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Lead edit
Pubarche usually results from rising levels of androgens[1] from the adrenal glands, ovaries, or testes but may also result from exposure to an anabolic steroid.
When pubarche occurs prematurely (in early or mid-childhood), it is referred to as premature pubarche or precocious puberty and may warrant an evaluation.
When adrenarche[2], an increase in adrenal androgen production, central puberty[3], and all disease-causing conditions have been excluded, the term isolated premature pubarche[3] is used to describe the unexplained development of pubic hair at an early age in people without other hormonal or physical changes of puberty.
Article body edit
Definition edit
Pubarche (pyü-bär-kē) refers to the first appearance of pubic hair at puberty and also it marks the beginning of puberty[4]. It is one of the physical changes of puberty and can occur independently of complete puberty. The early stage of sexual maturation, also known as adrenarche, is marked by characteristics including the development of pubic hair, axillary hair, adult apocrine body odor, acne, and increase oiliness of hair and skin.[5] The Encyclopedia of Child and Adolescent Health corresponds SMR2 (Sexual Maturity Rating) with pubarche, defining it as the development of pubic hair that occurs at a mean age of 11.6 years in females (range 9.3–13.9 years) and 12.6 years in males (range 10.7–14.5 years). It further describes that pubarche's physical manifestation is vellus hair over the labia or the base of the penis.[6] See Table 1. for the entirety of the sexual maturity rating description.
| Tanner Stage | Description of Pubic Hair Development |
|---|---|
| SMR 1 | Prepubertal - No pubic hair |
| SMR 2 | Pubarche - Sparse, fine, straight, downy hair over labia or penis |
| SMR 3 | Appearance of terminal hair - Adult quality, confined to the pubis |
| SMR 4 | Terminal hair fills the pubic region, not beyond inguinal crease |
| SMR 5 | Terminal hair extends onto medial thighs, achieving full adult distribution |
| SMR 6 | Terminal hair extends up the linea alba toward the umbilicus (only in males) |
A study researched whether thelarche pathway, beginning puberty with breast development alone, or the pubarche pathway, beginning puberty with pubic hair development alone, represents the true pubertal development. The study is an observational, longitudinal cohort study. The study cohort is limited to a group of black and white girls who were seen annually for ten years. It is concluded in the research that pubarche may represent true pubertal maturation. [7]
Assessment edit
The Tanner scale remains the gold standard for determining pubarche. In clinical settings, this is primarily conducted by physicians, nurses, or other trained healthcare providers as part of a physical examination to assess the stage of puberty in children and adolescents, though in some cases the stage of puberty can be self-assessed[8].
Premature Pubarche edit
Premature pubarche is when females younger than 8 years old or males younger than 9 year old develop sexual hairs.[9] Premature pubarche is linked to adrenarcheal androgen level: premature adrenarche, an adrenarcheal androgen levels with DHEAS of 40-130 ųg/dL, is the most common cause of premature pubarche.[10] Some other symptoms that often accompany premature pubarche include seborrhea, axillary hair, microcomedonal acne, and/or adult body odor and the increase in adrenal steroid C19 secretion, which includes the predominant adrenal C19 steroid hormones: dehydroepiandrosterone sulfate (DHEAS) and dehydroepiandrosterone (DHEA), by the zona reticularis is characteristic.[9] Premature pubarche is a subset of precocious puberty which divide into 1)true precocious puberty that includes complete and central precocious puberty and 2)incomplete puberty which has 3 subsets: premature thelacrche, premature pubarche and isolated menarche.[11] Scientists have traditionally thought that premature pubarche is benign, but it has been shown clinically now that it could be a forerunner of the metabolic syndrome, cause clinical ovarian androgen excess and hyperinsulinemia in adolescence.[12] Studies have shown that females with premature pubarche and lower birth weight obtained reduced height as adults because of early onset of puberty and a shorter duration of puberty.[12] There is ongoing study on metformin therapy in these female with the goal to improve final height.
