of critical illness with a further decline during the prolonged phase of critical illness (yellow line). It is currently unclear when the plasma levels of both IGF-1 and T3 fully normalize (dotted yellow line). Although TSH levels (green line) are not significantly altered during the first hours and days of critical illness, plasma concentration decreases when chronic critical illness sets in. When recovery is commenced, TSH transiently rise to supra-normal concentration before returning to physiological levels. Cortisol levels (red line) rise after a severe insult. High cortisol levels plateau in the first week of critical illness. When critical illness is prolonged, cortisol levels start to decrease. ACTH levels are rapidly reduced in acute critical illness but start to normalize after several days of critical illness. During the recovery phase, a rise in plasma concentrations of both ACTH and cortisol is seen (dotted blue line and dotted red line); however, when this rise is dampened and the circulating levels of ACTH and cortisol start to normalize is not clear.

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