{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T18:49:58Z","timestamp":1792694998659,"version":"4.5.0"},"reference-count":28,"publisher":"Walter de Gruyter GmbH","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,3,28]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec id=\"j_jpem-2017-0471_s_999_w2aab3b7c57b1b6b1aab1c15b1Aa\">\n                  <jats:title>Background:<\/jats:title>\n                  <jats:p>Achondroplasia is the most common form of inherited disproportionate short stature. Cross-sectional design studies of height show that, during childhood, height standard deviation scores (SDS) declines steadily and reaches a mean adult height at \u22126.42 and \u22126.72 SDS. However, there is a lack of knowledge about longitudinal growth and biological variables during puberty for children with achondroplasia. Here we report the growth velocity and biological parameters during puberty in children with achondroplasia.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jpem-2017-0471_s_998_w2aab3b7c57b1b6b1aab1c15b2Aa\">\n                  <jats:title>Methods:<\/jats:title>\n                  <jats:p>The study was an observational, cohort study. A total of 23 patients, 15 girls and eight boys with achondroplasia, who reached adult size were included. Growth data was collected from mid-childhood until final height by the same trained observer. Individual growth curves were estimated by fitting the Preece-Baines model 1 (PB1) to each individual\u2019s height for age data. Pubertal development was scored on Tanner scale on each visit.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jpem-2017-0471_s_997_w2aab3b7c57b1b6b1aab1c15b3Aa\">\n                  <jats:title>Results:<\/jats:title>\n                  <jats:p>In boys with achondroplasia the mean adult height was 129.18 cm. Age and velocity at peak velocity in puberty were 13.89 years and 4.86 cm\/year, respectively. The adolescent gain was 20.40 cm. Mean age at genital development 2 and 5 were 12.16 (0.60) and 14.97 (0.88), respectively. In girls the mean adult height was 118.67 cm. Age and velocity at peak velocity in puberty were 11.45 years and 4.40 cm\/year, respectively. The adolescent gain was 19.35 cm. Mean age at breast 2 and 4 were 10.20 (1.24) and 12.49 (1.07), respectively.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jpem-2017-0471_s_996_w2aab3b7c57b1b6b1aab1c15b4Aa\">\n                  <jats:title>Conclusions:<\/jats:title>\n                  <jats:p>Children with achondroplasia experienced an adolescent growth spurt, which was similar in shape and half the magnitude of the non-achondroplasia population.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1515\/jpem-2017-0471","type":"journal-article","created":{"date-parts":[[2018,2,27]],"date-time":"2018-02-27T10:48:39Z","timestamp":1519728519000},"page":"421-428","source":"Crossref","is-referenced-by-count":23,"title":["Growth velocity and biological variables during puberty in achondroplasia"],"prefix":"10.1515","volume":"31","author":[{"given":"Mariana","family":"del Pino","sequence":"first","affiliation":[{"name":"Growth and Development, Pediatric Garrahan Hospital , Combate de los Pozos 1881 , (1245) Buenos Aires , Argentina , Tel.: 00 54 9 11 4122 6221, Fax: 0054 9 11 43085325"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virginia","family":"Fano","sequence":"additional","affiliation":[{"name":"Growth and Development, Pediatric Garrahan Hospital , Buenos Aires , Argentina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paula","family":"Adamo","sequence":"additional","affiliation":[{"name":"Growth and Development, Pediatric Garrahan Hospital , Buenos Aires , Argentina"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"374","published-online":{"date-parts":[[2018,2,21]]},"reference":[{"key":"2021021322311602399_j_jpem-2017-0471_ref_001_w2aab3b7c57b1b6b1ab2b2b1Aa","doi-asserted-by":"crossref","unstructured":"Horton WA, Hall JG, Hecht JT. Achondroplasia. Lancet 2007;370:162\u201372.","DOI":"10.1016\/S0140-6736(07)61090-3"},{"key":"2021021322311602399_j_jpem-2017-0471_ref_002_w2aab3b7c57b1b6b1ab2b2b2Aa","doi-asserted-by":"crossref","unstructured":"Shiang R, Thompson LM, Zhu YZ, Church DM, Fielder TJ, et al. Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia. Cell 1994;78:335\u201342.","DOI":"10.1016\/0092-8674(94)90302-6"},{"key":"2021021322311602399_j_jpem-2017-0471_ref_003_w2aab3b7c57b1b6b1ab2b2b3Aa","unstructured":"Bellus GA, Hefferon TW, Ortiz de Luna RI, Hecht JT, Horton WA, et al. Achondroplasia is defined by recurrent G380R mutations of FGFR3. Am J Hum Genet 1995;56:368\u201373."},{"key":"2021021322311602399_j_jpem-2017-0471_ref_004_w2aab3b7c57b1b6b1ab2b2b4Aa","doi-asserted-by":"crossref","unstructured":"Spranger JW. Achondroplasia. In: Spranger JW, Brill PW, Poznanski A, editors. 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