Linear growth in relation to the circulating concentrations of insulin-like growth factor I, parathyroid hormone, and 25-hydroxy vitamin D in children with nutritional rickets before and after treatment: endocrine adaptation to vitamin D deficiency

Soliman, Ashraf T.; Khalaf, F. Al; AlHemaidi, Noura; Ali, Maryam Al; Zyoud, Mahmoud; Yakoot, Khaled

doi:10.1016/j.metabol.2007.08.011

Cited by 82 publications

(82 citation statements)

References 31 publications

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“…Thresholds as high as 80 to 90 nmol/L for serum 25(OH)D have been proposed to ensure optimal bone health during growth on the basis of crosssectional studies evaluating the 25(OH)D levels required to keep PTH levels low. (34,35) Our data do not support the hypothesis that elevated PTH levels are a relevant marker of altered bone mass accrual during puberty inasmuch as PTH levels in the highnormal range may favor bone formation and therefore not be detrimental to bone health during growth. (45) Assays of the other bone markers have not been informative in terms of understanding the mechanism(s) underlying the defective mineralization of girls' lumbar spine during late puberty.…”

Section: Discussioncontrasting

confidence: 86%

“…(27)(28)(29) Most clinicians agree that serum 25(OH)D levels below 25 to 30 nmol/L (10 to 12 ng/mL) may lead to nutritional rickets, hypocalcemic convulsions, dental problems, and poor growth in children and adolescents. (30)(31)(32)(33)(34)(35)(36) But the lower threshold of optimal vitamin D status for bone health and calcium homeostasis during growth is still under discussion, with cutoff values proposed from 25 to 30 to 70 to 90 nmol/L in children, (9,10,23,36) as in adults. (12) Differences in the 25(OH)D assays used might explain some discrepancies, especially because results have not been validated systematically using external control assessment schemes.…”

Section: Introductionmentioning

confidence: 99%

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Adverse interaction of low-calcium diet and low 25(OH)D levels on lumbar spine mineralization in late-pubertal girls

Esterle

Nguyen

Walrant-Debray

et al. 2010

Journal of Bone and Mineral Research

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No consensus has been reached on the serum 25-hydroxyvitamin D [25(OH)D] levels required to ensure optimal bone health around menarche. We searched for a possible interaction of 25(OH)D levels and calcium intake on lumbar spine mineralization and on biologic features of bone metabolism in healthy late-pubertal girls. Lumbar spine parameters (ie, area, mineral content, and density) and calcium intake were evaluated in 211 healthy white adolescent girls at pubertal stages IV-V (11 to 16.9 years), together with biologic markers of calcium and bone metabolism and with International External Quality Assessment Scheme for Vitamin D Metabolite (DEQAS)-validated serum 25(OH)D levels. A high prevalence of 25(OH)D levels 30 nmol/L (41%), 40 nmol/L (61%), and 50 nmol/L (70%) was found during winter-spring. Parathyroid hormone (PTH) levels were inversely associated with 25(OH)D levels ( p ¼ .0021). In contrast, lumbar spine mineral content and density were not associated with 25(OH)D, excepted when calcium intake was below 600 mg/day ( p ¼ .0081). Girls with such low calcium intake and 25(OH)D levels of 40 nmol/L or less (9% of the cohort) had a 0.4 to 0.7 SD lower mean areal bone mineral density Z-score than girls with higher calcium intake and/or higher 25(OH)D status. The adverse association between lumbar spine mineralization and combined calcium deficiency-low 25(OH)D levels remained significant in the 91 girls who could be followed over 4 years after their initial evaluation. We conclude that low 25(OH)D levels ( 40 nmol/L) are observed frequently during winterspring in late-pubertal European girls, which may exacerbate the negative impact of calcium deficiency on lumbar spine mineralization. ß

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Section: Discussioncontrasting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Adverse interaction of low-calcium diet and low 25(OH)D levels on lumbar spine mineralization in late-pubertal girls

Esterle

Nguyen

Walrant-Debray

et al. 2010

Journal of Bone and Mineral Research

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“…A significant direct correlation between 25(OH)D and IGF1 levels was found in patients with a 25(OH)D deficiency or severe deficiency. Similarly, Soliman et al [8] demonstrated a direct correlation between 25(OH)D and IGF1 levels, before and after administration of vitamin D, in children with rickets, a disease caused by a severe 25(OH)D deficit. The 25(OH)D-related IGF1 reduction found in DM1 might partially influence muscle metabolism and performance in those patients, although direct nongenomic effects of vitamin D on skeletal muscle mediated by its receptor should be also considered.…”

