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Radiological, biochemical, and hormonal changes in malnourished children with rachitic manifestations
A T Soliman1, E H Madina, M R Morsi
1Department of Pediatrics, Alexandria University Children's Hospital, Egypt.
Insights
Severe malnutrition in children can cause rickets and affect bone health. Decreased insulin-like growth factor-I (IGF-I) during malnutrition may impair bone growth and mineralization, independent of growth hormone (GH) levels.
Area of Science:
- Pediatric Endocrinology
- Nutritional Science
- Skeletal Biology
Background:
- Severe protein-energy malnutrition (PEM) can present with or without rickets.
- Rickets, often linked to vitamin D deficiency, affects bone mineralization.
- Growth hormone (GH) and insulin-like growth factor-I (IGF-I) play roles in bone development.
Purpose of the Study:
- To compare radiological, biochemical, and GH/IGF-I profiles in children with severe PEM and rickets, PEM without rickets, vitamin D-deficient rickets, and healthy controls.
- To investigate the role of GH and IGF-I in bone mineralization in malnourished children with rickets.
Main Methods:
- Evaluated 4 groups of children: PEM with rickets (n=10), PEM without rickets (n=10), vitamin D-deficient rickets (n=10), and healthy controls (n=10).
- Assessed serum calcium, phosphorus, albumin, and alkaline phosphatase (ALP).
- Performed radiological bone assessments and measured basal and stimulated GH and IGF-I levels.
Main Results:
- PEM groups showed decreased calcium, phosphorus, and albumin. Malnourished children with rickets had higher ALP than those without rickets.
- Radiological findings in rickets (demineralization, osteoid, metaphyseal changes) were similar in well-nourished and malnourished groups, but fractures were more common in malnourished children.
- Malnourished children exhibited elevated GH and depressed IGF-I; GH/IGF-I levels were normal in vitamin D-deficient rickets compared to controls.
Conclusions:
- Circulating GH and IGF-I may not be primary factors in bone mineralization in rachitic children.
- Reduced IGF-I production during malnutrition can inhibit epiphyseal growth and contribute to long bone demineralization.
Abstract:
We evaluated the radiological, biochemical and growth hormone (GH)/insulin-like growth factor-I (IGF-I) changes in 10 children with severe protein-energy malnutrition (PEM) who had rachitic manifestations (group 1), 10 children with severe PEM without clinical signs of rickets (group 2), and 10 children with normal body weight-for-length and -age, suffering from vitamin-D-deficiency with signs of florid rickets (group 3) and 10 normal age-matched children (group 4). Serum calcium (Ca2+), phosphorus (PO4), and albumin concentrations were markedly decreased in the two groups with PEM. Malnourished children with rickets had significantly higher serum alkaline phosphatase (ALP) concentrations compared to the malnourished group without rachitic manifestations. Radiological evaluation of the two groups who had rachitic manifestations revealed demineralization of long bones, thinning of the bony cortex, increased formation of osteoid tissue, and metaphyseal changes including cupping, fraying, and flaring. The incidence of these radiological findings did not differ among the well-nourished and the malnourished groups with clinical signs of rickets. However, the incidence of fracture of the shaft was higher (40 per cent) in the malnourished group compared to the well-nourished group (10 per cent) with rickets. In the malnourished group without clinical evidence of rickets, demineralization and cortical thinning was detected in 40 per cent without significant metaphyseal changes. Basal concentrations of GH and peak GH response to clonidine were significantly elevated and IGF-I concentrations were significantly depressed in the malnourished groups v. the other two groups. There were no significant differences in the fasting and the clonidine provoked GH levels or IGF-I concentrations between the rachitic children (group 3) and the normal children. These data suggest that in rachitic children there is not a major role for circulating GH (and by implication IGF-I) on bone mineralization. However, during malnutrition decreased IGF-I production can slow or stop epiphyseal growth and might contribute to the demineralization of the cortex of long bones.