Current opinion in pharmacology
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Curr Opin Pharmacol · Dec 2004
ReviewHormonal and metabolic strategies to attenuate catabolism in critically ill patients.
During the prolonged phase of critical illness, the ongoing hypermetabolic response leads to loss of lean tissue mass. Although the cachexia of prolonged illness is usually associated with low concentrations of anabolic hormones, most endocrine interventions attempting to correct the hormone balance have shown to be ineffective and their indiscriminate use is even harmful. Thus, a detailed understanding of the neuroendocrinology of the stress response is warranted, especially as the acute and chronic phases show remarkable differences. ⋯ By contrast, the pulsatile secretion of anterior pituitary hormones is uniformly decreased in the prolonged phase of the disease, leading to proportionally reduced concentrations of peripheral anabolic hormones. As hypothalamic secretagogues can restore the pulsatile secretion of the anterior pituitary and increase peripheral target hormones, tissues are at least partially sensitive to the anterior pituitary hormones in this phase of illness. Therefore, a combination of hypothalamic secretagogues that reactivates the anterior pituitary to a greater extent could be a more physiological and effective strategy to induce anabolism in patients with prolonged critical illness.
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Status epilepticus is a neurological emergency requiring prompt pharmacological intervention. Recent advances in the treatment of this condition include the introduction of treatment algorithms that are tailored more specifically to clinical situations, a trend towards more aggressive therapies if initial treatment with front-line agents fail, and a better understanding of the role of treatment for patients in status epilepticus in the out-of-hospital setting.
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Curr Opin Pharmacol · Feb 2003
ReviewCytokines: regulation of the hypothalamo-pituitary-adrenocortical axis.
Many of the pro-inflammatory cytokines that are released in response to immune/inflammatory insults exert marked stimulatory influences on the hypothalamo-pituitary-adrenocortical axis. Thus, they provoke the release of glucocorticoids that, in turn, temper the ensuing immune/inflammatory response, and thereby complete a homeostatic neuroendocrine loop. The mechanisms by which cytokines cause glucocorticoid release are complex and can be affected by repeated or sustained cytokine exposure, gender and age, or counter-regulatory mechanisms.