{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:20:58Z","timestamp":1791937258974,"version":"4.3.4"},"reference-count":130,"publisher":"Wiley","issue":"23","license":[{"start":{"date-parts":[[2006,7,12]],"date-time":"2006-07-12T00:00:00Z","timestamp":1152662400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J of Med Genetics Pt A"],"published-print":{"date-parts":[[2006,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Hutchinson\u2013Gilford progeria syndrome (HGPS) is a rare but well known entity characterized by extreme short stature, low body weight, early loss of hair, lipodystrophy, scleroderma, decreased joint mobility, osteolysis, and facial features that resemble aged persons. Cardiovascular compromise leads to early demise. Cognitive development is normal. Data on 10 of our own cases and 132 cases from literature are presented. The incidence in the last century in the Netherlands was 1:4,000,000. Sex ratio was 1.2:1. Main first symptoms were failure to thrive (55%), hair loss (40%), skin problems (28%), and lipodystrophy (20%). Mean age at diagnosis was 2.9 years. Growth in weight was more disturbed than growth in height, and growth delay started already prenatally. Mean height\u2009&gt;\u200913 years was 109.0 cm, mean weight was 14.5 kg. Osteolysis was wide\u2010spread but not expressed, except in the viscerocranium, and remained limited to membranous formed bone. Lipodystrophy is generalized, only intra\u2010abdominal fat depositions remain present. Cardiovascular problems are extremely variable, both in age of onset and nature. Stroke and coronary dysfunctioning are most frequent. Pathologic findings in coronaries and aorta resemble sometimes the findings in elderly persons, but can also be much more limited. Loss of smooth muscle cells seems the most important finding. Mean age of demise was 12.6 years. Patients can be subdivided in patients with classical HGPS, which follows an autosomal dominant pattern of inheritance, (almost) all cases representing spontaneous mutations, and in non\u2010classical progeria, in whom growth can be less retarded, scalp hair remains present for a longer time, lipodystrophy is more slowly progressive, osteolysis is more expressed except in the face, and survival well into adulthood is not uncommon. Pattern of inheritance of non\u2010classical progeria is most probably autosomal recessive. The cause of HGPS is an abnormally formed Lamin A, either directly by a mutated\n                    <jats:italic>LMNA<\/jats:italic>\n                    gene, or through abnormal posttranslational processing (\n                    <jats:italic>ZMPSTE24<\/jats:italic>\n                    gene mutations). Of 34\n                    <jats:italic>LMNA<\/jats:italic>\n                    mutations found in progeria patients, there were 26 classical p.G608G mutations (76%). Pathogenesis is most likely to follow several different pathways. Potential therapeutic strategies are developed along these lines and include RNA interference techniques and inhibition of the dominant\u2010negative influence of abnormally formed Lamin A on polymerization with normally formed Lamin A. \u00a9 2006 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/ajmg.a.31346","type":"journal-article","created":{"date-parts":[[2006,7,12]],"date-time":"2006-07-12T18:10:21Z","timestamp":1152727821000},"page":"2603-2624","source":"Crossref","is-referenced-by-count":499,"title":["Hutchinson\u2013Gilford progeria syndrome: Review of the phenotype"],"prefix":"10.1002","volume":"140A","author":[{"given":"Raoul C.M.","family":"Hennekam","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,7,12]]},"reference":[{"key":"e_1_2_20_2_1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1080\/pdp.21.1.1.13","article-title":"Hutchinson\u2013Gilford Progeria syndrome: A pathologic study","volume":"21","author":"Ackerman J","year":"2002","journal-title":"Pediatr Pathol Molec Med"},{"key":"e_1_2_20_3_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddg213"},{"key":"e_1_2_20_4_1","doi-asserted-by":"publisher","DOI":"10.5144\/0256-4947.1995.631"},{"key":"e_1_2_20_5_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM195406242502503"},{"key":"e_1_2_20_6_1","first-page":"384","article-title":"Cardiovascular abnormalities in Progeria","volume":"105","author":"Baker PB","year":"1981","journal-title":"Arch Pathol Lab Med"},{"key":"e_1_2_20_7_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-263X.2002.00401.x"},{"key":"e_1_2_20_8_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.192460799"},{"key":"e_1_2_20_9_1","first-page":"164","article-title":"Progeria with unusual ocular manifestations: Report of a case with a review of the literature","volume":"2","author":"Bhakoo ON","year":"1964","journal-title":"Indian Pediatr"},{"key":"e_1_2_20_10_1","first-page":"945","article-title":"Progeria","volume":"34","author":"Biswas AC","year":"1997","journal-title":"Indian Pediatr"},{"key":"e_1_2_20_11_1","first-page":"786","article-title":"Progeria. 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