{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T04:09:13Z","timestamp":1781064553174,"version":"3.54.1"},"reference-count":58,"publisher":"The Endocrine Society","issue":"1","funder":[{"DOI":"10.13039\/100000038","name":"US Food and Drug Administration","doi-asserted-by":"publisher","award":["R01 FD-R-002568"],"award-info":[{"award-number":["R01 FD-R-002568"]}],"id":[{"id":"10.13039\/100000038","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000038","name":"US Food and Drug Administration","doi-asserted-by":"publisher","award":["R01 FD-R-003409"],"award-info":[{"award-number":["R01 FD-R-003409"]}],"id":[{"id":"10.13039\/100000038","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R21 HD078864"],"award-info":[{"award-number":["R21 HD078864"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["M01 RR00052"],"award-info":[{"award-number":["M01 RR00052"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Albright hereditary osteodystrophy (AHO) is caused by heterozygous inactivating mutations in GNAS. Depending on the parental origin of the mutated allele, patients develop either pseudohypoparathyroidism type 1A (PHP1A), with multihormone resistance and severe obesity, or pseudopseudohypoparathyroidism (PPHP), without hormonal abnormalities or marked obesity. Subcutaneous ossifications (SCOs) are a source of substantial morbidity in both PHP1A and PPHP.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>This study investigated the previously undetermined prevalence of SCO formation in PHP1A vs PPHP as well as possible correlations with genotype, sex, age, hormonal resistance, and body mass index (BMI).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>This study evaluated patients with AHO for SCOs by physical examination performed by one consistent physician over 16 years.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Setting<\/jats:title>\n                  <jats:p>Albright Clinic, Kennedy Krieger Institute; Institute for Clinical and Translational Research, Johns Hopkins Hospital; Albright Center, Connecticut Children\u2019s Medical Center.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Patients<\/jats:title>\n                  <jats:p>We evaluated 67 patients with AHO (49 with PHP1A, 18 with PPHP) with documented mutations in GNAS.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcome Measures<\/jats:title>\n                  <jats:p>Relationships of SCOs to genotype, sex, age, hormonal resistance, and BMI.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Forty-seven of 67 participants (70.1%) had SCOs. Patients with PHP1A and PPHP had similar prevalences and degrees of ossification formation. Patients with frameshift and nonsense mutations had much more extensive SCOs than those with missense mutations. Males were affected more than females. There was no correlation with hormonal status or BMI.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>There is a similar prevalence of SCOs in PHP1A and PPHP, and the extent of SCO formation correlates with the severity of the mutation. Males are affected more extensively than females, and the SCOs tend to worsen with age.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/jc.2017-00860","type":"journal-article","created":{"date-parts":[[2017,10,19]],"date-time":"2017-10-19T18:07:01Z","timestamp":1508436421000},"page":"158-168","source":"Crossref","is-referenced-by-count":30,"title":["Ossifications in Albright Hereditary Osteodystrophy: Role of Genotype, Inheritance, Sex, Age, Hormonal Status, and BMI"],"prefix":"10.1210","volume":"103","author":[{"given":"Parissa","family":"Salemi","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Endocrinology, Johns Hopkins University School of Medicine, Baltimore, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie M","family":"Skalamera Olson","sequence":"additional","affiliation":[{"name":"Albright Clinic, Kennedy Krieger Institute, Baltimore, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren E","family":"Dickson","sequence":"additional","affiliation":[{"name":"Albright Center and Center for Rare Bone Disorders, Division of Pediatric Endocrinology & Diabetes, Connecticut Children\u2019s Medical Center, Farmington, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily L","family":"Germain-Lee","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Endocrinology, Johns Hopkins University School of Medicine, Baltimore, Maryland"},{"name":"Albright Clinic, Kennedy Krieger Institute, Baltimore, Maryland"},{"name":"Albright Center and Center for Rare Bone Disorders, Division of Pediatric Endocrinology & Diabetes, Connecticut Children\u2019s Medical Center, Farmington, Connecticut"},{"name":"Department of Pediatrics, University of Connecticut School of Medicine, Farmington, 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