Between Scylla and Charybdis: Where does the treatment of Addison's disease in late-life depression go first?

2016 ◽  
Vol 33 (S1) ◽  
pp. S382-S382 ◽  
Author(s):  
S. Petrykiv ◽  
M. Arts ◽  
L. de Jonge

IntroductionOlder adults with adrenocortical insufficiency, including Addison's disease (AD), are at an increased risk for developing late-life depression. Treatment of AD with glucocorticoid replacement therapy may exacerbate depressive symptoms and may complicate treatment of late-life depression.ObjectivesTo present a case with algorithm of decision-making in a particular case of glucocorticoid induced depression in patient with syndrome of Addison.AimsTo report a case-study, describing treatment of Addison's disease in LLD.MethodsA case report is presented and discussed, followed by a literature review.ResultsA 77-year-old female, diagnosed with Addison's disease, was referred with persistent fatigue, weakness, weight loss, sleep disturbances, and depressive symptoms over the previous 6 months. She was taken losartan 100 mg/day, zolpidem 10 mg/day, fludrocortisone 100 μg/day, and hydrocortisone 35 mg/day. There was no personal or family history of psychiatric problems. Clinical examination was normal aside from skin hyperpigmentation. After initial minimal dose reduction of glucocorticoids, Addison's disease remained under control. One week later, her depressive symptoms disappeared without administration of antidepressants.ConclusionThe association between glucocorticoid replacement therapy and late-life depression is not well understood. The current case shows that treatment of glucocorticoid-induced depression in subjects with Addison's disease is achievable by minimal adjustments in glucocorticoid regiment. However, collaboration with endocrinology is of vital importance to prevent an Addison's crisis. Pharmacokinetic dose-finding studies are required to find optimal glucocorticoid adjustment strategy.Disclosure of interestThe authors have not supplied their declaration of competing interest.

2009 ◽  
Vol 160 (6) ◽  
pp. 993-1002 ◽  
Author(s):  
Kristian Løvås ◽  
Clara G Gjesdal ◽  
Monika Christensen ◽  
Anette B Wolff ◽  
Bjørg Almås ◽  
...  

ContextPatients with primary adrenal insufficiency (Addison's disease) receive more glucococorticoids than the normal endogenous production, raising concern about adverse effects on bone.ObjectiveTo determine i) the effects of glucocorticoid replacement therapy on bone, and ii) the impact of glucocorticoid pharmacogenetics.Design, setting and participantsA cross-sectional study of two large Addison's cohorts from Norway (n=187) and from UK and New Zealand (n=105).Main outcome measuresBone mineral density (BMD) was measured; the Z-scores represent comparison with a reference population. Blood samples from 187 Norwegian patients were analysed for bone markers and common polymorphisms in genes that have been associated with glucocorticoid sensitivity.ResultsFemoral neck BMD Z-scores were significantly reduced in the patients (Norway: mean −0.28 (95% confidence intervals (CI) −0.42, −0.16); UK and New Zealand: −0.21 (95% CI −0.36, −0.06)). Lumbar spine Z-scores were reduced (Norway: −0.17 (−0.36, +0.01); UK and New Zealand: −0.57 (−0.78, −0.37)), and significantly lower in males compared with females (P=0.02). The common P-glycoprotein (ABCB1) polymorphism C3435T was significantly associated with total BMD (CC and CT>TT P=0.015), with a similar trend at the hip and spine.ConclusionsBMD at the femoral neck and lumbar spine is reduced in Addison's disease, indicating undesirable effects of the replacement therapy. The findings lend support to the recommendations that 15–25 mg hydrocortisone daily is more appropriate than the higher conventional doses. A common polymorphism in the efflux transporter P-glycoprotein is associated with reduced bone mass and might confer susceptibility to glucocorticoid induced osteoporosis.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gwenn S. Smith ◽  
Clifford I. Workman ◽  
Hillary Protas ◽  
Yi Su ◽  
Alena Savonenko ◽  
...  

