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Adrenal Insufficiency in Critical Illness

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Adrenal Insufficiency in Critical Illness Adrenal Insufficiency in Critical Illness Mark Stuart Cooper, BM BCh, MRCP, PhD Paul Michael Stewart, MD, FRCP, FmedSci metabolism, and action and how these changes will One of the more controversial areas in critical care in recent decades relates to the issue of adrenal insufficiency be affected by various types of illness. We will illus- and its treatment in critically ill patients. There is no con- trate adrenal function testing and how interpreta- sensus on which patients to test for adrenal insufficiency, tion of these tests will depend on the underlying which tests to use and how to interpret them, whether to illness being treated. There are inherent difficulties use corticosteroids, and, if so, who to treat and with what in interpreting the effects of glucocorticoid replace- dose. This review illustrates the complexity and diversity of pathophysiological changes in glucocorticoid secretion, ment during critical illness, including the diversity metabolism, and action and how these are affected by var- of effects of glucocorticoids on various tissues. We ious types of illness. It will review adrenal function testing offer advice as to when glucocorticoids should be and give guidance on corticosteroid replacement regimens given on the basis of the available evidence. based on current published literature. There remain inher- ent difficulties in interpreting the effects of glucocorticoid replacement during critical illness because of the diversity of effects of glucocorticoids on various tissues. Investigation Corticosteroid Physiology and treatment will depend on whether the likely cause of corticosteroid insufficiency is adrenal or central in origin. Corticosteroids are synthesized in the adrenal cortex Key words: corticosteroids, hydrocortisone, cortisol, sepsis, adrenal and can be divided into mineralocorticoids and glu- insufficiency, Addison’s disease cocorticoids. The main mineralocorticoid is aldos- terone and the main glucocorticoid cortisol. In addition, the adrenal secretes a large amount of One of the more controversial areas in critical care androgens through dehydroepiandrosterone (DHEA) in recent decades relates to the issue of adrenal and its sulphated derivative DHEAS. Aldosterone insufficiency in critically ill patients and whether binds to mineralocorticoid receptors (MRs) and is these patients should receive glucocorticoid ther- important in sodium handling in the kidney and apy. Although this subject has been discussed in other mineralocorticoid target tissues. Although the recent reviews [1-5], there is currently no consensus supply of the initial precursors for aldosterone pro- on which patients to test for adrenal insufficiency, duction is regulated by pituitary adrenocorticotropic which tests to use and how to interpret them, whether hormone (ACTH), a more important regulator is the glucocorticoids are beneficial, and, if so, who should renin–angiotensin system. Aldosterone production be treated and with what dose. This review illustrates is thus maintained in adrenal insufficiency induced the complexity and diversity of physiological and by pituitary disease but is lost at an early stage in pathological changes in glucocorticoid secretion, conditions that destroy the adrenal gland (eg, autoimmune Addison’s disease). From the Department of Endocrinology, Division of Medical Cortisol is the main glucocorticoid synthesized in Sciences, Institute of Biomedical Research, The University of humans. An area of potential confusion is that cortisol Birmingham, United Kingdom. is traditionally called hydrocortisone when adminis- Received October 3, 2006. Accepted for publication December 18, tered as a pharmaceutical. Cortisol can bind to the 2006. glucocorticoid receptor (GR), which is expressed at Address correspondence to Mark Stuart Cooper, BM BCh, MRCP, varying levels in almost all cells. This binding PhD, Department of Endocrinology, Division of Medical Sciences, accounts for the majority of responses seen in Institute of Biomedical Research, The University of Birmingham, healthy individuals. Cortisol also has some miner- Birmingham B15 2TT, United Kingdom, e-mail: m.s.cooper@ alocorticoid activity because it can bind to the MR. bham.ac.uk. This binding is normally limited by the presence of Cooper MS, Stewart PM. Adrenal insufficiency in critical illness. an enzyme in mineralocorticoid target tissues, 11β- J Intensive Care Med. 2007;22:348-362. hydroxysteroid dehydrogenase type 2 (11β-HSD2), DOI: 10.1177/0885066607307832 which rapidly inactivates cortisol to its inactive 348 Copyright © 2007 Sage Publications Adrenal Insufficiency metabolite cortisone [6]. This enzyme does not inac- In normal physiology, the metabolism