Early
pubic hair,
breast, or
genital development may result from natural early maturation or from several other conditions.
Central If the cause can be traced to the
hypothalamus or
pituitary, the cause is considered central. Other names for this type are
complete or
true precocious puberty. Causes of central precocious puberty can include: •
hypothalamic hamartoma produces pulsatile
gonadotropin-releasing hormone (GnRH) •
Langerhans cell histiocytosis •
McCune–Albright syndrome Central precocious puberty can also be caused by
brain tumors, infection (most commonly
tuberculous meningitis, especially in developing countries), trauma,
hydrocephalus, and
Angelman syndrome. Precocious puberty is associated with advancement in bone age, which leads to early fusion of epiphyses, thus resulting in reduced final height and short stature. Adrenocortical oncocytomas are rare with mostly benign and nonfunctioning tumors. There have been only three cases of functioning adrenocortical oncocytoma that have been reported up until 2013. Children with adrenocortical oncocytomas will present with "premature pubarche, clitoromegaly, and increased serum dehydroepiandrosterone sulfate and testosterone" which are some of the presentations associated with precocious puberty. Precocious puberty in girls begins before the age of 8. The youngest mother on record is
Lina Medina, who gave birth at the age of either 5 years, 7 months and 17 days or 6 years 5 months as mentioned in another report. "Central precocious puberty (CPP) was reported in some patients with suprasellar
arachnoid cysts (SAC), and SCFE (
slipped capital femoral epiphysis) occurs in patients with CPP because of rapid growth and changes of growth hormone secretion." If no cause can be identified, it is considered
idiopathic or constitutional.
Peripheral Secondary sexual development induced by
sex steroids from other abnormal sources is referred to as
peripheral precocious puberty or
precocious pseudopuberty. It typically presents as a severe form of disease with children. Symptoms are usually as a sequelae from adrenal hyperplasia (because of
21-hydroxylase deficiency or
11-beta hydroxylase deficiency, the former being more common), which includes but is not limited to hypertension, hypotension, electrolyte abnormalities, ambiguous genitalia in females, signs of virilization in females. Blood tests will typically reveal high level of
androgens with low levels of cortisol. Causes can include: • Endogenous sources •
Gonadal tumors (such as
arrhenoblastoma) •
Adrenal tumors •
Germ cell tumor •
Congenital adrenal hyperplasia •
McCune–Albright syndrome •
Silver–Russell syndrome •
Familial male-limited precocious puberty (testotoxicosis) • Exogenous hormones •
Environmental exogenous hormones • As treatment for another condition
Isosexual and heterosexual Generally, patients with precocious puberty develop
phenotypically appropriate
secondary sexual characteristics. This is called
isosexual precocity. In some cases, a patient may develop characteristics of the opposite sex. For example, a male may
develop breasts and other feminine characteristics, while a female may develop a deepened voice and facial hair. This is called
heterosexual or
contrasexual precocity. It is very rare in comparison to isosexual precocity and is usually the result of unusual circumstances. As an example, children with a very rare genetic condition called
aromatase excess syndrome – in which exceptionally high circulating levels of estrogen are present – usually develop precocious puberty. Males and females are hyper-feminized by the syndrome. "Obese girls, defined as at least 10 kilograms (22 pounds) overweight, had an 80 percent chance of developing breasts before their ninth birthday and starting menstruation before age 12 – the western average for menstruation is about 12.7 years." "Factors other than obesity, however, perhaps genetic and/or environmental ones, are needed to explain the higher prevalence of early puberty in black versus white girls." "Increasing rates of obese and overweight children in the United States may be contributing to a later onset of puberty in boys, say researchers at the University of Michigan Health System." The ACE's with significant influence on a girl's development are sexual and physical abuse. A 2026 study states that self-identification as a sexual minority correlates with earlier puberty compared to a child's heterosexual peers. High levels of beta-hCG in serum and
cerebrospinal fluid observed in a 9-year-old boy suggest a pineal gland tumor. The tumor is called a
chorionic gonadotropin secreting pineal tumor. Radiotherapy and chemotherapy reduced tumor and beta-hCG levels normalized. In a study using neonatal melatonin on rats, results suggest that elevated melatonin could be responsible for some cases of early puberty. Familial cases of idiopathic central precocious puberty (ICPP) have been reported, leading researchers to believe there are specific genetic modulators of ICPP. Mutations in genes such as
LIN28, and LEP and LEPR, which encode
leptin and the leptin receptor, have been associated with precocious puberty. The association between LIN28 and puberty timing was validated experimentally in vivo, when it was found that mice with ectopic over-expression of
LIN28 show an extended period of pre-pubertal growth and a significant delay in puberty onset. Mutations in the kisspeptin (KISS1) and its receptor, KISS1R (also known as GPR54), involved in GnRH secretion and puberty onset, are also thought to be the cause for ICPP However, this is still a controversial area of research, and some investigators found no association of mutations in the LIN28 and KISS1/KISS1R genes to be the common cause underlying ICPP. The gene MKRN3, which is a maternally imprinted gene, was first cloned by Jong et al. in 1999. MKRN3 was originally named Zinc finger protein 127. It is located on human chromosome 15 on the long arm in the
Prader-Willi syndrome critical region2, and has since been identified as a cause of premature sexual development or CPP. The identification of mutations in MKRN3 leading to sporadic cases of CPP has been a significant contribution to better understanding the mechanism of puberty. MKRN3 appears to act as a "brake" on the central hypothalamic-pituitary access. Thus, loss of function mutations of the protein allow early activation of the GnRH pathway and cause phenotypic CPP. Patients with a MKRN3 mutation all display the classic signs of CCP including early breast and testes development, increased bone aging and elevated hormone levels of GnRH and LH. == Diagnosis ==