Megestrol acetate therapy and secondary adrenal suppression

Naing, Ko K.; Dewar, John; Leese, Graham

doi:10.1002/(sici)1097-0142(19990915)86:6<1044::aid-cncr21>3.0.co;2-c

Cited by 55 publications

(23 citation statements)

References 20 publications

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“…29 Diabetes mellitus, inflammation, hypertension, obstructive sleep apnoea and genetic polymorphisms can also potentiate ACTH and cortisol release. 48 Confounding factors are anxiety, trauma, stress, illness, sleep loss, inanition, systemic disease, day-to-night schedule, 49 and medications, 50 such as benzodiazepines, antidepressants, synthetic progestins and glucocorticoids. In addition, interactions between the pituitary gland and the immune system constitute a growing focus in ageing research.…”

Section: Hpa Axis In Ageingmentioning

confidence: 99%

“…Interpretative limitations of pituitary studies in an ageing population include prevalent comorbidities, sex-specific effects, sex hormone deficiency or replacement, disrupted sleep, altered body composition, reduced physical activity, elevated inflammatory mediators, increased medication use and methodological inconsistencies (Box 2). 50 Moreover, rigorous evidence-based decisions require adequately powered, longitudinal, double-blind, randomized, placebo-controlled interventions replicated across multiple centres.…”

Section: Limitations Of Pituitary Studies In Ageingmentioning

confidence: 99%

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Changes in pituitary function with ageing and implications for patient care

Veldhuis

2013

Nat Rev Endocrinol

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The pituitary gland has a role in puberty, reproduction, stress-adaptive responses, sodium and water balance, uterine contractions, lactation, thyroid function, growth, body composition and skin pigmentation. Ageing is marked by initially subtle erosion of physiological signalling mechanisms, resulting in lower incremental secretory-burst amplitude, more disorderly patterns of pituitary hormone release and blunted 24 h rhythmic secretion. Almost all pituitary hormones are altered by ageing in humans, often in a manner dependent upon sex, body composition, stress, comorbidity, intercurrent illness, medication use, physical frailty, caloric intake, immune status, level of exercise, and neurocognitive decline. The aim of this article is to critically discuss the mechanisms mediating clinical facets of changes in the hypothalamic–pituitary axis during ageing, and the extent to which confounding factors operate to obscure ageing effects.

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Section: Hpa Axis In Ageingmentioning

confidence: 99%

Section: Limitations Of Pituitary Studies In Ageingmentioning

confidence: 99%

Changes in pituitary function with ageing and implications for patient care

Veldhuis

2013

Nat Rev Endocrinol

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“…Secondary adrenal insufficiency may also follow drug therapy (Table 1) [11]. Previous treatments with glucocorticoids induce prolonged suppression of CRH and ACTH synthesis, and result in slow onset secondary adrenal insufficiency that may outlast exposure to this treatment [12].…”

Section: Mechanisms Of Glucocorticoid Insufficiencymentioning

confidence: 99%

Science review: Mechanisms of impaired adrenal function in sepsis and molecular actions of glucocorticoids

2004

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This review describes current knowledge on the mechanisms that underlie glucocorticoid insufficiency in sepsis and the molecular action of glucocorticoids. In patients with severe sepsis, numerous factors predispose to glucocorticoid insufficiency, including drugs, coagulation disorders and inflammatory mediators. These factors may compromise the hypothalamic–pituitary axis (i.e. secondary adrenal insufficiency) or the adrenal glands (i.e. primary adrenal failure), or may impair glucocorticoid access to target cells (i.e. peripheral tissue resistance). Irreversible anatomical damages to the hypothalamus, pituitary, or adrenal glands rarely occur. Conversely, transient functional impairment in hormone synthesis may be a common complication of severe sepsis. Glucocorticoids interact with a specific cytosolic glucocorticoid receptor, which undergoes conformational changes, sheds heat shock proteins and translocates to the nucleus. Glucocorticoids may also interact with membrane binding sites at the surface of the cells. The molecular action of glucocorticoids results in genomic and nongenomic effects. Direct and indirect transcriptional and post-transcriptional effects related to the cytosolic glucocorticoid receptor account for the genomic effects. Nongenomic effects are probably subsequent to cytosolic interaction between the glucocorticoid receptor and proteins, or to interaction between glucocorticoids and specific membrane binding sites.

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“…MA likely contributed to his adrenal insufficiency. MA has an inhibitory effect on the HPA axis by direct suppressing at the hypothalamic level . In addition, MA possesses glucocorticoid activity and thus can suppress the HPA axis .…”

Section: Discussionmentioning

confidence: 99%