Salivary Cortisol day curves in assessing glucocorticoid replacement therapy in Addison’s disease

HORMONES ◽  
2013 ◽  
Vol 12 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Lisanne Smans ◽  
Eef Lentjes ◽  
Ad Hermus ◽  
Pierre Zelissen
Keyword(s):  
Replacement Therapy ◽  
Salivary Cortisol ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Glucocorticoid Replacement Therapy

scholarly journals Continuous subcutaneous hydrocortisone infusion in Addison’s disease

2007 ◽  
Vol 157 (1) ◽  
pp. 109-112 ◽  
Author(s):  
Kristian Løvås ◽  
Eystein S Husebye
Keyword(s):  
Replacement Therapy ◽  
Salivary Cortisol ◽  
Short Form ◽  
Circadian Variation ◽  
Addison’S Disease ◽  
Subjective Health ◽  
Addison's Disease ◽  
Subjective Health Status ◽  
Daily Dose ◽  
Design And Methods

Objective: The conventional replacement therapy in Addison’s disease (AD) does not restore the normal diurnal cortisol rhythm. We explored the feasibility and safety of continuous s.c. hydrocortisone infusion (CSHI) as a novel mode of glucocorticoid replacement therapy. Design and methods: Seven patients with AD were treated with CSHI in an open-labelled clinical study for up to three months. Adequacy of glucocorticoid replacement was assessed by 24 h blood and saliva sampling in one patient and by salivary cortisol day curves in six outpatients. Subjective health status was monitored by the Short Form-36 questionnaire. Results: CSHI re-established the circadian variation and normal levels of cortisol in the patients, with minor day-to-day variation. Most of the patients could reduce their glucocorticoid dose considerably without adverse reactions. The treatment was well tolerated and positively evaluated by the patients. Conclusions: CSHI is technically feasible and safe in patients with AD. A daily dose of ~10 mg/m2 body surface area/day restores the circadian variation and normal levels of salivary cortisol in most patients, which is close to the estimated daily requirement. We hypothesise that selected patients will benefit from restoration of the circadian cortisol rhythm.

scholarly journals Glucocorticoid replacement therapy and pharmacogenetics in Addison's disease: effects on bone

2009 ◽  
Vol 160 (6) ◽  
pp. 993-1002 ◽  
Author(s):  
Kristian Løvås ◽  
Clara G Gjesdal ◽  
Monika Christensen ◽  
Anette B Wolff ◽  
Bjørg Almås ◽  
...  
Keyword(s):  
New Zealand ◽  
Lumbar Spine ◽  
Femoral Neck ◽  
Replacement Therapy ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Mineral Density ◽  
Cross Sectional ◽  
Glucocorticoid Replacement Therapy ◽  
The Impact

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.

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
Keyword(s):  
Depressive Symptoms ◽  
Replacement Therapy ◽  
Sleep Disturbances ◽  
Addison’S Disease ◽  
Late Life ◽  
Addison's Disease ◽  
Late Life Depression ◽  
Current Case ◽  
Increased Risk ◽  
Glucocorticoid Replacement Therapy

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.

Oral dehydroepiandrosterone (DHEA) replacement therapy in women with Addison's disease

2000 ◽  
Vol 52 (6) ◽  
pp. 775-780 ◽  
Author(s):  
Gennet Gebre-Medhin ◽  
Eystein S. Husebye ◽  
Hans Mallmin ◽  
Lotti Helström ◽  
Christian Berne ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Addison’S Disease ◽  
Addison's Disease
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