Hypercorticism blunts circadian variations of osteocalcin regardless of nutritional status

Vergély, N.; Lafage-Proust, Marie-Hélène; Caillot-Augusseau, Anne; Millot, L.; Lang, François; Estour, Bruno

doi:10.1016/s8756-3282(01)00677-9

Cited by 18 publications

(14 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Elsa Ost-Nat (Cis Bio Intl., Gif-sur-Yvette, France), a two-site assay, was used to quantify intact osteocalcin. Intraassay and interassay CVs were less than 5% (23,24). The manufacturer's mean and reference range for females 21-30 yr were 13.4 and 7.6 -25.6 g/ml, respectively.…”

Section: Hormonal and Bone Marker Studymentioning

confidence: 90%

Constitutional Thinness: Unusual Human Phenotype of Low Bone Quality

Galusca

Zouch

Germain

et al. 2008

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

Context: Low fat mass and hormonal or nutritional deficiencies are often incriminated in bone loss related to thinness. Constitutional thinness has been described in young women with low body mass index (BMI) but close-to-normal body composition, physiological menstruation, no hormonal abnormalities, and no anorexia nervosa (AN) psychological profile.Objective: Our objective was to determine whether constitutional thinness is associated with impaired bone quality.Design, Setting, and Participants: This was an observational, cross-sectional study on 25 constitutionally thin and 44 AN young women with similar low BMI (Ͻ16.5 kg/m 2 ) and 28 age-matched controls. Main Outcome Measures:Femoral and lumbar spine bone mineral density by dual-energy x-ray absorptiometry, distal tibia and radius bone architecture and breaking strength by three-dimensional peripheral quantitative computed tomography, and bone turnover markers were determined. Results:Constitutionally thin subjects displayed a higher percentage of fat mass than AN subjects but had similar lumbar and femoral bone mineral density, which were significantly lower than in controls (P Ͻ 0.001). Constitutionally thin subjects displayed more markedly impaired trabecular and cortical bone parameters in the distal tibia than in the radius. AN bone structure was impaired only in subjects with a long history of disease. Calculated breaking strength was decreased in constitutional thinness and long-standing AN in both the radius and the tibia. Bone markers in constitutionally thin subjects were similar to those of controls. Osteoprotegerin to receptor activator of nuclear factor B ligand ratio was higher in constitutionally thin subjects than in controls or AN women. Conclusions:Young women with constitutional thinness present an unexpectedly high prevalence of low bone mass (44%) associated with small bone size, overall diminished breaking strength, but normal bone turnover. Mechanisms related to insufficient skeletal load and/or genetics are proposed to explain this new phenotype of impaired bone quality. In middle-aged and elderly patients, bone loss has been related to thinness, mainly in a context of low fat mass (FM) (2). Consumptive (3), infectious (4), digestive (5), or chronic Abbreviations: AN, Anorexia nervosa; bALP, bone alkaline phosphatase; BMD, bone mineral density; BMI, body mass index; BV/TV, relative bone volume as a percentage of total volume, derived from trabecular density; CT, constitutional thinness; CTh, absolute thickness of cortical bone; CV, coefficient of variation; 3D-pQCT, three-dimensional peripheral quantitative computed tomography; D100, mean whole bone (cortical and trabecular) density; Dcomp, bone density of cortical bone; DHEAS, sulfate salt of dehydroepiandrosterone; Dinn, density of the central part of trabecular bone;Dmeta,densityofthesubcorticalareaoftrabecularbone;Dtrab,densityofthetrabeculararea of bone; DXA, dual-energy x-ray absorptiometry; FFM, fat-free mass; FM, fat mass; HA, hydroxyapatite; MOI, moment of inertia; OPG, oste...

show abstract

Section: Hormonal and Bone Marker Studymentioning

confidence: 90%

Constitutional Thinness: Unusual Human Phenotype of Low Bone Quality

Galusca

Zouch

Germain

et al. 2008

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

show abstract

“…This method has demonstrated highly significant deficits in the number of bone trabeculae, increased distance Strong inverse correlation with bone formation markers, but not resorption markers. 49,90 Possibly decreases bone formation Ghrelin resistance Perhaps mediated by high cortisol and GH resistance, and lack of response to the signal to increase nutritional intake in anorexia 29,86 Increased osteoprogerin Decreases bone resorption. Increased levels are indicative of a compensatory (yet suboptimal) bone remodelling process 91 …”

Section: Bone Health In An Backgroundmentioning

confidence: 99%

Current concepts in bone and reproductive health in adolescents with anorexia nervosa

