eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Precocious Puberty: Follow-up

Author: Paul B Kaplowitz, MD, PhD, Professor of Pediatrics, George Washington University School of Medicine and Health Sciences; Chief of Endocrinology, Children's National Medical Center
Contributor Information and Disclosures

Updated: Jun 30, 2009

Follow-up

Further Outpatient Care

  • Patients with precocious puberty treated with gonadotropin-releasing hormone (GnRH) agonists
    • Follow up every 4-6 months to ensure that progression of puberty has been arrested.
    • Favorable signs include normalization of accelerated growth, reduction (or at least no increase) in size of breasts, and suppression of gonadotropin levels after a challenge of GnRH.
    • The ideal testing frequency has not been established. A suggested timeline for girls is to obtain a GnRH test about 4 months after starting the drug to confirm suppression and then no more often than yearly, as long as clinical indicators suggest that the drug is working as intended. Some clinicians advocate dispensing with formal GnRH testing as long as growth has slowed and breasts have decreased in size. In boys, a decrease in the size of the testes and a fall in serum testosterone level to less than 20 ng/dL are good indications of efficacy.
    • Monitor bone age yearly to confirm that the rapid advancement seen in the untreated state has slowed, typically to a half year of bone age per year or less.
  • Patients not treated with GnRH agonists: In many cases, the physician may elect to observe the child with central precocious puberty (CPP), either because the age is borderline (ie, 7-8 y) and the child and family are coping well or because the progression of puberty is not rapid and the bone age is only mildly advanced (ie, £ 1 y), so that predicted adult height falls well within the reference range. In these cases, follow-up at 6-month intervals is appropriate. Testing and treatment may be initiated if the tempo of puberty begins to accelerate and predicted adult height deteriorates.

Prognosis

  • Without treatment
    • Most girls with early puberty who are aged 6-8 years at the onset of puberty achieve an adult height within the reference range. Treatment with GnRH analogues such as Lupron is usually associated with only a modest gain in final height in this age group.
    • Consider therapy following initial evaluation for girls who then have predicted heights less than 4 ft 11 in or who are well below their target height (ie, average of parents' heights, less 2.5 in) when the patient also has very advanced bone age, a height below the 25th percentile, or both.
    • Controversy surrounds the significance of several studies (mostly with small numbers of patients with no control group) that appear to indicate that girls with CPP are at increased risk for significant behavior problems, such as poor self-esteem and higher anxiety, irritability, or withdrawal. Other studies have not shown such problems. A recent review of this topic by Walvoord and Mazur concluded that CPP may become a risk factor for psychosocial problems, mainly in the setting of other risk factors; they cautioned against medical therapy in order to avoid presumed negative psychological consequences of precocious puberty.15
  • With treatment
    • Most studies show significant improvement in adult height compared with height predicted at the start of therapy, but the extent of this improvement depends to some extent on the age of onset of CPP.
    • A recent study from Israel showed that height gained in girls after discontinuation of GnRH analogue therapy at age 11-12 years (and bone age 12-12.5 y) is greater for girls with onset of CPP before age 6 years than at age 6-8 years or after age 8 years. Mean final height was better than genetic target height in the younger group and less-than-target height in the group whose puberty started after age 8 years.16 This supports the view that the benefit of treatment in terms of increased adult height is the greatest in patients who are diagnosed with CPP and started on GnRH analogues at younger ages.
    • Normal adult height can be achieved in most cases if treatment is started before bone maturation is too advanced (>12 y in girls, >13 y in boys) and if good gonadal suppression is maintained for several years. Treatment allows growth to continue while dramatically slowing the rate of bone maturation.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Failure to diagnose a CNS tumor
    • In girls, most cases of central precocious puberty (CPP) are idiopathic; however, the risk of a tumor or other CNS abnormality is greater in girls younger than 6 years who have rapid progression of puberty or any CNS signs or symptoms (eg, headaches, visual disturbances, seizures). Because some of these tumors are malignant (eg, gliomas, astrocytomas), failure to consider this possibility and to perform CT scanning or MRI in high-risk cases could result in delayed diagnosis, increased morbidity, and poorer chance of a cure.
    • In boys, organic causes of precocious puberty are more likely. CT scanning or MRI should be part of the evaluation once the child is diagnosed with CPP.
 


More on Precocious Puberty

Overview: Precocious Puberty
Differential Diagnoses & Workup: Precocious Puberty
Treatment & Medication: Precocious Puberty
Follow-up: Precocious Puberty
Multimedia: Precocious Puberty
References
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References

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Further Reading

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Keywords

precocious puberty, early puberty, central precocious puberty, CPP, premature thelarche, premature pubarche, precocious pseudopuberty, hyperovarianism, early onset of puberty, sexual precocity, precocious puberty, idiopathic CPP, inappropriate sexual behaviors, increased masturbation, short stature, breast enlargement, clitoral enlargement, enlarged testes, congenital adrenal hyperplasia, familial male precocious puberty, Leydig-cell tumors, HCG-secreting tumors, premature adrenarche, increased body fat, astrocytomas, gliomas, germ cell tumors secreting human chorionic gonadotropin, germ cell tumors secreting HCG, hypothalamic hamartomas, hydrocephalus, arachnoid cysts, suprasellar cysts, treatment, diagnosis

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Contributor Information and Disclosures

Author

Paul B Kaplowitz, MD, PhD, Professor of Pediatrics, George Washington University School of Medicine and Health Sciences; Chief of Endocrinology, Children's National Medical Center
Paul B Kaplowitz, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Indevus Consulting fee Review panel membership

Medical Editor

Phyllis W Speiser, MD, Chief of Pediatric Endocrinology, Schneider Children's Hospital; Professor of Pediatrics, New York University School of Medicine
Phyllis W Speiser, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Lynne Lipton Levitsky, MD, Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor, Department of Pediatrics, Harvard University Medical School
Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Pfizer Grant/research funds P.I.; Tercica Grant/research funds PI, also occasional consultant

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and Arkansas Children's Hospital
Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research
Disclosure: Genentech, Inc. Honoraria Speaking and teaching; Pfizer, Inc. Honoraria Consulting

 
 
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