AbstractDepression in late-life is associated with increased risk of cognitive decline and development of all-cause dementia. The neurobiology of late-life depression (LLD) may involve both neurochemical and neurodegenerative mechanisms that are common to depression and dementia. Transgenic amyloid mouse models show evidence of early degeneration of monoamine systems. Informed by these preclinical data, the hypotheses were tested that a spatial covariance pattern of higher beta-amyloid (Aβ) and lower serotonin transporter availability (5-HTT) in frontal, temporal, and parietal cortical regions would distinguish LLD patients from healthy controls and the expression of this pattern would be associated with greater depressive symptoms. Twenty un-medicated LLD patients who met DSM-V criteria for major depression and 20 healthy controls underwent PET imaging with radiotracers for Aβ ([11C]-PiB) and 5-HTT ([11C]-DASB). A voxel-based multi-modal partial least squares (mmPLS) algorithm was applied to the parametric PET images to determine the spatial covariance pattern between the two radiotracers. A spatial covariance pattern was identified, including higher Aβ in temporal, parietal and occipital cortices associated with lower 5-HTT in putamen, thalamus, amygdala, hippocampus and raphe nuclei (dorsal, medial and pontine), which distinguished LLD patients from controls. Greater expression of this pattern, reflected in summary 5-HTT/Aβ mmPLS subject scores, was associated with higher levels of depressive symptoms. The mmPLS method is a powerful approach to evaluate the synaptic changes associated with AD pathology. This spatial covariance pattern should be evaluated further to determine whether it represents a biological marker of antidepressant treatment response and/or cognitive decline in LLD patients.


HORMONES ◽  
2013 ◽  
Vol 12 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Lisanne Smans ◽  
Eef Lentjes ◽  
Ad Hermus ◽  
Pierre Zelissen

2021 ◽  
Vol 30 ◽  
Author(s):  
Shiyu Lu ◽  
Tianyin Liu ◽  
Gloria H. Y. Wong ◽  
Dara K. Y. Leung ◽  
Lesley C. Y. Sze ◽  
...  

Abstract Aims Late-life depression has substantial impacts on individuals, families and society. Knowledge gaps remain in estimating the economic impacts associated with late-life depression by symptom severity, which has implications for resource prioritisation and research design (such as in modelling). This study examined the incremental health and social care expenditure of depressive symptoms by severity. Methods We analysed data collected from 2707 older adults aged 60 years and over in Hong Kong. The Patient Health Questionnaire-9 (PHQ-9) and the Client Service Receipt Inventory were used, respectively, to measure depressive symptoms and service utilisation as a basis for calculating care expenditure. Two-part models were used to estimate the incremental expenditure associated with symptom severity over 1 year. Results The average PHQ-9 score was 6.3 (standard deviation, s.d. = 4.0). The percentages of respondents with mild, moderate and moderately severe symptoms and non-depressed were 51.8%, 13.5%, 3.7% and 31.0%, respectively. Overall, the moderately severe group generated the largest average incremental expenditure (US$5886; 95% CI 1126–10 647 or a 272% increase), followed by the mild group (US$3849; 95% CI 2520–5177 or a 176% increase) and the moderate group (US$1843; 95% CI 854–2831, or 85% increase). Non-psychiatric healthcare was the main cost component in a mild symptom group, after controlling for other chronic conditions and covariates. The average incremental association between PHQ-9 score and overall care expenditure peaked at PHQ-9 score of 4 (US$691; 95% CI 444–939), then gradually fell to negative between scores of 12 (US$ - 35; 95% CI - 530 to 460) and 19 (US$ -171; 95% CI - 417 to 76) and soared to positive and rebounded at the score of 23 (US$601; 95% CI -1652 to 2854). Conclusions The association between depressive symptoms and care expenditure is stronger among older adults with mild and moderately severe symptoms. Older adults with the same symptom severity have different care utilisation and expenditure patterns. Non-psychiatric healthcare is the major cost element. These findings inform ways to optimise policy efforts to improve the financial sustainability of health and long-term care systems, including the involvement of primary care physicians and other geriatric healthcare providers in preventing and treating depression among older adults and related budgeting and accounting issues across services.


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