{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T21:59:53Z","timestamp":1781647193192,"version":"3.54.5"},"reference-count":28,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2026,4,10]],"date-time":"2026-04-10T00:00:00Z","timestamp":1775779200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,4,10]],"date-time":"2026-04-10T00:00:00Z","timestamp":1775779200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"name":"Universit\u00e4tsklinikum Ulm"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Mol Cell Pediatr"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Genetic screening for maturity-onset diabetes of the young (MODY) involves sequencing of the coding regions of known disease-associated genes. We describe the complex and challenging diagnostic journey of a patient with early-onset diabetes with a novel, intronic\u00a0\n                      <jats:italic>HNF1A<\/jats:italic>\n                      \u00a0variant likely affecting a branching site.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Case presentation<\/jats:title>\n                    <jats:p>\n                      The patient was diagnosed with diabetes at the age of 10\u00a0years after incidental hyperglycemia (HbA1c 8.1%, C-peptide 3.0\u00a0\u03bcg\/dl), without polyuria, polydipsia, or weight loss. Type 1 diabetes associated autoantibodies were negative, but the patient had a strong family history of early-onset diabetes (classified as type 1 or type 2 diabetes). Initial genetic testing for\u00a0\n                      <jats:italic>HNF4A<\/jats:italic>\n                      ,\u00a0\n                      <jats:italic>GCK<\/jats:italic>\n                      ,\u00a0\n                      <jats:italic>HNF1A<\/jats:italic>\n                      , and\u00a0\n                      <jats:italic>HNF1B<\/jats:italic>\n                      \u00a0coding regions (including exon\/intron boundaries\u2009\u00b1\u200920\u00a0bp) and MLPA were negative. Sulfonylureas provided good glycemic control until age 16, when insulin was added. At age 18, an expanded targeted next-generation sequencing (NGS) panel for MODY was also negative. At age 24, whole-exome-sequencing via NGS and additional analysis was conducted, focusing on synonymous and intronic variants, and revealed a heterozygous\u00a0\n                      <jats:italic>HNF1A<\/jats:italic>\n                      \u00a0variant (c.327-28A\u2009&gt;\u2009G;p.?) in the patient and four affected relatives. The variant co-segregated with diabetes, and was predicted to affect splicing via branching site disruption, suggesting pathogenicity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In summary, this case highlights the importance of a comprehensive diagnostic approach that combines clinical, biochemical, and extended genetic evaluation. When MODY is strongly suspected despite negative targeted testing, broader sequencing\u2014including intronic and regulatory regions\u2014should be pursued. Accurate variant interpretation remains essential to prevent misclassification and to optimize diagnosis, treatment, and understanding of the genetic complexity of monogenic diabetes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s40348-026-00229-0","type":"journal-article","created":{"date-parts":[[2026,4,10]],"date-time":"2026-04-10T09:59:05Z","timestamp":1775815145000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The conundrum in diagnosing Maturity-Onset Diabetes of the Young (MODY) in a large German pedigree with early-onset diabetes and a novel HNF1A variant"],"prefix":"10.1186","volume":"13","author":[{"given":"Eleni Z.","family":"Giannopoulou","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abubakar","family":"Moawia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josef","family":"H\u00f6gel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanna","family":"Lerner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefanie","family":"Zorn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Denzer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Reiner","family":"Siebert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Wabitsch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,10]]},"reference":[{"issue":"4","key":"229_CR1","doi-asserted-by":"publisher","first-page":"670","DOI":"10.1016\/j.ajhg.2020.08.016","volume":"107","author":"S Althari","year":"2020","unstructured":"Althari S, Najmi LA, Bennett AJ, Aukrust I, Rundle JK, Colclough K, Molnes J, Kaci A, Nawaz S, van der Lugt T, Hassanali N, Mahajan A, Molven A, Ellard S, McCarthy MI, Bj\u00f8rkhaug L, Nj\u00f8lstad PR, Gloyn AL (2020) Unsupervised clustering of missense variants in HNF1A using multidimensional functional data aids clinical interpretation. 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