Jayasinghe

Grover

Zacharin

2008

BJOG

View full text Add to dashboard Cite

Anorexia nervosa (AN) initiates an adaptive response at the level of the hypothalamus, which results in a complex interplay involving most elements of the neuroendocrine axis. Consequences of onset of disease in adolescence include amenorrhoea, pubertal arrest with potential loss of target height, and osteoporosis with reduced capacity for future attainment of peak bone mass. With recovery, delay in restoration of menses is common. Hormonal therapies for restoration of bone mineral density (BMD) in adolescents have shown limited efficacy. This review will discuss the reproductive endocrine effects of AN in adolescence, and discuss new investigative tools for monitoring restoration of reproductive function and BMD in this population.Keywords Adolescence, amenorrhoea, anorexia nervosa, bone mineral density, eating disorders. IntroductionNinety percent of eating disorders present before the age of 25 years, and in the early stages they may present with menstrual dysfunction. 1 Therefore, it is important that gynaecologists have a good understanding of current concepts of hypothalamic regulation, as those physicians may be the first point of contact in subsyndromal eating disorders. Leptin, a hormone produced by adipocytes, appears to be the critical link between energy homeostasis and neuroendocrine regulation. 2 Since its discovery in 1994, 3 rapid gains in understanding of the hormonal and nutritional regulation of anorexia nervosa (AN) have occurred. 4 These findings are likely to have a significant impact on clinical management of the reproductive-endocrine aspects of AN. Bone loss consequent upon estrogen deficiency may be severe, of long duration with reduced capacity for recovery. Understanding bone loss mechanisms, correct interpretation of bone density measurements and consideration of treatment modalities to ameliorate the problems of eating disorders are an essential part of overall management strategies. EpidemiologyThe Society for Adolescent Medicine together with other medical bodies has recognised that strict Diagnostical and Statistical Manual of Mental Health Disorders-IV (DSM-IV) criteria 5 for AN (particularly requiring weight below 85% of normal and amenorrhoea for 3 months), may not apply to all women. 6,7 This is particularly so in adolescents because of their normal variability in development, and also because adverse health effects occur even in partial syndromes. In adolescence, prevalence of AN is 0.5%, bulimia nervosa is 1% and partial syndromes (eating disorders not otherwise specified) is 2.4-5.0%. 6,[8][9][10] Clinical sequelaeThe clinical sequelae of AN depend on timing of disease in relation to puberty. These may include pubertal delay and primary amenorrhoea, pubertal arrest with potential loss of target height, or secondary amenorrhoea. 11-13 Amenorrhoea has been reported to precede weight loss in 20% of women, which may lead to diagnostic confusion.Low bone mineral density (BMD) is an established risk in AN, with 50% of anorexics demonstrating osteopenia within 20 months of ameno...

show abstract

“…One of the important factors to be considered is the current psychological condition and the psychological follow-up provided, as it is known that hypercortisolaemia is a negative factor. Vergely, LafageProust, Caillot-Augusseau, MilIot, Lang, and Estour (2002) demonstrated that hypercortisolism decreases the levels of osteocalcin. We also know the importance of genetic factors in the pathogenesis of osteoporosis (Ralston, 1999).…”

mentioning

confidence: 99%

A study of bone density change in patients with anorexia nervosa

Carmo

Mascarenhas

Macedo³

et al. 2007

Euro Eating Disorders Rev

View full text Add to dashboard Cite

In patients with anorexia nervosa (AN) several factors combine to cause osteoporosis, and the risk of osteoporosis increases with chronicity of illness. The authors carried out a follow-up study in patients who attended the Eating Disorders department of the Hospital de Santa Maria. The average follow-up period was of 7.6 years. Fifteen patients were included. Patients answered clinical history questions and underwent neck of femur and spine densitometry. The most important variable with negative correlations to bone recovery was disease duration. A positive correlation between bone recovery and time since the first menstrual cycle post-amenorrhea was also found. However, AN is a condition in which once weight improves and menstrual cycles become regular, severe damage to bone structure is still likely to be maintained.

show abstract

Hypercorticism blunts circadian variations of osteocalcin regardless of nutritional status

Cited by 18 publications

References 43 publications

Constitutional Thinness: Unusual Human Phenotype of Low Bone Quality

Constitutional Thinness: Unusual Human Phenotype of Low Bone Quality

Current concepts in bone and reproductive health in adolescents with anorexia nervosa

A study of bone density change in patients with anorexia nervosa

Contact Info

Product

Resources

About