{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T11:15:17Z","timestamp":1790680517795,"version":"4.1.0"},"reference-count":31,"publisher":"The Endocrine Society","issue":"12","license":[{"start":{"date-parts":[[2020,9,7]],"date-time":"2020-09-07T00:00:00Z","timestamp":1599436800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Wellcome Trust Senior Investigator","award":["098395\/Z\/12\/Z"],"award-info":[{"award-number":["098395\/Z\/12\/Z"]}]},{"name":"Diabetes UK RD Lawrence Fellow","award":["19\/005971"],"award-info":[{"award-number":["19\/005971"]}]},{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000288","name":"Royal Society","doi-asserted-by":"publisher","award":["105636\/Z\/14\/Z"],"award-info":[{"award-number":["105636\/Z\/14\/Z"]}],"id":[{"id":"10.13039\/501100000288","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Biallelic mutations in the PTF1A enhancer are the commonest cause of isolated pancreatic agenesis. These patients do not have severe neurological features associated with loss-of-function PTF1A mutations. Their clinical phenotype and disease progression have not been well characterized.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>To evaluate phenotype and genotype characteristics and long-term follow-up of patients with PTF1A enhancer mutations.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Setting<\/jats:title>\n                  <jats:p>Twelve tertiary pediatric endocrine referral centers.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Patients<\/jats:title>\n                  <jats:p>Thirty patients with diabetes caused by PTF1A enhancer mutations. Median follow-up duration was 4 years.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcome Measures<\/jats:title>\n                  <jats:p>Presenting and follow-up clinical (birthweight, gestational age, symptoms, auxology) and biochemical (pancreatic endocrine and exocrine functions, liver function, glycated hemoglobin) characteristics, pancreas imaging, and genetic analysis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Five different homozygous mutations affecting conserved nucleotides in the PTF1A distal enhancer were identified. The commonest was the Chr10:g.23508437A&amp;gt;G mutation (n\u2005=\u200518). Two patients were homozygous for the novel Chr10:g.23508336A&amp;gt;G mutation. Birthweight was often low (median SDS\u2005=\u2005\u20133.4). The majority of patients presented with diabetes soon after birth (median age of diagnosis: 5 days). Only 2\/30 presented after 6 months of age. All patients had exocrine pancreatic insufficiency. Five had developmental delay (4 mild) on long-term follow-up. Previously undescribed common features in our cohort were transiently elevated ferritin level (n\u2005=\u200512\/12 tested), anemia (19\/25), and cholestasis (14\/24). Postnatal growth was impaired (median height SDS: \u20132.35, median BMI SDS: \u20130.52 SDS) with 20\/29 (69%) cases having growth retardation.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>We report the largest series of patients with diabetes caused by PTF1A enhancer mutations. Our results expand the disease phenotype, identifying recurrent extrapancreatic features which likely reflect long-term intestinal malabsorption.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgaa613","type":"journal-article","created":{"date-parts":[[2020,9,7]],"date-time":"2020-09-07T11:24:04Z","timestamp":1599477844000},"page":"e4351-e4359","source":"Crossref","is-referenced-by-count":17,"title":["Clinical Characteristics and Long-term Follow-up of Patients with Diabetes Due To <i>PTF1A<\/i> Enhancer Mutations"],"prefix":"10.1210","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6374-5884","authenticated-orcid":false,"given":"Huseyin","family":"Demirbilek","sequence":"first","affiliation":[{"name":"Hacettepe University Faculty of Medicine, Department of Pediatric Endocrinology, Ankara, Turkey"},{"name":"Diyarbak\u0131r Children\u2019s Hospital, Clinics of Pediatric Endocrinology, Diyarbakir, 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