Poor quality of life, depressed mood, and memory impairment may be mediated by sleep disruption in patients with Addison's disease

In this article, we review published studies covering epidemiology, natural course and mortality in primary adrenal insufficiency (PAI) or Addison's disease. Autoimmune PAI is a rare disease with a prevalence of 100-220 per million inhabitants. It occurs as part of an autoimmune polyendocrine syndrome in more than half of the cases. The patients experience impaired quality of life, reduced parity and increased risk of preterm delivery. Following a conventional glucocorticoid replacement regimen leads to a reduction in bone mineral density and an increase in the prevalence of fractures. Registry studies indicate increased mortality, especially evident in patients diagnosed with PAI at a young age and in patients with the rare disease autoimmune polyendocrine syndrome type-1. Most notably, unnecessary deaths still occur because of adrenal crises. All these data imply the need to improve the therapy and care of patients with PAI.

Section: Health-related Quality Of Lifementioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Epidemiology, quality of life and complications of primary adrenal insufficiency: a review

Bensing

Hulting

Husebye

et al. 2016

“…Recent studies, over a decade later, confirmed these observations, that health-related quality of life is significantly impaired in Addisonian patients compared with the age-matched and gender-matched general population, despite the proper use of the recommended oral hydrocortisone doses (131,132). The mental fatigue, accounting for a significant portion of these patient's poorer quality of life, is characterised by higher prevalence of mood disorders (mainly depression), memory impairment and sleep disorders (133). Similar findings have been reported in patients with Cushing's syndrome after long-term remission, where the health-related quality of life remains impaired regardless of aetiology, presence of hormonal deficiencies and different treatment strategies (134).…”

Section: Is There a Relationship Between Gc-based Therapeutics And Nementioning

confidence: 90%

MECHANISMS IN ENDOCRINOLOGY: Does circadian and ultradian glucocorticoid exposure affect the brain?

Kalafatakis

Russell

Lightman

2019

Glucocorticoids are a class of systematically secreted hormones, vital for mammalian life, which are intensively investigated for more than 80 years. They regulate multiple body processes like metabolism, fluid homeostasis, immune and stress system responsivity, as well as brain function. Glucocorticoids have a complex rhythm by which they are released to circulation from the adrenal cortex. The hormone exhibits a circadian variation, with high hormonal levels being secreted just prior and during the active part of the day, and progressively lower and lower amounts being released during the inactive part of it. Underlying this diurnal variation there is a more dynamic, ultradian rhythm composed of frequent episodes of glucocorticoid secretion (hormonal pulses). Accumulating evidence from observational, in silico, in vitro and in vivo, preclinical and clinical studies suggest that both aspects of glucocorticoid rhythmicity are preserved among mammalian species and are important for brain function. The central nervous system is exposed to both aspects of the hormonal rhythm and has developed mechanisms able to perceive them and translate them to differential cellular events, genomic and non-genomic. Thus, glucocorticoid rhythmicity regulates various physiological neural and glial processes, under baseline and stressful conditions, and hormonal dysrhythmicity has been associated with cognitive and behavioural defects. This raises a number of clinical implications concerning (i) glucocorticoid involvement in neuropsychiatric disease and (ii) improving the therapeutic efficacy or expanding the role of glucocorticoid-based treatments in such conditions.

“…Hydrocortisone administration in the late afternoon or early evening leads to relatively elevated cortisol concentrations during the early part of the night (9), but the medication's short half-life results in cortisol deficiencies during the latter part of the night and the early morning (10). Given the importance of the HPA axis in sleep regulation (4), high night-time cortisol during the early hours of sleep, accompanied by high night-time ACTH and CRH, may be one reason why patients with AD frequently report experiencing disrupted, unrefreshing sleep (11,12,13).…”

Section: Introductionmentioning

confidence: 99%

“…Nonetheless, and especially in light of sizable literature describing relationships between irregular HPA axis activity and altered sleep architecture in both psychiatric and healthy samples (16,17,18), it is plausible to suggest that hypo-or hyperactivity of that endocrinological system might play a role in explaining why patients with AD self-report, and objectively experience, poorer sleep quality and more frequent sleep disturbances than healthy controls (11,12,14,19).…”

Section: Introductionmentioning

confidence: 99%

Reduced slow-wave sleep and altered diurnal cortisol rhythms in patients with Addison’s disease

Henry

Ross

Thomas³

2018

Self Cite

Overall, these results suggest that patients with AD demonstrate different patterns of night-time cortisol concentrations to healthy controls, and that relatively elevated concentrations are associated with a reduction of SWS. These hormonal and sleep architectural aberrations may disrupt the routine sleep-dependent processes of memory consolidation, and hence may explain, at least partially, the memory impairments often experienced by patients with AD.