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Serum 25-hydroxyvitamin D in infantile rickets
Insights
Serum 25-hydroxyvitamin D (25-OH-D) levels decrease with the severity of vitamin D deficiency in children. Familial hypophosphatemia patients showed normal 25-OH-D levels, suggesting parathyroid hormone
Area of Science:
- Pediatric Endocrinology
- Nutritional Biochemistry
- Metabolic Bone Disease
Background:
- Nutritional vitamin D deficiency is a common concern in pediatric populations.
- 25-hydroxyvitamin D (25-OH-D) is the primary indicator of vitamin D status.
- Understanding 25-OH-D dynamics is crucial for managing deficiency-related conditions.
Purpose of the Study:
- To correlate serum 25-hydroxyvitamin D concentrations with the clinical stages of nutritional vitamin D deficiency in children.
- To investigate 25-OH-D levels in children with familial hypophosphatemia.
- To explore the potential role of parathyroid hormone in 25-OH-D depletion.
Main Methods:
- Serum 25-OH-D levels were measured in pediatric patients.
- Clinical disease staging was performed for nutritional vitamin D deficiency.
- Comparison of 25-OH-D levels between deficient children, familial hypophosphatemia patients, and healthy controls.
Main Results:
- Serum 25-OH-D was low but within normal limits in the early hypocalcemic stage of deficiency (16-20 ng/ml).
- 25-OH-D levels decreased further (<15 ng/ml) in advanced stages of vitamin D deficiency.
- Children with familial hypophosphatemia exhibited normal serum 25-OH-D concentrations, similar to controls.
Conclusions:
- Serum 25-OH-D concentration is a valuable biomarker that reflects the severity of nutritional vitamin D deficiency in children.
- Familial hypophosphatemia appears to have a different pathophysiology regarding vitamin D metabolism compared to nutritional deficiency.
- Endogenous parathyroid hormone may contribute to the reduction of serum 25-OH-D in deficiency states.
Abstract:
In small children with nutritional vitamin D deficiency, the serum concentration of 25-hydroxyvitamin D (25-OH-D), the major circulating metabolite of vitamin D, was correlated with the stage of clinical disease. It was low (16 to 20 ng/ml) but within the normal range in the earliest (hypocalcemic) stage of the deficiency syndrome and decreased (less than 15 ng/ml) in the more advanced stages. In patients with familial hypophosphatemia (X-linked dominant), mean serum 25-OH-D concentration was the same as in age-matched normal controls. Evidence is presented that endogenous parathyroid hormone may have a role in the depletion of serum 25-OH0D in deficiency states.
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