{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T06:26:12Z","timestamp":1787293572020,"version":"build-2736575974"},"reference-count":26,"publisher":"Springer Science and Business Media LLC","issue":"9","license":[{"start":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:00:00Z","timestamp":1779408000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:00:00Z","timestamp":1779408000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J Endocrinol Invest"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>\n                      To estimate the global prevalence of genetic carriers of primary bilateral macronodular adrenal hyperplasia (PBMAH)-associated variants in\n                      <jats:italic>ARMC5<\/jats:italic>\n                      and\n                      <jats:italic>KDM1A<\/jats:italic>\n                      using a large genomic database.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We analyzed sequencing data from 807,162 unrelated individuals in gnomAD v4.1. Two prespecified variant-selection strategies were applied. Strict criteria included\n                      <jats:italic>ARMC5<\/jats:italic>\n                      and\n                      <jats:italic>KDM1A<\/jats:italic>\n                      variants classified as pathogenic\/likely pathogenic (P\/LP) in ClinVar\/LOVD and germline P\/LP variants reported in the literature. Liberal criteria included all strict variants plus rare predicted deleterious variants (nonsense, frameshift, loss of start codon and splice-disrupting variants predicted to be deleterious by in silico analysis) and PBMAH-reported somatic\n                      <jats:italic>ARMC5<\/jats:italic>\n                      variants from the literature as candidate germline susceptibility alleles. Carrier prevalence was estimated by aggregating allele frequencies of qualifying variants overall and by ancestry.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      For\n                      <jats:italic>ARMC5<\/jats:italic>\n                      , estimated carrier prevalence was 37.5\/100,000 under strict criteria and 64.1\/100,000 under liberal criteria. Prevalence varied by ancestry, highest in East Asian individuals (strict: 111.4\/100,000; liberal: 173.7\/100,000) and lowest in Middle Eastern (strict: 0; liberal: 33.0\/100,000) and Ashkenazi Jewish groups (strict: 6.8; liberal: 27.0\/100,000). For\n                      <jats:italic>KDM1A<\/jats:italic>\n                      , only three variants met strict criteria; liberal criteria yielded an estimated carrier prevalence of 33.8\/100,000, highest in Middle Eastern (66.0\/100,000) and lowest in Finnish (6.2\/100,000). Several variants were enriched in specific ancestries (e.g.,\n                      <jats:italic>ARMC5<\/jats:italic>\n                      p.Arg454Trp in East Asians;\n                      <jats:italic>ARMC5<\/jats:italic>\n                      p.Arg879Trp and\n                      <jats:italic>KDM1A<\/jats:italic>\n                      p.Arg196AsnfsTer6 in non-Finnish Europeans).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Population-scale data suggest PBMAH genetic susceptibility due to\n                      <jats:italic>ARMC5<\/jats:italic>\n                      and\n                      <jats:italic>KDM1A<\/jats:italic>\n                      variants may be more common than implied by clinical series and differs across ancestries, underscoring the need for improved variant curation and phenotype-linked studies.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s40618-026-02920-5","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T07:50:38Z","timestamp":1779436238000},"page":"2291-2303","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Global prevalence of genetic carriers for ARMC5- and KDM1A-associated primary bilateral macronodular adrenal hyperplasia: insights from a large multiethnic genomic database"],"prefix":"10.1007","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6501-6180","authenticated-orcid":false,"given":"Nipith","family":"Charoenngam","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taweesak","family":"Wannachalee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,22]]},"reference":[{"issue":"11","key":"2920_CR1","doi-asserted-by":"publisher","first-page":"699","DOI":"10.1038\/s41574-022-00718-y","volume":"18","author":"IP Cavalcante","year":"2022","unstructured":"Cavalcante IP, Berthon A, Fragoso MC, Reincke M, Stratakis CA, Ragazzon B, Bertherat J (2022) Primary bilateral macronodular adrenal hyperplasia: definitely a genetic disease. 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