Section: Discussionmentioning

confidence: 83%

“…Vitamin D receptor has genomic and non-genomic effects, all promoting muscle differentiation and proliferation. Interestingly, one of its genomic actions is through the stimulation of the insulinlike growth factor-1 (IGF1) axis [7]; accordingly, vitamin D administration in children with vitamin D deficiency resulted in an increase of circulating levels of IGF-1 [8].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D deficiency in myotonic dystrophy type 1

et al. 2013

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Myotonic dystrophy type 1 (DM1) is a multisystemic\ud disorder affecting, among others, the endocrine\ud system, with derangement of steroid hormones functions.\ud Vitamin D is a steroid recognized for its role in calcium\ud homeostasis. In addition, vitamin D influences muscle\ud metabolism by genomic and non-genomic actions,\ud including stimulation of the insulin-like-growth-factor 1\ud (IGF1), a major regulator of muscle trophism. To verify\ud the presence of vitamin D deficit in DM1 and its possible\ud consequences, serum 25-hydroxyvitamin D (25(OH)D),\ud calcium, parathormone (PTH), and IGF1 levels were\ud measured in 32 DM1 patients and in 32 age-matched\ud controls. Bone mineral density (BMD) and proximal\ud muscle strength were also measured by DXA and a\ud handheld dynamometer, respectively. In DM1 patients,\ud 25(OH)D levels were reduced compared to controls, and a\ud significant decrease of IGF1 was also found. 25(OH)D\ud levels inversely correlated with CTG expansion size,\ud while IGF1 levels and muscle strength directly correlated\ud with levels of 25(OH)D lower than 20 and 10 ng/ml,\ud respectively. A significantly higher percentage of DM1\ud patients presented hyperparathyroidism as compared to\ud controls. Calcium levels and BMD were comparable\ud between the two groups. Oral administration of cholecalciferol\ud in 11 DM1 patients with severe vitamin D deficiency\ud induced a normal increase of circulating 25(OH)D,\ud ruling out defects in intestinal absorption or hepatic\ud hydroxylation. DM1 patients show a reduction of circulating\ud 25(OH)D, which correlates with genotype and may\ud influence IGF1 levels and proximal muscle strength. Oral\ud supplementation with vitamin D should be considered in\ud DM1 and might mitigate muscle weakness

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“…The 25OH-D3 concentrations were significantly correlated with the IGF-I levels both before and after treatment, and a significant correlation was found between growth velocity after vitamin D treatment and the increase in IGF-I and 25OH-D3 levels. These data denote that accelerated linear growth after treatment of nutritional vitamin D deficiency is mediated through activation of the GH/IGF-I system and suggests an important role of vitamin D as a link between the proliferating cartilage cells of the growth plate and GH/ IGF-I secretion [21]. These data have been confirmed by Ameri et al, who prospectively measured IGF-I levels before and after 12 weeks of treatment with oral vitamin D3 (5000 or 7000 IU/week) vs. no intervention in 39 healthy adults.…”

Section: Vitamin D and Igf-imentioning

confidence: 61%

Vitamin D across growth hormone (GH) disorders: From GH deficiency to GH excess

Ciresi

Giordano

2017

Growth Hormone & IGF Research

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The interplay between vitamin D and the growth hormone (GH)/insulin-like growth factor (IGF)-I system is very complex and to date it is not fully understood. GH directly regulates renal 1 alpha-hydroxylase activity, although the action of GH in modulating vitamin D metabolism may also be IGF-I mediated. On the other hand, vitamin D increases circulating IGF-I and the vitamin D deficiency should be normalized before measurement of IGF-I concentrations to obtain reliable and unbiased IGF-I values. Indeed, linear growth after treatment of nutritional vitamin D deficiency seems to be mediated through activation of the GH/IGF-I axis and it suggests an important role of vitamin D as a link between the proliferating cartilage cells of the growth plate and GH/IGF-I secretion. Vitamin D levels are commonly lower in patients with GH deficiency (GHD) than in controls, with a variable prevalence of insufficiency or deficiency, and this condition may worsen the already known cardiovascular and metabolic risk of GHD, although this finding is not common to all studies. In addition, data on the impact of GH treatment on vitamin D levels in GHD patients are quite conflicting. Conversely, in active acromegaly, a condition characterized by a chronic GH excess, both increased and decreased vitamin D levels have been highlighted, and the interplay between vitamin D and the GH/IGF-I axis becomes even more complicated when we consider the acromegaly treatment, both medical and surgical. The current review summarizes the available data on vitamin D in the main disorders of the GH/IGF-I axis, providing an overview of the current state of the art.

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Linear growth in relation to the circulating concentrations of insulin-like growth factor I, parathyroid hormone, and 25-hydroxy vitamin D in children with nutritional rickets before and after treatment: endocrine adaptation to vitamin D deficiency

Cited by 82 publications

References 31 publications

Adverse interaction of low-calcium diet and low 25(OH)D levels on lumbar spine mineralization in late-pubertal girls

Adverse interaction of low-calcium diet and low 25(OH)D levels on lumbar spine mineralization in late-pubertal girls

Vitamin D deficiency in myotonic dystrophy type 1

Vitamin D across growth hormone (GH) disorders: From GH deficiency to GH excess

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