Apparent free Cortisol concentrations in patients with anorexia nervosa at different stages of the disease

Rolla, M; Chicca, M.G. Del; Andreoni, A.; Belliti, D.; Vescovi, S. De; Andreani, Giacomo; Clerico, Aldo

doi:10.1007/bf03348432

Cited by 6 publications

(3 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, given that AN is associated with undernutrition and hypogonadism, one would expect low, rather than high, CBG levels. The binding capacity of CBG for cortisol does not differ in adults with AN compared with controls (12), and elevations have been reported not only in total, but also in free plasma cortisol in adult AN women (20,37). To determine whether an acquired partial glucocorticoid resistance is the cause of hypercortisolemia in AN, investigators have examined expression of glucocorticoid receptors in adults with this disorder.…”

Section: Discussionmentioning

confidence: 99%

Alterations in Cortisol Secretory Dynamics in Adolescent Girls with Anorexia Nervosa and Effects on Bone Metabolism

Misra

Miller

Almazan

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

224

170

View full text Add to dashboard Cite

Anorexia nervosa (AN) is associated with low bone density in adolescents and adults. Hypercortisolemia has been reported in adults with this disorder and has been hypothesized to be a factor in bone loss. However, the secretory dynamics of cortisol in adolescents with AN and the contribution of alterations in cortisol secretion to bone metabolism in AN have not been examined. We examined the dynamics of cortisol secretion by Cluster and deconvolutional analysis in 23 girls with AN and 21 healthy adolescents of comparable age and maturity. Cortisol sampling was performed every 30 min for 12 h overnight. Twenty-four-hour urinary free cortisol (UFC) and creatinine (cr) were obtained for all subjects. The surface area (SA) of the subjects was calculated. Markers of bone turnover (type 1 procollagen, osteocalcin, and N-telopeptide) were examined. Subjects with AN were prospectively followed over 1 yr, and those who recovered weight (defined as a 10% increase in body mass index) were again studied. On Cluster analysis, girls with AN had significantly higher mean cortisol (8.6 +/- 2.0 vs. 5.9 +/- 1.1 microg/dl; P < 0.0001), nadir cortisol (5.5 +/- 2.3 vs. 3.4 +/- 1.2 microg/dl; P = 0.0008), valley mean cortisol (7.0 +/- 2.7 vs. 4.7 +/- 1.5 microg/dl; P = 0.001), peak amplitude (12.6 +/- 4.4 vs. 7.8 +/- 3.0 microg/dl; P = 0.0004), peak area (652 +/- 501 vs. 340 +/- 238 microg/dl; P = 0.02), and total area under the curve (6112 +/- 1467 vs. 4117 +/- 802 microg/dl; P < 0.0001) than healthy adolescents. On deconvolutional analysis, the frequency of nocturnal secretory bursts (7.0 +/- 1.2 vs. 5.8 +/- 1.3 /12 h; P = 0.001), total nocturnal pulsatile cortisol secretion (69.3 +/- 14.7 vs. 53.9 +/- 11.1 microg/dl; P = 0.0003), and total cortisol secretion (89.6 +/- 18.8 vs. 71.2 +/- 17.6 microg/dl; P = 0.002) were significantly higher in girls with AN than in healthy controls. Cortisol half-life trended higher in girls with AN. However, basal cortisol secretion and approximate entropy did not differ between the groups. UFC/cr and UFC/cr.SA were significantly higher in girls with AN than in controls [0.050 +/- 0.028 vs. 0.036 +/- 0.017 (P = 0.04) and 0.035 +/- 0.020 vs. 0.023 +/- 0.012 (P = 0.03)]. Six of 23 girls with AN had UFC/cr.SA values that were more than 2 sd above those in healthy controls. An inverse correlation was noted between measures of cortisol concentration as well as pulsatile secretion and measures of nutritional status (body mass index, fat mass, leptin, insulin, and IGF-I). An oral glucose load suppressed cortisol levels in healthy adolescents, but not in AN patients. Weight recovery was associated with a significant decrease in the number of secretory bursts. In girls with AN, strong inverse correlations were noted between levels of cortisol (mean, nadir, and total area under the curve) and levels of markers of bone formation (C-terminal propeptide of type 1 procollagen and osteocalcin). Conversely, in healthy controls, cortisol values did not predict levels of markers of bone turnover. Adolescent girls with...

show abstract

Section: Discussionmentioning

confidence: 99%

Alterations in Cortisol Secretory Dynamics in Adolescent Girls with Anorexia Nervosa and Effects on Bone Metabolism

Misra

Miller

Almazan

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

224

170

View full text Add to dashboard Cite

show abstract

“…Moreover, the hyperactivity of the HPA axis differs in depression and AN, with a greater involvement of AVP in depressive disorder and perhaps more reliance on CRH to drive the axis in AN [98] . Some authors proposed malnutrition as the main determinant responsible for HPA axis alterations, because of the significant correlation between pathological DST results and the weight loss already mentioned [114][115][116][117] . Consistent with this interpretation is that the weight recovery is associated with a normalization of plasmatic and urinary cortisol levels [94,97] and with a significant decrease in the number of secretory bursts [97] .…”

Section: The Hpa Axis In the Specific Eating Disordersmentioning

confidence: 99%

Stress, Hypothalamic-Pituitary-Adrenal Axis and Eating Disorders

et al. 2008

View full text Add to dashboard Cite

The etiopathogenesis of eating disorders (ED) is complex and poorly understood. Biological, psychological and environmental factors have all been considered to be involved in the onset and the persistence of these syndromes, often with conflicting results. The recent literature focused on the possible role of hormonal pathways, in particular the hypothalamic-pituitary-adrenal (HPA) axis, as a relevant factor capable of influencing the onset and the course of ED. Other studies have suggested that the onset of ED is often preceded by severe life events, and that chronic stress is associated with the persistence of these disorders. As the biological response to stress is the activation of the HPA axis, the available literature considering the relationships between stress, HPA axis functioning and anorexia nervosa, bulimia nervosa and binge eating disorder is reviewed by the present article.

show abstract

“…Studies on anorexia patients also have demonstrated increased plasma cortisol, reflecting both increased production and decreased metabolism of this hormone (Walsh et al, 1981). Although these anomalies normalize after weight restoration (Rolla et al, 1984), they may play a significant role in maintaining the disorder. Underweight anorexics have low levels of CSF leptin (Hebebrand et al, 1997).…”

Section: Pathophysiologymentioning

confidence: 99%