{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,14]],"date-time":"2023-10-14T06:43:05Z","timestamp":1697265785934},"reference-count":35,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,6,16]],"date-time":"2004-06-16T00:00:00Z","timestamp":1087344000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2004,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold><jats:sc>objective\u2002<\/jats:sc><\/jats:bold> Congenital adrenal hyperplasia (CAH) due to 21\u2010hydroxylase deficiency (21\u2010OHD) is characterized by high androgen levels, ambiguous genitalia or premature pubarche, increased height velocity and skeletal maturation. Considering the possibility of changes in the IGF system components depending on the state of clinical control, the objective of the present study was to analyse serum IGF\u2010I, IGF\u2010II and IGFBP levels in children with 21\u2010OHD under two states of clinical control.<\/jats:p><jats:p><jats:bold><jats:sc>patients and design\u2002<\/jats:sc><\/jats:bold> We studied 12 prepubertal children with 21\u2010OHD CAH aged 4\u00b70\u00a0\u00b1\u00a00\u00b77\u00a0years. They were classified as good (GC) or poor control (PC) based on growth rate, signs of adrenal insufficiency or Cushing syndrome, progression of sexual characteristics and serum androgens levels. Blood samples were obtained from each patient in two different states of clinical control (GC and PC) for biochemical measurements.<\/jats:p><jats:p><jats:bold><jats:sc>measurements\u2002<\/jats:sc><\/jats:bold> IGF\u2010I, IGF\u2010II, IGFBP\u20101, IGFBP\u20102 and IGFBP\u20103 were determined by immunoassays. IGFBPs were also analysed by Western ligand blotting (WLB).<\/jats:p><jats:p><jats:bold><jats:sc>results\u2002<\/jats:sc><\/jats:bold> Levels of IGF\u2010I (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b703) and IGFBP\u20103 (<jats:italic>P<\/jats:italic>\u00a0= 0\u00b701) were higher in GC than in PC while IGFBP\u20101 (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7004) concentrations were lower in GC patients. A trend towards higher levels of IGF\u2010II (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b708) and lower levels of IGFBP\u20102 (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b708) was observed in GC children. Increased IGFBP\u20104 band intensity was observed in GC children (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b703).<\/jats:p><jats:p><jats:bold><jats:sc>conclusion\u2002<\/jats:sc><\/jats:bold> Higher levels of IGF\u2010I, IGFBP\u20103 and IGFBP\u20104, but lower levels of IGFBP\u20101, were associated with better control in children with 21\u2010OHD CAH. These findings are different from those observed in children with other causes of increasing androgens levels and are likely to be related to the insufficient glucocorticoid status.<\/jats:p>","DOI":"10.1111\/j.1365-2265.2004.02075.x","type":"journal-article","created":{"date-parts":[[2004,6,22]],"date-time":"2004-06-22T11:27:09Z","timestamp":1087903629000},"page":"94-101","source":"Crossref","is-referenced-by-count":7,"title":["Different states of clinical control are associated with changes in IGF\u2010I and IGFBPs in children with congenital adrenal hyperplasia due to 21\u2010hydroxylase deficiency"],"prefix":"10.1111","volume":"61","author":[{"given":"Heloisa Marcelina","family":"Cunha","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucila Leico Kagohara","family":"Elias","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cecilia","family":"Camacho\u2010H\u00fcbner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ayrton Cust\u00f3dio","family":"Moreira","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"Jr","given":"Carlos Eduardo","family":"Martinelli","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2004,6,16]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1159\/000023176"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.1990.tb03893.x"},{"key":"e_1_2_6_4_1","doi-asserted-by":"crossref","first-page":"11949","DOI":"10.1016\/S0021-9258(19)49788-3","article-title":"Identification of the forms of insulin\u2010like growth factor\u2010binding proteins produced by human fibroblasts and the mechanisms that regulate their secretion","volume":"267","author":"Camacho\u2010H\u00fcbner C.","year":"1992","journal-title":"Journal of Biological Chemistry"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1159\/000181790"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.87.5.2238"},{"key":"e_1_2_6_7_1","first-page":"140","article-title":"Cortisol increases plasma insulin\u2010like growth factor binding protein\u20101 in humans","volume":"128","author":"Conover C.A.","year":"1993","journal-title":"Acta Endocrinologica"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1210\/en.136.4.1403"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-67-5-882"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2002-020896"},{"key":"e_1_2_6_11_1","doi-asserted-by":"crossref","first-page":"353","DOI":"10.1152\/physrev.1979.59.2.353","article-title":"Inborn errors of steroid biosynthesis","volume":"59","author":"Finkelstein M.","year":"1979","journal-title":"Physiological Reviews"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.81.2.482"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1210\/en.140.12.5579"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1097\/00000441-195909000-00030"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1055\/s-2008-1043931"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1530\/eje.0.1400271"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(19981001)71:1<96::AID-JCB10>3.0.CO;2-G"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(86)90507-5"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.80.10.3059"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2265.1996.711531.x"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1210\/endo-124-3-1576"},{"key":"e_1_2_6_22_1","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1650557"},{"key":"e_1_2_6_23_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.1994.tb03792.x"},{"key":"e_1_2_6_24_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2265.1999.00724.x"},{"key":"e_1_2_6_25_1","first-page":"117A","article-title":"A criterion to define therapeutic control in children with congenital adrenal hyperplasia due to 21\u2010hydroxylase deficiency","volume":"49","author":"Martinelli C.E.","year":"2001","journal-title":"Pediatric Research"},{"key":"e_1_2_6_26_1","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1360525"},{"key":"e_1_2_6_27_1","doi-asserted-by":"crossref","first-page":"277","DOI":"10.1016\/S0889-8529(18)30269-X","article-title":"Congenital adrenal hyperplasia caused by 21\u2010hydroxylase deficiency. 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