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Ann Pediatr Endocrinol Metab > Volume 28(3); 2023 > Article
Lee: Central precocious puberty: is routine brain MRI screening necessary for girls?: Commentary on “Brain magnetic resonance imaging (MRI) findings in central precocious puberty patients: is routine MRI necessary for newly diagnosed patients?”
Central precocious puberty (CPP) is defined by the early activation of hypothalamicpituitary- gonadal axis before the age of 8 years in girls and 9 years in boys [1,2]. With a ratio of 1:5 to 1:10, precocious puberty is more common in girls than in boys. The onset of puberty is a multifaceted phenomenon influenced by a combination of genetic and environmental factors, including factors such as obesity and endocrine disruptors. In addition, the onset of typical puberty shows individual variability and is determined by a variety of genetic factors, including both rare and common variations [3-7].
Approximately 90% to 95% of girls have idiopathic form of CPP, but approximately 40% to 75% of boys with CPP have pathological brain lesions, including hypothalamic hamartoma, pituitary adenoma, and germinoma. Therefore, magnetic resonance imaging (MRI) of the brain can be performed to evaluate children with CPP and rule out the possibility of pathological brain lesions. In global consensus statement on CPP, all boys with CPP and girls younger than 6 years of age with CPP should undergo a brain MRI as a part of etiological investigation [8]. However, there is controversy as to whether brain MRI should be performed on girls with precocious puberty between the ages of 6 and 8.
CPP cases, as well as the benefit of brain MRI in girls with age at puberty onset older than 6 years without neurological abnormality. Yoon et al. [9] reported that when brain MRI was performed on girls diagnosed with precocious puberty at an average age of 6.8 years, 91.8% showed normal findings. Also, any pathological lesions among girls with CPP were not detected. In recent systematic review, the prevalence of brain lesions in patients with CPP was 12% in girls younger than 7 years old and only 3% in girls between 7–8 years old [10]. In a recent study by Oh et al. [11], a pathological brain lesion which was diagnosed as hypothalamic hamartoma was only detected in one girl (6.1 years of age) out 199 girls with CPP. The detection rate of brain lesions not only in girls but also in boys is not higher in recent studies compared to previous literature [12]. Out of 138 boys with CPP who underwent brain MRI, brain lesions including pituitary hyperplasia, thickening of the pituitary stalk, and Rathke cleft cyst were found in 10 boys (7%). Oh et al. [11] reported that 4 of 24 boys (16.6%) with CPP had pituitary abnormalities, but no pathological brain lesions were not observed.
Recent westernized eating habits and the increase in obesity are thought to be related to the increased incidence of precocious puberty. As the degree of obesity increases, the incidence of precocious puberty in obese children is higher than in children of normal weight. Therefore, alterations in an individual's nutritional status may affect the lowering the risk of presenting pathological brain lesions.
In conclusion, true pathological brain lesions in patients with CPP are relatively rare, especially in girls diagnosed with CPP between the ages of 6 and 8. Therefore, routine MRI of the brain in patients with CPP should be carefully considered in girls with CPP who are older than 6 years of age.

Notes

Conflicts of interest

No potential conflict of interest relevant to this article was reported.

References

1. Cho AY, Ko SY, Lee JH, Kim EY. Effects of gonadotropinreleasing hormone agonist treatment on final adult height in boys with idiopathic central precocious puberty. Ann Pediatr Endocrinol Metab 2021;26:259–65.
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2. Lee HS, Yoon JS, Hwang JS. Luteinizing hormone secretion during gonadotropin-releasing hormone stimulation tests in obese girls with central precocious puberty. J Clin Res Pediatr Endocrinol 2016;8:392–8.
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3. Shim YS, Lee HS, Hwang JS. Aberrant notch signaling pathway as a potential mechanism of central precocious puberty. Int J Mol Sci 2022;23:3332.
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4. Lee HS, Jeong HR, Rho JG, Kum CD, Kim KH, Kim DW, et al. Identification of rare missense mutations in NOTCH2 and HERC2 associated with familial central precocious puberty via whole-exome sequencing. Gynecol Endocrinol 2020;36:682–6.
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5. Huynh QTV, Ho BT, Le NQK, Trinh TH, Lam LHT, Nguyen NTK, et al. Pathological brain lesions in girls with central precocious puberty at initial diagnosis in Southern Vietnam. Ann Pediatr Endocrinol Metab 2022;27:105–12.
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6. Lee SY, Kim JM, Kim YM, Lim HH. Single random measurement of urinary gonadotropin concentration for screening and monitoring girls with central precocious puberty. Ann Pediatr Endocrinol Metab 2021;26:178–84.
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7. Jeon MJ, Choe JW, Chung HR, Kim JH. Short-term efficacy of 1-month and 3-month gonadotropin-releasing hormone agonist depots in girls with central precocious puberty. Ann Pediatr Endocrinol Metab 2021;26:171–7.
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8. Carel JC, Eugster EA, Rogol A, Ghizzoni L, Palmert MR, Antoniazzi F, et al. Consensus statement on the use of gonadotropin-releasing hormone analogs in children. Pediatrics 2009;123:e752. –62.
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9. Yoon JS, So CH, Lee HS, Lim JS, Hwang JS. Prevalence of pathological brain lesions in girls with central precocious puberty: possible overestimation? J Korean Med Sci 2018;33:e329.
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10. Cantas-Orsdemir S, Garb JL, Allen HF. Prevalence of cranial MRI findings in girls with central precocious puberty: a systematic review and meta-analysis. J Pediatr Endocrinol Metab 2018;31:701–10.
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11. Oh YR, Kim YJ, Oh KE, Park GH, Kang E, Nam HK, et al. Brain magnetic resonance imaging (MRI) findings in central precocious puberty patients: is routine MRI necessary for newly diagnosed patients? Ann Pediatr Endocrinol Metab 2023;28:200–5.
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12. Yoon JS, So CH, Lee HS, Lim JS, Hwang JS. The prevalence of brain abnormalities in boys with central precocious puberty may be overestimated. PLoS One 2018;13:e0195209.
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