Evaluation of markers of bone and collagen turnover in patients with active and preclinical Cushing's syndrome and in patients with adrenal incidentaloma

Sartório, Alessandro; Conti, Antonio; Ferrero, S.; Giambona, Salvatore; Re, T.; Passini, E.; Ambrosi, Bruno

doi:10.1530/eje.0.1380146

Cited by 73 publications

(74 citation statements)

References 29 publications

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“…The serum level is influenced by renal function (20) but otherwise well correlated with bone formation, as judged by histomorphometry (21) and calcium kinetics (22). This study confirms the findings of previous biochemical investigations (7,(9)(10)(11)(12) indicating decreased bone formation in endogenous CS. The low serum level of osteocalcin cannot be explained by alteration in renal function, as it did not differ between patients and controls.…”

Section: Discussionsupporting

confidence: 92%

“…Bone mineral content (BMC) and density (BMD) are markedly decreased in untreated CS, with significant improvement following treatment (5)(6)(7)(8). Biochemical markers of bone turnover have consistently shown decreased serum levels of formative parameters (7,(9)(10)(11)(12), whereas the resorptive markers, so far, have been inconclusive. In a recent study of normal subjects treated with prednisolone (20 mg daily) (13), a prompt decline in formative markers was shown, whereas renal calcium excretion was markedly increased, as was serumparathyroid hormone.…”

Section: Introductionmentioning

confidence: 99%

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Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Godang

Ueland

Bollerslev

1999

European Journal of Endocrinology

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It is well established that chronic excess of glucocorticoids has negative effects on bone and collagen turnover, and that secondary osteoporosis is a known clinical complication of endogenous Cushing's syndrome (CS). The aim of the present study was to evaluate bone dimension and bone mineral content in relation to biochemical markers of bone and collagen turnover, in a consecutive series of 23 patients with endogenous CS (18 with pituitary adenoma and 5 with adrenal tumor; 17 women, 6 men; mean age 39.7 Ϯ 2.8 (S.E.M.) and 44.3 Ϯ 3.1 years respectively), compared with 23 age-, sex-and body mass index-matched healthy controls.Bone mineral densities were uniformly reduced in the different regions analyzed: lumbar spine (16.1%, P < 0.001), femoral neck (15.2%, P < 0.001), total body (11.5%, P < 0.001), and the subregions of arms (8.4%, P < 0.05), legs (10.1%, P < 0.05) and trunk (15.8%, P < 0.001). Similar results were observed for bone mineral content, although these were less prominent. The calculated area was significantly decreased in trunk (13.8%, P < 0.01) and total body (11.6%, P < 0.05).Serum levels of osteocalcin were significantly decreased (28%, P < 0.03) in patients with CS. No significant differences were observed for the formative markers carboxyterminal propeptide of type I procollagen and aminoterminal propeptide of type I procollagen. Markers of bone resorption, serum Crosslaps and carboxyterminal cross-linked telopeptide of type I collagen were increased in patients compared with controls, although only significantly for Crosslaps (P < 0.02). No correlations between formative and resorptive markers were found in the patients, but in controls, the formative markers were positively correlated with resorptive markers.In conclusion, bone dimension and bone mineral content of the entire skeleton are found to be decreased in endogenous CS. As judged by biochemical markers of bone remodeling, this is caused by decreased bone formation and an increased bone resorption.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Godang

Ueland

Bollerslev

1999

European Journal of Endocrinology

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“…In conclusion, this study confirms and extends previous observations on the negative effects of endogenous hypercortisolism on bone density, bone turnover, and fracture incidence (7,8,40,41). Our data suggest that bone demineralization and spinal fractures are frequent at any degree of cortisol excess, being partly counterbalanced by increased BMI and androgen levels, whereas preserved menstrual cycles had protective effects only in women with less severe, i.e.…”

Section: Discussionsupporting

confidence: 90%

“…This study confirms that patients with cortisol excess are at risk for bone loss and vertebral fractures, regardless of its severity and origin (exogenous or endogenous) (1,7,8,(37)(38)(39)(40)(41). Back pain and stature shortening should be investigated in all patients with endogenous hypercortisolism, and a radiogram of the spine is required in order to assess morphology of vertebral bodies also in non-symptomatic patients.…”

Section: Discussionsupporting

confidence: 70%

Effects of sex steroids on bone in women with subclinical or overt endogenous hypercortisolism

