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Since the clinical phenotype of MFS is highly heterogeneous, with certain symptoms appearing as children age, the diagnostic process and establishing a genotype-phenotype association in childhood MFS can be challenging. The lack of sufficient childhood studies also makes it difficult to interpret the subject. This study aims to evaluate the relationship between clinical symptoms used as diagnostic criteria and <jats:italic>FBN1<\/jats:italic> variations in children with MFS. This study investigated the relationships between genotypes and phenotypes in 131 children suspected of having Marfan syndrome (MFS). Diagnosis of MFS was made according to the revised Ghent nosology. <jats:italic>FBN1<\/jats:italic> variants were categorized based on exon regions, type of variant, and pathogenicity classes. These <jats:italic>FBN1<\/jats:italic> variants were then correlated with the clinical manifestations including cardiovascular, ocular, facial, and skeletal abnormalities. Out of the children, 43 were diagnosed with MFS. <jats:italic>FBN1<\/jats:italic> variant was identified in 32 (74.4%) of the MFS children. MFS diagnosis could not be made in five (15.6%) <jats:italic>FBN1<\/jats:italic> variant-positive children. The most common cardinal finding is cardiac anomalies <jats:italic>n<\/jats:italic>\u2009=\u200938 (88.3%). The most common <jats:italic>FBN1<\/jats:italic> pathogenic variant was c.1786\u00a0T\u2009&gt;\u2009C\/p.Cys596Arg <jats:italic>n<\/jats:italic>\u2009=\u20094 (12.5%). The distribution of pathogenic variants was as follows: 29 (90.6%) missense, 2 (6.3%) frameshift, and 1 (3.1%) nonsense. The numbers of AD and EL of the variant-positive children were 16 (50%) and 14 (43.7%), respectively. Ocular abnormalities were more common in children with <jats:italic>FBN1-<\/jats:italic>positive MFS (<jats:italic>p<\/jats:italic>\u2009=\u20090.009). There was no difference in the number of cardiac abnormalities between <jats:italic>FBN1<\/jats:italic>-positive and <jats:italic>FBN1<\/jats:italic>-negative MFS patients (<jats:italic>p<\/jats:italic>\u2009=\u20090.139).<\/jats:p><jats:p>\u00a0 \u00a0<jats:italic>Conclusion<\/jats:italic>: This study examines the relationship between <jats:italic>FBN1<\/jats:italic> variants and clinical features used as diagnostic criteria in MFS children. The findings emphasize the importance of long-term monitoring of heterogeneous clinical phenotypes and bioinformatic reanalysis in determining the genotype-phenotype relationship in children, as MFS symptoms can vary with age.<\/jats:p><jats:p><jats:table-wrap><jats:table><jats:tbody>\n                    <jats:tr>\n                      <jats:td colspan=\"2\"><jats:bold>What is Known:<\/jats:bold><jats:italic>\u2022 Marfan syndrome has highly variable phenotypic heterogeneity.<\/jats:italic><jats:italic>\u2022 The genotype-phenotype relationship in childhood Marfan syndrome is not clear enough due to the variation in the time of onset of the findings.<\/jats:italic><\/jats:td>\n                    <\/jats:tr>\n                    <jats:tr>\n                      <jats:td colspan=\"2\"><jats:bold>What is New:<\/jats:bold><jats:italic>\u2022 This article provides regional data for the field of research on genotype-phenotype relationships in childhood Marfan syndrome.<\/jats:italic><jats:italic>\u2022 Long-term follow-up of clinical findings and bioinformatics reanalysis is an important requirement for a well-established genotype-phenotype relationship in childhood Marfan syndrome.<\/jats:italic><\/jats:td>\n                    <\/jats:tr>\n                  <\/jats:tbody><\/jats:table><\/jats:table-wrap><\/jats:p>","DOI":"10.1007\/s00431-024-05579-3","type":"journal-article","created":{"date-parts":[[2024,5,3]],"date-time":"2024-05-03T15:42:16Z","timestamp":1714750936000},"page":"3219-3232","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genotype and clinical phenotype of children with Marfan syndrome in Southeastern Anatolia"],"prefix":"10.1007","volume":"183","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2861-3568","authenticated-orcid":false,"given":"Murat","family":"Karaoglan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8512-8833","authenticated-orcid":false,"given":"Gulper","family":"Nacarkahya","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8385-4049","authenticated-orcid":false,"given":"Emel Hatun","family":"Aytac","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5544-8991","authenticated-orcid":false,"given":"Mehmet","family":"Keskin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2024,5,3]]},"reference":[{"issue":"1","key":"5579_CR1","doi-asserted-by":"publisher","first-page":"279","DOI":"10.1016\/j.gene.2016.07.033","volume":"591","author":"LY Sakai","year":"2016","unstructured":"Sakai LY, Keene DR, Renard M, De Backer J (2016) FBN1: the disease-causing gene for Marfan syndrome and other genetic disorders. 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All the procedures carried out in the research with the participation of humans were in compliance with the ethical standards of the National Research Ethics Committee and with the Helsinki Declaration of 1964 and its subsequent changes or with comparable ethics standards. The study was approved by the Gaziantep University Clinical Research Ethics Committee.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethical approval"}},{"value":"Informed voluntary consent was obtained from every participant of the study\".","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent to participate"}},{"value":"The authors declare no competing interests.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflict of interest"}}]}}