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Review
. 2008;11(2):187-207.
doi: 10.1007/s11102-008-0112-8.

Systemic illness

Affiliations
Review

Systemic illness

Marta Bondanelli et al. Pituitary. 2008.

Abstract

Systemic illnesses are associated with alterations in the hypothalamic-pituitary-peripheral hormone axes, which represent part of the adaptive response to stressful events and may be influenced by type and severity of illness and/or pharmacological therapy. The pituitary gland responds to an acute stressful event with two secretory patterns: adrenocorticotropin (ACTH), prolactin (PRL) and growth hormone (GH) levels increase, while luteinizing hormone (LH), follicle-stimulating hormone (FSH) and thyrotropin (TSH) levels may either decrease or remain unchanged, associated with a decreased activity of their target organ. In protracted critical illness, there is a uniformly reduced pulsatile secretion of ACTH, TSH, LH, PRL and GH, causing a reduction in serum levels of the respective target-hormones. These adaptations are initially protective; however, if inadequate or excessive they may be dangerous and may contribute to the high morbidity and mortality risk of these patients. There is no consensus regarding the type of approach, as well as the criteria to use to define pituitary axis function in critically ill patients. We here provide a critical approach to pituitary axis evaluation during systemic illness.

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References

    1. J Clin Endocrinol Metab. 1981 Oct;53(4):764-71 - PubMed
    1. Crit Care Med. 1993 Mar;21(3):396-401 - PubMed
    1. N Engl J Med. 2004 Apr 15;350(16):1629-38 - PubMed
    1. J Clin Endocrinol Metab. 1991 Nov;73(5):1106-10 - PubMed
    1. Arch Intern Med. 1999 Apr 12;159(7):658-65 - PubMed

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