Increased rates of cortisol production and urinary free cortisol excretion in elderly women 2 weeks after proximal femur fracture

Barton, R. N.; Weijers, J. W. M.; Horan, Michael A.

doi:10.1111/j.1365-2362.1993.tb00757.x

Cited by 16 publications

(4 citation statements)

References 16 publications

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“…One explanation for the decrease in S‐OC could be a trauma‐related elevation in serum cortisol. (29) The biosynthesis of OC is suppressed by glucocorticoids,(30) serum OC levels decrease after glucocorticoid administration,(31) and are lower in women with recent hip fracture than in elderly controls. (32) Increase in cortisol after the trauma may also explain the slight, but nonsignificant, decrease observed in S‐PINP soon after fracture (Table 2).…”

Section: Discussionmentioning

confidence: 99%

Effect of Fracture on Bone Turnover Markers: A Longitudinal Study Comparing Marker Levels Before and After Injury in 113 Elderly Women

Ivaska

Gerdhem

Åkesson

et al. 2007

Journal of Bone and Mineral Research

154

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In this longitudinal, prospective, and population-based study (n = 1044), seven BTMs were assessed before and after trauma in 113 elderly women (85 with fractures). Markers were not altered in the immediate postfracture period but were clearly elevated during fracture repair. Recent fracture should thus be taken into account when markers are used in clinical practice.Introduction: Fracture may influence the levels of bone turnover markers (BTM) and have implications for their use in clinical practice. In this longitudinal, prospective, and population-based study, we assessed prefracture levels of BTMs and compared them with postfracture levels of the same individuals immediately after fracture and during fracture repair. This is the first study in which the effect of fracture on bone markers has been evaluated with prefracture samples available. Materials and Methods: Serum and urine were collected at the emergency unit from 85 women (77.9 ± 1.8 yr) who sustained a fracture after low-energy trauma and 28 controls (77.8 ± 2.0 yr) with similar trauma but no fracture. All were participants of the Malmö OPRA study (n ‫ס‬ 1044), and pretrauma samples were collected 1.05 ± 0.85 yr before. Results: BTMs sampled within a few hours after fracture were not altered from preinjury levels. Both bone formation and bone resorption markers were, however, significantly increased 4 mo after fracture. The elevation was most pronounced after hip fracture. Bone turnover remained elevated up to 12 mo after fracture. Conclusions: We believe this study extends our knowledge on the skeletal postfracture metabolic processes. In addition, it may provide a basis for future means to monitor pharmacological intervention promoting fracture healing.

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Section: Discussionmentioning

confidence: 99%

Effect of Fracture on Bone Turnover Markers: A Longitudinal Study Comparing Marker Levels Before and After Injury in 113 Elderly Women

Ivaska

Gerdhem

Åkesson

et al. 2007

Journal of Bone and Mineral Research

154

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“…Stud ies of HPA axis sensitivity to cortisol feedback inhibition in the very old and in the substantial proportion of older persons with one or more chronic illnesses would be infor mative. Reduced feedback inhibition with aging may be a contributory mechanism to the enhanced ACTH and/or cortisol responses observed in older human subjects to some stimuli [27,[32][33][34][35] The age-related changes in human HPA function may also bear a mechanistic and etiologic relationship to the facilitation of HPA respon siveness [22] and decreased sensitivity to fast feedback [36] produced by chronic stress.…”

Section: Discussionmentioning

confidence: 99%

Decreased Hypothalamic-Pituitary Adrenal Axis Sensitivity to Cortisol Feedback Inhibition in Human Aging

