Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Radiological, biochemical, and hormonal changes in malnourished children with rachitic manifestations. 882 Jun 18

Growth retardation in children with thalassaemia major is multifactorial. We studied the growth hormone (GH) response to provocation by clonidine and glucagon, measured the circulating concentrations of insulin, insulin-like growth factor-I (IGF-I), IGF-binding protein-3 (IGFBP3), and ferritin, and evaluated the spontaneous nocturnal (12 h) GH secretion in prepubertal patients with thalassaemia and age-matched children with constitutional short stature (CSS) (height SDS < -2, but normal GH response to provocation). The anatomy of the hypothalamic pituitary area was studied in patients with abnormal GH secretion using MRI scanning. Children with thalassaemia had significantly lower peak GH response to provocation by clonidine and glucagon (8.8 +/- 2.3 micrograms/l and 8.2 +/- 3.1 micrograms/l respectively) than did controls (17.6 +/- 2.7 micrograms/l and 15.7 +/- 3.7 micrograms/l respectively). They had significantly decreased circulating concentrations of IGF-I and IGFBP3 (68.5 +/- 19 ng/ml and 1.22 +/- 0.27 mg/l respectively) compared to controls (153 +/- 42 ng/ml and 2.16 +/- 0.37 mg/l respectively). Seven of the thalassaemic children had a GH peak response of < 7 micrograms/l after provocation. Those with a normal GH response after provocation also had significantly lower IGF-I and IGFBP3 concentrations than controls. Analysis of their spontaneous nocturnal GH secretion revealed lower mean (2.9 +/- 1.77 micrograms/l) and integrated (2.53 +/- 1.6 micrograms/l) concentrations compared to controls (4.9 +/- 0.29 micrograms/l and 5.6 +/- 0.52 micrograms/l respectively). Five of them had mean nocturnal GH concentration < 2 micrograms/l and four had maximum nocturnal peak below 10 micrograms/l. These data denoted defective spontaneous GH secretion in some of these patients. MRI studies revealed complete empty sella (n = 2), marked diminution of the pituitary size (n = 4), thinning of the pituitary stalk (n = 3) with its posterior displacement (n = 2), and evidence of iron deposition in the pituitary gland and midbrain (n = 7) in those patients with defective GH secretion (n = 9). Serum ferritin concentration was correlated significantly with the circulating IGF-I (r = -0.47, p < 0.01) and IGFBP3 (r = -0.43, p < 0.01) concentrations. These data prove a high prevalence of defective GH secretion in thalassaemic children associated with structural abnormality of their pituitary gland.
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PMID:Spontaneous and provoked growth hormone (GH) secretion and insulin-like growth factor I (IGF-I) concentration in patients with beta thalassaemia and delayed growth. 1066 1