Precocious puberty

Source: Wikipedia, the free encyclopedia.
Precocious puberty
Other namesEarly puberty
Idiopathic, brain tumor

In

sex steroid production. The opposite condition is delayed puberty.[2][3]

The term is used with several slightly different meanings that are usually apparent from the context. In its broadest sense, and often simplified as early puberty, "precocious puberty" sometimes refers to any physical

sex hormone effect, due to any cause, occurring earlier than the usual age, especially when it is being considered as a medical problem. Stricter definitions of "precocity" may refer only to central puberty starting before a statistically specified age based on percentile in the population (e.g., 2.5 standard deviations below the population mean),[4] on expert recommendations of ages at which there is more than a negligible chance of discovering an abnormal cause, or based on opinion as to the age at which early puberty may have adverse effects. A common definition for medical purposes is onset before 8 years in girls or 9 years in boys.[5]

Causes

Early

genital
development may result from natural early maturation or from several other conditions.

Central

If the cause can be traced to the

pituitary, the cause is considered central. Other names for this type are complete or true precocious puberty.[6]

Causes of central precocious puberty can include:

Central precocious puberty can also be caused by brain tumors, infection (most commonly tuberculous meningitis, especially in developing countries), trauma, hydrocephalus, and Angelman syndrome.[7] 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.[8]

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.[9][10]

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[11] or 6 years 5 months as mentioned in another report.[12]

"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."[13]

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:

Isosexual and heterosexual

Generally, patients with precocious puberty develop

secondary sexual characteristics. This is called isosexual precocity.[16]

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.[16] The "opposite" case would be the hyper-masculinisation of both male and female patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency, in which there is an excess of androgens. Thus, in the aromatase excess syndrome the precocious puberty is isosexual in females and heterosexual in males, whilst in the CAH it's isosexual in males and heterosexual in females.[citation needed]

Research

Although the causes of early puberty are still somewhat unclear, girls who have a high-fat diet and are not physically active or are obese are more likely to physically mature earlier.[17][18][19] "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."[19] In addition to diet and exercise habits, exposure to chemicals that mimic estrogen (known as xenoestrogens) is another possible cause of early puberty in girls. Bisphenol A, a xenoestrogen found in hard plastics, has been shown to affect sexual development.[20] "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."[18] While more girls are increasingly entering puberty at younger ages, new research indicates that some boys are actually starting later (delayed puberty).[21][22] "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."[22]

High levels of beta-hCG in serum and

pineal tumor. Radiotherapy and chemotherapy reduced tumor and beta-hCG levels normalized.[23]

In a study using neonatal melatonin on rats, results suggest that elevated melatonin could be responsible for some cases of early puberty.[24]

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,[25][26] and LEP and LEPR, which encode leptin and the leptin receptor,[27] 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.[28]

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[29][30] 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.[31]

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.[32] The identification of mutations in MKRN3 leading to sporadic cases of CPP has been a significant contribution to better understanding the mechanism of puberty.[33] 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.[34]

Diagnosis

Studies indicate that breast development in girls and the appearance of pubic hair in both girls and boys are starting earlier than in previous generations.[18][35][36] As a result, "early puberty" in children as young as 8 and 9 is no longer considered abnormal, particularly with girls. Although it is not considered as abnormal, it may be upsetting to parents[21][37] and can be harmful to children who mature physically at a time when they are immature mentally.[38]

No age reliably separates normal from abnormal processes in children, but the following age thresholds for evaluation are thought to minimize the risk of missing a significant medical problem:

Medical evaluation is sometimes necessary to recognize the few children with serious conditions from the majority who have entered puberty early but are still medically normal. Early sexual development warrants evaluation because it may:

  • induce early
    bone maturation
    and reduce eventual adult height
  • indicate the presence of a tumour or other serious problem
  • cause the child, particularly a girl, to become an object of adult sexual interest.[19][39][40]

Treatment

One possible treatment is with

follicle stimulating hormone (FSH) and luteinizing hormone (LH).[why?][41] Triptorelin depot is widely used to treat central precocious puberty (CPP) in children.[42]

