Central precocious puberty in Boston boys: A 10-year single center experience

• Published in: PloS one 2018-06, Vol.13 (6), p.e0199019-e0199019
• Main Authors: Topor, Lisa Swartz, Bowerman, Kimberly, Machan, Jason T, Gilbert, Courtney L, Kangarloo, Tairmae, Shaw, Natalie D
• Format: Article
• Language: English
• Subjects: Age; Biology and Life Sciences; Body weight; Boston - epidemiology; Boys; Brain research; Care and treatment; Central nervous system; Child; Children & youth; Design standards; Diagnosis; Diagnostic software; Diagnostic systems; Endocrinology; Evaluation; Follicle Stimulating Hormone - blood; Genetic disorders; Genetics; Health status indicators; Hospitals; Humans; Laboratories; Luteinizing Hormone - blood; Male; Medical diagnosis; Medical imaging; Medical records; Medical research; Medical schools; Medicine and Health Sciences; Mutation; Neurofibromatosis; Neuroimaging; Neurological disorders; Neurology; Overweight; Patients; Pediatrics; Precocious puberty; Puberty; Puberty, Precocious - blood; Puberty, Precocious - epidemiology; Research and Analysis Methods; Retrospective Studies; Testosterone - blood; Tumors
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0199019

Recent studies in the US and abroad suggest that boys are undergoing puberty at a younger age. It is unknown if this secular trend extends to boys with central precocious puberty (CPP), who sit at the extreme end of the pubertal spectrum, and if neuroimaging should remain a standard diagnostic tool. Retrospective chart review of all boys with CPP seen by Endocrinology at a US pediatric hospital from 2001-2010. Fifty boys had pubertal onset at an average age of 7.31 years (95CI 6.83-7.89), though many did not present until nearly one year thereafter, by which time 30% were mid-to-late pubertal. Boys were predominantly non-Hispanic White and 64% were overweight/obese. The majority (64%) of boys had neurogenic CPP (CNS-CPP) with neurofibromatosis type I being the most common diagnosis. Diagnosis of CPP led to discovery of a neurogenic lesion in only 3 of 32 (9%) CNS-CPP cases. The remaining boys, with idiopathic CPP (36%), were indistinguishable from those with CNS-CPP aside from four boys who endorsed a family history of PP (22% vs. 0% among CNS-CPP cases). Importantly, there was no change in the incidence of male CPP after accounting for the increase in clinic volume during this time period. In this contemporary Boston-based cohort of 50 boys with CPP, most cases were neurogenic, consistent with older literature. Several idiopathic cases had a family history of PP but were otherwise indistinguishable from CNS-CPP cases. Thus, neuroimaging remains a critical diagnostic tool. We find no evidence for an increase in the prevalence of male CPP.