Corticotropin deficiency

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Pituitary corticotropin normally stimulates the adrenal cortex to secrete a cascade of steroids including cortisol, and its own secretion is principally stimulated by hypothalamic corticotropin-releasing hormone and arginine vasopressin ( ThorneLMM 1992). Cortisol exerts negative feedback inhibition at the basophil cell level.

An intact pituitary adrenocortical axis is of vital importance, particularly in critical illness ( Van,den B®Egh®.,.aQd..d®,Z®gh§I,.1996.). The stress of critical illness normally induces elevated serum cortisol concentrations with loss of circadian rhythm. This hypothalamic-pituitary-adrenal response to prolonged stress induced by trauma or sepsis was recently found to be biphasic. In the first phase, lasting for a few days, the high cortisol levels appear to be induced by augmented corticotropin release, which in turn is presumably driven by cytokines and the noradrenergic system. In the second phase, there is a discrepancy between low corticotropin and high cortisol levels, suggesting that cortisol release is stimulated through an alternative pathway. The hypercortisolism elicited by disease or trauma can be interpreted as an attempt of the organism to mute its own inflammatory cascade, thus protecting itself against possible endogenous over-responses as virtually all the components of the immune response are inhibited by cortisol. Moreover, the acute cortisol-induced shifts in carbohydrate and protein metabolism result in instantly available energy and postpone anabolism. Therefore inability to activate the hypothalamic-pituitary-adrenocortical axis acutely in response to illness or stress hampers survival if left untreated.

DHEAS, the most abundant steroid secreted by the zona reticularis of the adrenal cortex after adrenarche, is under pituitary control, possibly through corticotropin and/or prolactin (Xhorner, et,al 1992). Pan-hypopituitarism is always associated with low levels of DHEAS. It circulates as a prohormone and is peripherally converted into the active dehydroepiandrosterone (DHEA), which is a weak androgen and an anabolic agent, as well as a modulator of the immune response. DHEA stimulates the Th1-cell function directly through a specific intracellular receptor and enhances T-lymphocyte function indirectly through a glucocorticoid-antagonizing effect. Low levels of DHEAS, which occur gradually with advancing age and acutely in severe illness, may contribute to T-lymphocyte dysfunction.

Corticotropin deficiency is almost always accompanied by deficiency of other pituitary hormones. The usual presentations are similar to those of primary adrenocortical failure, except for two characteristics.

1. Because of corticotropin and related pro-opiomelanocortin-derived peptide deficiency, the characteristic hyperpigmentation of Addison's disease is absent and patients have pallid skin and diminished tanning after exposure to sunlight.

2. Because of the primary dependence of aldosterone secretion on the renin-angiotensin system, the clinical features of mineralocorticoid deficiency are usually absent in corticotropin deficiency in the unstressed state.

Dehydration, volume depletion, and electrolyte abnormalities are not usually seen. Hypotension is less severe except in acute presentations. Although corticotropin deficiency is usually partial, a full-blown Addisonian-like crisis with shock may occur, with the latter unresponsive to vasopressor therapy until glucocorticoids are replaced. Such an acute presentation can occur in the undiagnosed corticotropin-deficient patient during acute illness or surgery, in the glucocorticoid-treated patient whose glucocorticoid dosage was not increased in such circumstances, and in pituitary apoplexia.

Dopamine infused as part of intensive care suppresses serum concentrations of DHEAS whereas the increased cortisol levels appear to be dopamine independent, suggesting a differential regulation of adrenal androgen and cortisol metabolism in critical illness ( V§n .d.eD B§Egh§.,.aQd..d§,Z§gh§I,.1996.). This DHEAS suppression may be mediated in part by the concomitant hypoprolactinemia. Low serum levels of prolactin, growth hormone, and DHEAS in the presence of high cortisol concentrations may contribute to the anergy-type immune dysfuction, the protein hypercatabolism, and the myopathy distinctively associated with prolonged critical illness.

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