Prognosis

Early puberty is posited to put girls at higher risk of sexual abuse;[19][40] however, a causal relationship is, as yet, inconclusive.[40] Early puberty also puts girls at a higher risk for teasing or bullying, mental health disorders and short stature as adults.[19][39][43] Girls as young as 8 are increasingly starting to menstruate, develop breasts and grow pubic and underarm hair; these "biological milestones" typically occurred only at 13 or older in the past. African-American girls are especially prone to early puberty.[18]

Though boys face fewer problems from early puberty than girls do, early puberty is not always positive for boys. Early sexual maturation in boys can be accompanied by increased aggressiveness due to the surge of pubertal hormones.[44] Because they appear older than their peers, pubescent boys may face increased social pressure to conform to adult norms; society may view them as more emotionally advanced, although their cognitive and social development may lag behind their physical development.[44] Studies have shown that early-maturing boys are more likely to be sexually active and are more likely to participate in risky behaviors.[45]

History

Pubertas praecox is the

Jungian "complexional" causes, or general or local "plethora" (blood excess).[46] Endocrinological (hormonal) theories and discoveries are a twentieth-century development.[citation needed
]

See also

References

  1. ^ "Precocious Puberty". KidsHealth. Retrieved 2013-09-09.
  2. S2CID 4772278
    .
  3. .
  4. ^ precocious+puberty at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
  5. ^ "default - Stanford Children's Health". www.stanfordchildrens.org. Retrieved 2021-02-16.
  6. ^ David Gardner, Dolores Shoback. Basic And Clinical Endocrinology. McGraw-Hill Medical; 2011. 9th Edition. Pg. 550
  7. PMID 15349080
    .
  8. .
  9. . So far, in the pediatric age group, only three cases of functioning adrenocortical oncocytoma have been reported. We report a case of functioning adrenocortical oncocytoma in a 3 1/2-year-old female child who presented with premature pubarche, clitoromegaly, and increased serum dehydroepiandrosterone sulfate and testosterone. She was managed successfully with right adrenalectomy, and the tumor histology was consistent with adrenal oncocytoma.
  10. .
  11. The Telegraph. August 27, 2002. Archived from the original
    on July 22, 2009. Retrieved April 13, 2016.
  12. ^ "Little Mother". Time. December 16, 1957. Archived from the original on April 22, 2009. Retrieved January 9, 2008.
  13. S2CID 27162486
    .
  14. .
  15. .
  16. ^ .
  17. ^ (Tanner, 1990).
  18. ^
    PMID 11483799
    .
  19. ^ a b c d e McKenna, Phil (2007-03-05). "Childhood obesity brings early puberty for girls". New Scientist. Archived from the original on 2008-04-19. Retrieved 2010-05-22.
  20. PMID 19479018
    .
  21. ^ a b Cooney, Elizabeth (2010-02-11). "Puberty gap: Obesity splits boys, girls. Adolescent males at top of the BMI chart may be delayed". NBC News. Retrieved 2010-05-22.
  22. ^
    Science Daily
    . February 2010. Retrieved 2010-05-22.
  23. PMID 16767969
    .
  24. .
  25. .
  26. .
  27. .
  28. .
  29. .
  30. .
  31. .
  32. .
  33. .
  34. .
  35. .
  36. ^ Roberts, Michelle (2005-05-15). "Why puberty now begins at seven". BBC News. Retrieved 2010-05-22.
  37. ^ Ritter, Jim (2000-08-02). "Parents worried by girls' earlier start of puberty". Chicago Sun-Times.
  38. ^ Diana Zuckerman (2001). "Early Puberty in Girls". The Ribbon. Cornell University Program on Breast Cancer and Environmental Risk Factors. Retrieved 18 February 2018.
  39. ^ a b (Stattin & Magnussion, 1990)
  40. ^
    PMID 25419091
    .
  41. .
  42. .
  43. ^ (Caspi et al.1993: Lanza and Collins, 2002)
  44. ^ a b Garn, SM. Physical growth and development. In: Friedman SB, Fisher M, Schonberg SK, editors. Comprehensive Adolescent Health Care. St Louis: Quality Medical Publishing; 1992. Retrieved on 2009-02-20
  45. ^ Susman, EJ; Dorn, LD; Schiefelbein, VL. Puberty, sexuality, and health. In: Lerner MA, Easterbrooks MA, Mistry J., editors. Comprehensive Handbook of Psychology. New York: Wiley; 2003. Retrieved on 2009-02-20
  46. PMID 33186444
    .

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