Abstract
The hypothesis of a defect in growth hormone (GH) binding has been suggested to explain the growth failure of thalassemic children. We have measured GH binding sites in membrane fractions prepared from liver biopsies. 6 girls and 11 boys with thalassemia major, aged 3 to 15, all prepubertal, were studied at the time of splenectomy. A liver biopsy was performed for histological studies. Part of it (about 500 mg wet weight) was used to prepare a microsomal membrane fraction. Specific binding of 125I-hGH (human GH) expressed in percentage of total radioactivity per mg membrane protein ranged from 4 to 51%. Activities of 2 other membrane markers varied much less than hGH binding: the range of insulin binding was 93-179% of total radioactivity per mg membrane protein and the ratio hGH binding/5'nucleotidase activity varies in the same proportion (10 fold) as does the binding of hGH. Histological hepatic changes were assessed with respect to siderosis, fibrosis, inflammation and necrosis. No correlation was found between these parameters and hGH binding. All patients had retarded growth (mean SDS of -2.6) and no relationship was found between the growth failure and the level or hGH binding. Maximum plasma GH peak during 2 pharmacological tests was normal in 13 children, low in 2, not obtained in 2. Plasma IGF-1 levels were low (mean 170±36 mu/ml). In conclusion: 1) Specific hGH binding to liver microsomal membranes was observed and showed Creat variations; 2) Insulin and hGH binding to liver membranes do not show parallel changes, which suggests that possible membrane alterations are not the only reason for the variations in hGH binding: 3) Plasma IGF-I levels were not related to GH binding. Thus, a defect in GH binding to liver membranes is probably not the main cause for the growth retardation of thalassemic children.
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Postel-Vinay, M., Girot, R., Leger, J. et al. NO EVIDENCE FOR A DEFECT IN GROWTH HORMONE BINDING TO LIVER MEMBRANES OF THALASSEMIC CHILDREN. Pediatr Res 23, 105 (1988). https://doi.org/10.1203/00006450-198801000-00024
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DOI: https://doi.org/10.1203/00006450-198801000-00024