et al. 2007

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Objective: Glucocorticoid-induced osteoporosis is the most frequent cause of secondary osteoporosis. Nevertheless, limited data are available on bone status in patients with endogenous cortisol excess. This study is aimed at investigating the role of sex steroids and severity of hypercortisolism on bone mineral density (BMD) and prevalence of vertebral fractures in female patients. Design: Cross-sectional, case-control study. Patients: Seventy-one consecutive women were enrolled: 36 with overt hypercortisolism (26 with ACTH-secreting pituitary adenoma and 10 with cortisol-secreting adrenal tumor) and 35 with subclinical hypercortisolism due to adrenal incidentalomas. They were compared with 71 matched controls. Methods: At diagnosis, we measured serum cortisol, FSH, LH, estradiol, testosterone, androstenedione and DHEAS, and urinary cortisol excretion. BMD was determined by dual energy X-ray absorptiometry at the lumbar spine and femoral neck. Vertebral fractures were investigated by a semiquantitative scoring method. Results: Between women with overt and subclinical hypercortisolism BMD values and prevalence of any vertebral (69 vs 57%, PZ0.56), clinical (28 vs 11.4%, PZ0.22), and multiple vertebral fractures (36 vs 31%, PZ0.92) did not differ. Among patients with subclinical hypercortisolism, amenorrhoic women had a lower BMD (PZ0.035) and more frequent vertebral fractures (80 vs 40%; PZ0.043) when compared with the eumenorrhoic ones. Among women with overt hypercortisolism, there was no difference in lumbar BMD (PZ0.37) and prevalence of fractures (81 vs 60%; PZ0.26) between those amenorrhoic and eumenorrhoic. By logistic regression analysis, lumbar spine BMD values and cortisol-to-DHEAS ratio were the best predictors of vertebral fractures (P!0.01). Conclusions: Vertebral fractures are very common in women with endogenous cortisol excess, regardless of its severity. The deleterious effects of hypercortisolism on the spine may be partly counterbalanced by DHEAS increase at any degree of cortisol excess, and by preserved menstrual cycles in women with subclinical but not in those with overt hypercortisolism.

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“…Recently, a subtle cortisol over-production has been described in an increasing number of subjects with incidentally detected adrenal mass without clear clinical signs of cortisol excess (7±16). This pathological entity (subclinical CS) seems to be more frequent than overt CS and a decrease in bone mineral density (BMD) and alterations in bone turnover markers have been previously reported in patients with this disorder (5,6,17).…”

Section: Introductionmentioning

confidence: 93%

Bone loss determined by quantitative ultrasonometry correlates inversely with disease activity in patients with endogenous glucocorticoid excess due to adrenal mass

Tauchmanovà¹,

Rossi²,

Nuzzo³

et al. 2001

European Journal of Endocrinology

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Objective: Glucocorticoid excess is widely recognized as one of the most important causes of bone loss. The mechanism of glucocorticoid-induced osteoporosis is presumably multifactorial, and consists of the loss of organic and non-organic compounds. Efforts have been made to develop simple physical methods for the assessment of bone tissue for the screening of subjects at high risk of osteoporosis, without the use of radioactive sources or ionizing radiation. Quantitative ultrasonometry (QUS) has been suggested as a useful method for monitoring patients undergoing glucocorticoid therapy, which is the most common cause of glucocorticoid excess. QUS appears to detect more structural bone changes than the traditional methods and allows assessment of bone density and elasticity, both characteristics influenced by organic and non-organic bone compounds. However, the use of QUS has not yet been extensively investigated in subjects with endogenous cortisol excess. The aim of this study was to evaluate the usefulness and predictive power of QUS in assessing bone loss in subjects with differing degrees of endogenous cortisol excess due to adrenal mass. Design: Thirty-four patients (20 women and 14 men) aged between 21 and 59 years were evaluated; fifteen (9 women and 6 men; median age, 42 years) were affected by overt Cushing's syndrome (CS) and nineteen (11 women and 8 men; median age, 44 years) by subclinical CS, defined as lacking clinical signs of hormone excess despite the presence of at least two abnormalities in hypothalamic± pituitary±adrenal axis function, as assessed by routine endocrine tests. All women included were eumenorrhoic. Methods: QUS measurement of amplitude-dependent speed of sound was performed on the 2nd to 5th proximal phalanges of the non-dominant hand using a DBM Sonic 1200R bone profiler (Igea S.r.l, Italy). The results were compared with bone density assessed on lumbar vertebrae (L1±L4) and femoral neck sites by dual-energy X-ray absorptiometry (DEXA). Results: A strongly significant bone loss was detected by finger QUS measurement when the patients were considered either all together or as two subgroups P , 0X001, all). The bone density decrease in the fingers was similar to that found at the lumbar spine and femoral neck by the DEXA technique. Lumbar and finger Z-scores correlated inversely with 24 h urinary free cortisol (UFF) excretion P , 0X01, both). Finger Z-scores also correlated inversely with the estimated duration of subclinical CS P , 0X05X Concerning disease activity, only UFF was confirmed by multivariate analysis to be an independent factor influencing bone loss P , 0X05X A positive correlation between the results of the two techniques was found in controls P , 0X05 but not in patients. The lack of correlation between the two techniques in patients can probably be attributed to the different parameters of bone alteration measured by the techniques. Conclusions: The detection of bone loss in subclinical CS similar to that in overt CS suggests that all subjects with endog...

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Evaluation of markers of bone and collagen turnover in patients with active and preclinical Cushing's syndrome and in patients with adrenal incidentaloma

Cited by 73 publications

References 29 publications

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Effects of sex steroids on bone in women with subclinical or overt endogenous hypercortisolism

Bone loss determined by quantitative ultrasonometry correlates inversely with disease activity in patients with endogenous glucocorticoid excess due to adrenal mass

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