The Endocrine Society (ES) recently released a clinical practice guideline on central precocious puberty in an effort to address clinical questions associated with the diagnosis and treatment of pediatric patients with central precocious puberty. The overall goal of these guidelines was to provide clinicians with diagnostic and therapeutic strategies that will most likely provide net clinical benefits to patients.

Below, we showcase the ten recommendations featured in the ES clinical practice guideline, Central Precocious Puberty. View the full-text version of the clinical practice guideline for the most thorough explanation of the following recommendations, along with their accompanying clinical questions. The ES points out there is a substantial need for additional research for this patient population.

ES Recommendations in the 2026 Central Precocious Puberty Guideline
  • In girls who present with thelarche (Tanner B2) between ages 7 and 8 years, Endocrine Society (ES) suggests watchful waiting via periodic physical examinations rather than immediately performing evaluation with laboratory testing and/or radiologic imaging.
  • In girls younger than age 7 years with initial breast development (Tanner B2), ES suggests a four- to six-month period of observation to differentiate unsustained or slowly progressive puberty from rapidly progressive puberty before starting diagnostic evaluation.
  • In girls and boys with evidence of precocious puberty, ES suggests an initial evaluation with a basal luteinizing hormone concentration by ultrasensitive assay, rather than initially performing a gonadotropin-releasing hormone/gonadotropin-releasing hormone agonist stimulation test, in order to distinguish those with central precocious puberty from those without.
  • In girls ages 6 to 8 years and boys ages 8 to 9 years with central precocious puberty and without central nervous system findings, ES suggests that brain magnetic resonance imaging (MRI) should not be routinely performed.
  • For children with central precocious puberty, ES suggests against routine genetic testing (e.g., to identify loss-of-function mutations in Makorin ring finger protein 3 gene [MKRN3], delta-like non-canonical Notch ligand 1 gene [DLK1], and/or methyl-CpG-binding protein 2 gene [MECP2]).
  • For many children with central precocious puberty, ES suggests gonadotropin-releasing hormone agonist treatment, although certain patient subgroups may not achieve net benefit with such treatment.
  • In patients with central precocious puberty who will use a long-acting gonadotropin-releasing hormone agonist in the long term, ES suggests initiating therapy with the long-acting gonadotropin-releasing hormone agonist preparation rather than initiating therapy with a monthly gonadotropin-releasing hormone agonist.
  • In children being treated for central precocious puberty with a gonadotropin-releasing hormone agonist, ES suggests against routine biochemical testing (e.g., luteinizing hormone and sex steroid concentrations) to monitor pubertal suppression.
  • In children with central precocious puberty, ES suggests against the routine addition of growth hormone to gonadotropin-releasing hormone agonist therapy.
  • In children being treated for central precocious puberty, ES suggests against routinely continuing gonadotropin-releasing hormone agonist treatment beyond chronological age 10–11 years (girls) or 11–12 years (boys) and/or bone age 11–12 years (girls) or 12–13 years (boys).

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