15 research outputs found

    Vitamin D in adults: update on testing and supplementation

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    Hypovitaminosis D, a frequent condition in adults, is accompanied by adverse skeletal and non-skeletal events. The objective of the present article was to propose an update on the indications and use of vitamin D testing and supplementation in adults. Among healthy middle-aged adults, the serum 25-hydroxyvitamin D (25(OH)D) target concentration is 50 nmol/L. Natural intakes (sun exposure and diet) are sufficient, and there is no indication for systematic blood test or supplementation. In middle-aged adults who are either sick or dependent or frail, natural intakes are generally insufficient but should be encouraged. In this population, the loading phase of the supplementation targets a 25(OH)D concentration of 75 nmol/L, and the pattern of supplementation (200,000 to 400,000 IU orally over 2 months) depends on the measure of circulating 25(OH)D (which is not reimbursed outside the scope defined by the French national authority for health). In adults over 65 years of age, the loading phase of the supplementation should be systematic and targets a concentration of 75 nmol/L (pattern of 300,000 IU orally over 3 months). Regardless of age, the loading phase should be followed by a long-term maintenance phase of supplementation to maintain the 25(OH)D concentration above the target. A measure of serum 25(OH)D is useful after 9 months of supplementation to adjust the frequency or dosage of supplements if necessary

    Parathormone and vitamin D

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    Vitamin D in the elderly: 5 points to remember

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    Vitamin D is a secosteroid hormone. Vitamin D receptors are present in the majority of body tissues. The manifestations of hypovitaminosis D - linked to dysfunction of target tissues - are various, including osteoporosis, cancer, tuberculosis, hypertension, multiple sclerosis, depression, dementia, sarcopenia, propensity to fall... The serum 25-hydroxyvitamin D threshold value to avoid these adverse health events is around 30 ng/mL. Only 15% of the elderly reach this target concentration. For the remaining 85% with no supplements, the severity of hypovitaminosis D appears to be a biomarker of chronic diseases and of frailty. Conversely, the supplementation for correction of hypovitaminosis D positively impacts bone and non-bone morbidities - such as risks of falls and fractures - and reduces the mortality rate. A daily intake of at least 800-1,000 IU supplemental vitamin D(3) per day is the key

    Pubertal origin of growth retardation in inborn errors of protein metabolism: A longitudinal cohort study.

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    Inherited amino-acid metabolism disorders (IAAMDs) require lifelong protein-restricted diet. We aimed to investigate: 1/ whether IAAMDs was associated with growth, pubertal, bone mineral apparent density (BMAD) or body composition impairments; 2/ associations linking height, amino-acid mixture (AAM), plasma amino-acids and IGF1 concentrations. Retrospective longitudinal study of 213 patients with neonatal-onset urea cycle disorders (UCD,n = 77), organic aciduria (OA,n = 89), maple syrup urine disease (MSUD,n = 34), or tyrosinaemia type 1 (n = 13). We collected growth parameters, pubertal status, BMAD, body composition, protein-intake, and IGF1 throughout growth. Overall final height (n = 69) was below target height (TH): -0.9(1.4) vs. -0.1(0.9) SD, p < 0.001. Final height was ≤ TH-2SD in 12 (21%) patients. Height ≤ - 2SD was more frequent during puberty than during early-infancy and pre-puberty: 23.5% vs. 6.9%, p = 0.002; and vs. 10.7%, p < 0.001. Pubertal delay was frequent (26.7%). Height (SD) was positively associated with isoleucine concentration: β, 0.008; 95%CI, 0.003 to 0.012; p = 0.001. In the pubertal subgroup, height (SD) was lower in patients with vs. without AAM supplementation: -1.22 (1.40) vs. -0.63 (1.46) (p = 0.02). In OA, height and median (IQR) isoleucine and valine concentrations(μmol/L) during puberty were lower in patients with vs. without AAM supplementation: -1.75 (1.30) vs. -0.33 (1.55) SD, p < 0.001; and 40 (23) vs. 60 (25) (p = 0.02) and 138 (92) vs. 191 (63) (p = 0.01), respectively. No correlation was found with IGF1. Lean-mass index was lower than fat-mass index: -2.03 (1.15) vs. -0.44 (0.89), p < 0.001. In IAAMDs, growth retardation worsened during puberty which was delayed in all disease subgroups. Height seems linked to the disease, AAM composition and lower isoleucine concentration, independently of the GH-IGF1 pathway. We recommend close monitoring of diet during puberty
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