E Toussirot, N U Nguyen, G Dumoulin, J Regnard, D Wendling
{"title":"强直性脊柱炎患者血清胰岛素样生长因子- 1和胰岛素样生长因子结合蛋白-3水平的变化。","authors":"E Toussirot, N U Nguyen, G Dumoulin, J Regnard, D Wendling","doi":"10.1093/rheumatology/37.11.1172","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Low bone mass, vertebral osteopenia and fractures have been described in patients with ankylosing spondylitis (AS), but the aetiology of this osteoporosis (OP) remains unknown. Insulin-like growth factor-I (IGF-I), a bone-promoting peptide, may be considered as reflecting osteoblast function as well as its main binding protein, insulin-like growth factor binding protein-3 (IGFBP-3). Both were found to be decreased in post-menopausal women and male patients with idiopathic OP. In this study, we aimed to measure the circulating IGF-I and IGFBP-3 in AS patients.</p><p><strong>Methods: </strong>Thirty-three AS patients were compared to 23 healthy controls. Bone mineral density (dual X-ray absorptiometry) was measured at the spine and the femoral neck. We determined the serum levels of growth hormone (GH), insulin, glycaemia, and the IGF-I and IGFBP-3 serum concentrations.</p><p><strong>Results: </strong>A lowered lumbar spine bone mineral density was found in the AS group (AS: 0.946 g/cm2, controls: 1.02 g/cm2; P = 0.05). AS patients had a higher glycaemia than controls, but results were in the normal range. There were no significant differences in the mean values for GH and insulin. Mean IGF-I serum levels were 218.3 ng/ml (+/-72.4) in patients and 212.1 (+/-71.1) in controls (P = 0.75). The serum concentrations of IGFBP-3 were significantly lower in AS (3.29+/-0.6 microg/ml) than in healthy subjects (3.63+/-0.6 microg/ml; P = 0.05). There was a negative correlation between the serum IGFBP-3 concentration and erythrocyte sedimentation rate (r = -0.39; P = 0.025).</p><p><strong>Conclusions: </strong>Since IGFBP-3 is an important cofactor for IGF-I and modulates its bioavailability and activity in bone, these data suggest that osteoblast cell function could be impaired in AS. Inflammation could play a role in this IGFBP-3/IGF-I axis involvement. However, further studies are warranted to determine the role of the other growth factors and their binding proteins in the OP of AS.</p>","PeriodicalId":9307,"journal":{"name":"British journal of rheumatology","volume":"37 11","pages":"1172-6"},"PeriodicalIF":0.0000,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/rheumatology/37.11.1172","citationCount":"27","resultStr":"{\"title\":\"Insulin-like growth factor-I and insulin-like growth factor binding protein-3 serum levels in ankylosing spondylitis.\",\"authors\":\"E Toussirot, N U Nguyen, G Dumoulin, J Regnard, D Wendling\",\"doi\":\"10.1093/rheumatology/37.11.1172\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Low bone mass, vertebral osteopenia and fractures have been described in patients with ankylosing spondylitis (AS), but the aetiology of this osteoporosis (OP) remains unknown. Insulin-like growth factor-I (IGF-I), a bone-promoting peptide, may be considered as reflecting osteoblast function as well as its main binding protein, insulin-like growth factor binding protein-3 (IGFBP-3). Both were found to be decreased in post-menopausal women and male patients with idiopathic OP. In this study, we aimed to measure the circulating IGF-I and IGFBP-3 in AS patients.</p><p><strong>Methods: </strong>Thirty-three AS patients were compared to 23 healthy controls. Bone mineral density (dual X-ray absorptiometry) was measured at the spine and the femoral neck. We determined the serum levels of growth hormone (GH), insulin, glycaemia, and the IGF-I and IGFBP-3 serum concentrations.</p><p><strong>Results: </strong>A lowered lumbar spine bone mineral density was found in the AS group (AS: 0.946 g/cm2, controls: 1.02 g/cm2; P = 0.05). AS patients had a higher glycaemia than controls, but results were in the normal range. There were no significant differences in the mean values for GH and insulin. Mean IGF-I serum levels were 218.3 ng/ml (+/-72.4) in patients and 212.1 (+/-71.1) in controls (P = 0.75). The serum concentrations of IGFBP-3 were significantly lower in AS (3.29+/-0.6 microg/ml) than in healthy subjects (3.63+/-0.6 microg/ml; P = 0.05). There was a negative correlation between the serum IGFBP-3 concentration and erythrocyte sedimentation rate (r = -0.39; P = 0.025).</p><p><strong>Conclusions: </strong>Since IGFBP-3 is an important cofactor for IGF-I and modulates its bioavailability and activity in bone, these data suggest that osteoblast cell function could be impaired in AS. Inflammation could play a role in this IGFBP-3/IGF-I axis involvement. However, further studies are warranted to determine the role of the other growth factors and their binding proteins in the OP of AS.</p>\",\"PeriodicalId\":9307,\"journal\":{\"name\":\"British journal of rheumatology\",\"volume\":\"37 11\",\"pages\":\"1172-6\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1998-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1093/rheumatology/37.11.1172\",\"citationCount\":\"27\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"British journal of rheumatology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/rheumatology/37.11.1172\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"British journal of rheumatology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/rheumatology/37.11.1172","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Insulin-like growth factor-I and insulin-like growth factor binding protein-3 serum levels in ankylosing spondylitis.
Objective: Low bone mass, vertebral osteopenia and fractures have been described in patients with ankylosing spondylitis (AS), but the aetiology of this osteoporosis (OP) remains unknown. Insulin-like growth factor-I (IGF-I), a bone-promoting peptide, may be considered as reflecting osteoblast function as well as its main binding protein, insulin-like growth factor binding protein-3 (IGFBP-3). Both were found to be decreased in post-menopausal women and male patients with idiopathic OP. In this study, we aimed to measure the circulating IGF-I and IGFBP-3 in AS patients.
Methods: Thirty-three AS patients were compared to 23 healthy controls. Bone mineral density (dual X-ray absorptiometry) was measured at the spine and the femoral neck. We determined the serum levels of growth hormone (GH), insulin, glycaemia, and the IGF-I and IGFBP-3 serum concentrations.
Results: A lowered lumbar spine bone mineral density was found in the AS group (AS: 0.946 g/cm2, controls: 1.02 g/cm2; P = 0.05). AS patients had a higher glycaemia than controls, but results were in the normal range. There were no significant differences in the mean values for GH and insulin. Mean IGF-I serum levels were 218.3 ng/ml (+/-72.4) in patients and 212.1 (+/-71.1) in controls (P = 0.75). The serum concentrations of IGFBP-3 were significantly lower in AS (3.29+/-0.6 microg/ml) than in healthy subjects (3.63+/-0.6 microg/ml; P = 0.05). There was a negative correlation between the serum IGFBP-3 concentration and erythrocyte sedimentation rate (r = -0.39; P = 0.025).
Conclusions: Since IGFBP-3 is an important cofactor for IGF-I and modulates its bioavailability and activity in bone, these data suggest that osteoblast cell function could be impaired in AS. Inflammation could play a role in this IGFBP-3/IGF-I axis involvement. However, further studies are warranted to determine the role of the other growth factors and their binding proteins in the OP of AS.
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