MARKERS OF BONE METABOLISM IN EUGONADAL FEMALE PATIENTS WITH Β-Thalassemia MAJOR

Angelopoulos, Nicholas; Goula, Anastasia; Katounda, Eugenia; Rombopoulos, Grigorios; Kaltzidou, Victoria; Kaltsas, Dimitrios; Konstandelou, Evangellia; Tolis, G.

doi:10.1080/08880010701533611

Cited by 11 publications

(10 citation statements)

References 21 publications

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“…At molecular level, although osteoblast dysfunction is considered to be the main pathogenetic mechanism (19), recent evidence has demonstrated that anemia, through stimulation of erythropoietin and subsequent bone marrow expansion, also increases expression of RANKL and thus promotes activation of osteoclast activity (21,25). In accordance with previous studies (20,26) bone resorption marker b-CTX was found significantly increased at baseline compared with the control group. In addition, P1NP but not osteocalcin was also found increased in these patients, reflecting increased bone turnover.…”

Section: Discussionsupporting

confidence: 79%

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Yavropoulou¹,

Tomos²,

Tsekmekidou³

et al. 2011

European Journal of Endocrinology

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Objective: Postprandial suppression of bone resorption is considered one of the main contributors in the circadian rhythm of bone turnover markers. The aim of this study was to investigate this physiological response of bone tissue in diseases that affect bone metabolism. Patients and methods: In this study, 118 patients (45 hypothyroid, 40 hyperthyroid, and 33 b-thalassemic patients) and 78 healthy individuals matched for age and body mass index were included. An oral glucose test (75 g glucose) was performed after overnight fasting. Serum levels of procollagen type-I N-terminal propeptide (P1NP), b-C-terminal telopeptide of type I collagen (b-CTX), and osteocalcin were assayed at 0, 60, and 120 min. Results: Baseline values of bone turnover markers were significantly elevated in hyperthyroid and b-thalassemic patients but not in hypothyroid patients compared with the control group. After oral glucose, the levels of b-CTX but not P1NP or osteocalcin were significantly suppressed in all groups (mean change from baseline is 46.9% for b-CTX, 7.9% for P1NP, and 8% for osteocalcin). The percentage change from baseline for b-CTX was significantly augmented in hypothyroidism (52 vs 42%, PZ0.009). Conclusion: The preservation or even augmentation of postprandial suppression of bone resorption in diseases that affect bone metabolism through distinct pathogenetic mechanisms suggests the importance of this physiological response to nutrients for the general homeostasis and functional integrity of the skeleton.

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Section: Discussionsupporting

confidence: 79%

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Yavropoulou¹,

Tomos²,

Tsekmekidou³

et al. 2011

European Journal of Endocrinology

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“…6,18 Accordingly, elevated markers of bone resorption have been found in TM subjects. 14,36 Endocrinopathies are common in TM patients, and these may also contribute to osteopenia-OP syndrome, particularly hypogonadotrophic hypogonadism. 37 Anti-resorption therapies, such as bisphosphonates in combination with hormone replacement regimens, lead to improvements in bone integrity in thalassemic patients.…”

Section: Discussionmentioning

confidence: 99%

Iron overload causes osteoporosis in thalassemia major patients through interaction with transient receptor potential vanilloid type 1 (TRPV1) channels

et al. 2014

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“…Most have reported increased bone resorption (serum CTx, urinary NTx, deoxypyridinoline) [1,10,34,35,36], with and without decreases in bone formation markers (bone specific alkaline phosphatase, osteocalcin) [1,32-35]. In 2003, Domrongkitchaiporn et al analyzed iliac crest bone biopsies and markers of bone turnover in 18 adult patients with thalassemia.…”

Section: 0 Discussionmentioning

confidence: 99%

“…Many factors contribute to the etiology of low bone mass including: ineffective erythropoiesis which leads to bone marrow hyperplasia [6], growth hormone and sex steroid deficiencies [1,2], hypothyroidism [7], vitamin D deficiency [8], and severe anemia [6,9] with presumed, but poorly characterized reduced physical activity. Even well transfused patients with normal gonadal function who are supplemented with calcium have been shown to have low bone mass by dual x-ray absorptiometry (DXA) [1,10], suggesting other factors are also involved.…”

Section: 0 Introductionmentioning

confidence: 99%

Characterization of low bone mass in young patients with thalassemia by DXA, pQCT and markers of bone turnover

Fung¹,

Vichinsky²,

Kwiatkowski

et al. 2011

Bone

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Previous reports using dual x-ray absorptiometry (DXA) suggest that up to 70% of adults with thalassemia major (Thal) have low bone mass. However, few studies have controlled for body size and pubertal delay, variables known to affect bone mass in this population. In this study, bone mineral content and areal density (BMC, aBMD) of the spine and whole body were assessed by DXA, and volumetric BMD and cortical geometries of the distal tibia by peripheral quantitative computed tomography (pQCT) in subjects with Thal (n=25, 11 male, 10 to 30 yrs) and local controls (n=34, 15 male, 7 to 30 yrs). Z-scores for bone outcomes were calculated from reference data from a large sample of healthy children and young adults. Fasting blood and urine were collected, pubertal status determined by self-assessment and dietary intake and physical activity assessed by written questionnaires. Subjects with Thal were similar in age, but had lower height, weight and lean mass index Z-scores (all p<0.001) compared to controls. DXA aBMD was significantly lower in Thal compared to controls at all sites. Adult Thal subjects (>18 yrs, n=11) had lower tibial trabecular vBMD (p=0.03), cortical area, cortical BMC, cortical thickness, periosteal circumference and section modulus Z-scores (all p<0.01) compared to controls. Cortical area, cortical BMC, cortical thickness, and periosteal circumference Z-scores (p=0.02) were significantly lower in young Thal (≤18 yrs, n=14) compared to controls. In separate multivariate models, tibial cortical area, BMC, and thickness and spine aBMD and whole body BMC Z-scores remained lower in Thal compared to controls after adjustment for gender, lean mass and/or growth deficits (all p<0.01). Tanner stage was not predictive in these models. Osteocalcin, a marker of bone formation, was significantly reduced in Thal compared to controls after adjusting for age, puberty and whole body BMC (p=0.029). In summary, we have found evidence of skeletal deficits that cannot be dismissed as an artifact of small bone size or delayed maturity alone. Given that reduced bone density and strength are associated with increased risk of fracture, therapies focused on increasing bone formation and bone size in younger patients are worthy of further evaluation.

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MARKERS OF BONE METABOLISM IN EUGONADAL FEMALE PATIENTS WITH Β-Thalassemia MAJOR

Cited by 11 publications

References 21 publications

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Iron overload causes osteoporosis in thalassemia major patients through interaction with transient receptor potential vanilloid type 1 (TRPV1) channels

Characterization of low bone mass in young patients with thalassemia by DXA, pQCT and markers of bone turnover

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