of cortisol tivate aldosterone, leaving this steroid free to bind is dominated by the liver and the kidney [14]. A to the MR. When cortisol levels are moderately high, proportion of the cortisol present in serum is con- however, the mineralocorticoid action of cortisol verted to cortisone within the kidney because of becomes clinically significant [7]. Cortisol is rapidly the presence of large amounts of the 11β-HSD2 synthesized in the adrenal cortex in response to enzyme within this organ. Cortisone is biologically ACTH synthesized in the pituitary. ACTH is secreted inactive but can be converted back to cortisol in tis- from the pituitary in response to corticotropin sues that express the 11β-hydroxysteroid dehydro- releasing hormone (CRH), which is secreted from genase type 1 (11β-HSD1) enzyme (as described the hypothalamus. CRH is released in response to a below). The liver is able to convert cortisone back range of factors, including neurological inputs entrain- to cortisol, but there are also a range of other ing the normal diurnal rhythm of cortisol secretion enzymes in the liver that can metabolize cortisol and a range of physiological and psychological and cortisone to less active, more polar metabolites stressors. that are then excreted in the urine. The balance DHEA is a weak adrenal androgen of uncertain between cortisol and cortisone interconversion and physiological importance. Most of the DHEA in the hepatic degradation is a major factor in determining circulation exists as DHEAS. DHEA is thought to the circulatory half-life of cortisol [15]. exert its actions primarily through downstream con- In recent years it has been realized that some version to more powerful androgens, such as tissues are able to generate active glucocorticoids androstenedione and testosterone in various tissues from inert circulating precursors [15]. This occurs by [8]. DHEA synthesis is ACTH dependent, but there the presence of the 11β-HSD1 enzyme that primarily may also be mechanisms within the adrenal gland converts inactive cortisone to active cortisol. This that can control the relative production of gluco- enzyme is expressed constitutively in liver, adipose, corticoids and adrenal androgens [9]. and bone tissue but additionally is expressed in a Steroid hormones bind to circulating binding pro- range of other tissues in response to inflammatory teins. Circulating cortisol is heavily bound to a spe- mediators [16-18]. The purpose of this inflammation- cific binding protein, cortisol binding globulin (CBG; induced glucocorticoid activating capacity is unclear, also known as transcortin), and to a lesser extent to but it may be important in dampening local inflam- albumin [10,11]. In healthy individuals, as little as 5% matory responses. Importantly, this is a situation of cortisol will be present as a free fraction in the cir- where cortisol production is not regulated by the culation, but only this fraction can diffuse into the tis- classical hypothalamic–pituitary–adrenal (HPA) axis. sues. Because the levels of CBG are very low at a tissue level under normal circumstances, the tissue cortisol level will actually be much lower than sug- gested by measurements of serum concentrations Changes in HPA (0.1-1 μg/dL [1-20 nmol/L] compared with 7-14 μg/dL Axis During Critical Illness [200-400 nmol/L]). Congenital or acquired alteration in binding protein levels or affinity for cortisol will Dramatic changes in HPA axis function occur at all profoundly affect serum levels of cortisol but not the levels during critical illness [2]. Some of these fea- tissue level of steroid [12]. The most important situa- tures appear common to all types of severe illness, tions in which CBG levels are elevated are pregnancy whereas others may vary depending on the under- and during use of estrogen-based oral contraceptives. lying condition. The nature and mechanisms under- CBG levels are low in patients with severe illness, as lying these changes probably change with disease described below. Current methods to directly mea- duration, and attempts have been made to break sure free cortisol are technically difficult to perform these down into distinct acute, chronic, and recov- and are not standardized for clinical use, although ery phases [19,20]. These anticipated changes are recent reports suggest that free cortisol estimation also modified by a range of external factors. These using CBG and albumin concentrations can give a include disease-related pathology (eg, infection or reasonable approximation [13]. hemorrhage) and treatment-related factors (eg, Whereas there has been great interest in the syn- drugs). Changes in HPA function can be divided thesis and secretion of corticosteroids, there has been into those attributable to changes in cortisol secre- much less interest in their metabolism. Variation in
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