Wilkinson

Peskind

Raskind³

1997

Neuroendocrinology

166

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Aging-related reduction in the sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis to glucocorticoid feedback inhibition has been demonstrated in rodents, but aging effects on glucocorticoid feedback inhibition in humans are unclear. This study assessed the influence of aging on the sensitivity of the human HPA axis to feedback inhibition induced by cortisol. Endogenous cortisol feedback inhibition was removed by treatment with metyrapone, which reduces cortisol synthesis by inhibiting 11β-hydroxylase. Feedback inhibition was then reintroduced by infusing exogenous cortisol. Sixteen young (26 ± 1 years old) and 16 older (70 ± 2 years old) subjects underwent three study conditions in random order. In the two cortisol infusion conditions, oral metyrapone treatment was followed by intravenous infusion of 0.03 mg/kg/h (83 nmol/kg/h) or 0.06 mg/kg/h (166 nmol/kg/h) cortisol for 150 min. Feedback sensitivity was estimated by the latency to and extent of decline of plasma ACTH concentration during and following the cortisol infusion. In a placebo condition, placebo tablets were substituted for metyrapone and normal saline infusion was substituted for cortisol. Blood samples were drawn twice prior to and at 15-min intervals for 4 h following the onset of the infusions, and plasma was assayed for 11-deoxycortisol, cortisol and ACTH. Plasma cortisol suppression and ACTH and 11-deoxycortisol elevations did not differ between age groups after metyrapone. Older subjects exhibited delayed and blunted ACTH responses to infused cortisol. Within older subjects, the ACTH response to the higher dose cortisol infusion was blunted in older women compared to older men. These data provide direct evidence for reduced responsiveness to glucocorticoid feedback inhibition in human aging.

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“…The increase in cortisol is substantial. At about 2 weeks after injury, urinary free cortisol excretion is about three times higher than in healthy subjects (3), and indirect estimates suggest a similar increase in the plasma free cortisol concentration averaged over 24 h (R N Barton, J G Rose & M A Horan, unpublished observations).…”

Section: Introductionmentioning

confidence: 96%

Sensitivity of mononuclear leucocytes to glucocorticoids in elderly hip-fracture patients resistant to suppression of plasma cortisol by dexamethasone

Rijen¹,

Harvey²,

Barton³

et al. 1998

European Journal of Endocrinology

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Objective: Elderly women with proximal femur fracture show a prolonged increase in plasma cortisol, which could have undesirable catabolic effects. Suppression of cortisol by dexamethasone is impaired, suggesting resistance to glucocorticoid effects at feedback inhibitory sites. We therefore wished to find out whether peripheral glucocorticoid sensitivity is normal. Design: Peripheral blood mononuclear leucocytes were used as a model tissue. Blood samples were taken from elderly women about 2 weeks after hip fracture and from elderly control women. Each patient was then given 1 mg dexamethasone at 2300 h followed by further sampling at 0800 and 1600 h the next day. Methods: Glucocorticoid-receptor binding parameters were measured by incubating whole cells with 3 H]thymidine than the control cells in the absence of dexamethasone. The percentage inhibition by a saturating concentration of dexamethasone was unchanged but the concentration giving half-maximal inhibition was decreased (sensitivity was increased) at the higher of the two concanavalin A concentrations used. Conclusions: These experiments in mononuclear leucocytes give no evidence of peripheral resistance to glucocorticoids in hip-fracture patients with impaired suppression of cortisol by dexamethasone. European Journal of Endocrinology 138 659-666

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Increased rates of cortisol production and urinary free cortisol excretion in elderly women 2 weeks after proximal femur fracture

Cited by 16 publications

References 16 publications

Effect of Fracture on Bone Turnover Markers: A Longitudinal Study Comparing Marker Levels Before and After Injury in 113 Elderly Women

Effect of Fracture on Bone Turnover Markers: A Longitudinal Study Comparing Marker Levels Before and After Injury in 113 Elderly Women

Decreased Hypothalamic-Pituitary Adrenal Axis Sensitivity to Cortisol Feedback Inhibition in Human Aging

Sensitivity of mononuclear leucocytes to glucocorticoids in elderly hip-fracture patients resistant to suppression of plasma cortisol by dexamethasone

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