RADIOLOGICAL, BIOCHEMICAL, AND HORMONAL CHANGES IN MALNOURISHED CHILDREN WITH RACHITIC MANIFESTATIONS

We evaluated the radiological, biochemical and growth hormone (GH)/ins ulin-like growth factor-I (IGF-I) changes in 10 children with severe p rotein-energy malnutrition (PEM) who had rachitic manifestations (grou p 1), 10 children with severe PEM without clinical signs of rickets (g roup 2), and 10 children with normal body weight-for-length and -age, suffering from vitamin-D-deficiency with signs of florid rickets (grou p 3) and 10 normal age-matched children (group 4). Serum calcium (Ca2), phosphorus (PO4), and albumin concentrations,were markedly decrease d in the two groups with PEM. Malnourished children with rickets had s ignificantly higher serum alkaline phosphatase (ALP) concentrations co mpared to the malnourished group without rachitic manifestations. Radi ological 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 includi ng 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 fract ure of the shaft was higher (40 per cent) in the malnourished group co mpared to the well-nourished group (10 per cent) with rickets. In the malnourished group without clinical evidence of rickets, demineralizat ion and cortical thinning was detected in 40 per cent without signific ant metaphyseal changes. Basal concentrations of GH and peak GH respon se to clonidine were significantly elevated and IGF-I concentrations w ere significantly depressed in the malnourished groups v. the other tw o groups. There were no significant differences in the fasting and the clonidine provoked GH levels or IGF-I concentrations between the rach itic children (group 3) and the normal children. These data suggest th at in rachitic children there is not a major role for circulating GH ( and by implication IGF-I) on bone mineralization. However, during maln utrition decreased IGF-I production can slow or stop epiphyseal growth and might contribute to the demineralization of the cortex of long bo nes.