Premature pubarche (PP) could represent the first manifestation of non-classic congenital adrenal hyperplasia caused by 21 hydroxylase deficiency (NC21OHD) (10-30% of cases). In the last 20 years, the necessity of performing an ACTH test to diagnose NC21OHD in all cases with PP has been questioned, with conflicting results. This study aims to retrospectively evaluate the predictive value of the basal androgens, 17-OHP levels, and auxological features in suggesting the presence of NC21OHD and, thus, the need for a standard ACTH test to confirm the diagnosis. In all, 111 consecutive patients (87 females) with PP and advanced bone age underwent an ACTH test. Of these, 6/111 cases (1 male) were diagnosed with NC21OHD. The mean baseline 17 hydroxyprogesterone (17-OHP), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), delta 4 androstenedione (Δ4A), and testosterone serum levels were higher in NC21OHD patients than in the others (p < 0.05). We found three predictive features for NC21OHD: basal 17 OHP of >200 ng/mL, bone age advance of >2 years, and DHEA-S levels of >228 ng/mL with sensitivity and specificity of 83.3% and 97.1%, 83.3% and 65.7%, and 83.3% and 96.2%, respectively. Our data confirm that the prevalence of NC21OHD is low among patients with PP. Serum 17-OHP of >200 ng/mL could be helpful to decide, in most cases, which patients should undergo the ACTH test. Bone age advance represented an inadequately specific predictive marker of NC21OHD. -https://pubmed.ncbi.nlm.nih.gov/36983190/
Insulin sensitization with metformin decreases hyperinsulinemia and hyperandrogenism in women with PCOS, restores eumenorrhea and increases the rate of spontaneous ovulation; the same effects have been observed in non-obese adolescents with premature pubarche [120–124]. We explored the preventive use of insulin sensitization to disrupt progression from premature pubarche to PCOS in formerly lean girls of low birth weight, who were 6–12 months postmenarche (age 12.4 years), with hyperinsulinemia, hyperandrogenemia, dyslipidemia, excess truncal and body fat, and reduced lean body mass, but without clinical signs or symptoms of androgen excess [125]. These girls were randomized to receive metformin [850 mg/day] or no treatment for 12 months. In untreated girls, insulin sensitivity, serum androgens, lipids, total and truncal fat mass, and lean body mass each deviated further from normal. In metformin-treated girls, each of these abnormalities reversed within 6 months, and body composition continued to improve between 6–12 months (Fig. 7). Most benefits of metformin were lost as soon as therapy was discontinued [125]. These results were subsequently replicated in another cohort of low birth weight girls with premature pubarche from the same population [40]; the addition of flutamide was beneficial only in a subset of girls identified by genetic markers as having greater androgen receptor activity [126]. -https://pubmed.ncbi.nlm.nih.gov/18726694/
The use of metformin has been shown clinically to prevent ovarian hyperandrogenism development in females with premature pubarche. A randomized control trial studied the effect of metformin 850 mg daily for 12 months compared to placebo. The results show that all abnormalities regarding insulini sensitivity, serum androgens, lipids, total and truncal fat mass, and lean body mass were reversed within 6 months. The untreated group had data that continued to deviate from the normal range. Later on, a cohort study replicated these results.
Average Age edit
See also: Tanner scale
The average beginning of pubarche varies due to many factors, including environmental exposures, nourishment, weight, race and ethnicity, and geographical location. First (and often transient) pubic hair resulting from adrenarche may appear between ages 10–12 at the beginning of puberty.
Chemical toxins in the environment are one of many factors influencing adolescent development. In the early 1970s, more than 4000 people were accidentally exposed to polybrominated biphenyls (PBBs).[13] A study was conducted in the child-bearing women exposed to the toxin, with their baby girls reaching menarche by the age of 11.6 years, compared to girls who had low exposure reaching menarche by the age of 12.2-12.6 years.[13] In every day life, people are exposed to a various number of pesticides, with a large amount found to be distruptive to the endocrine system. Although dichlorodiphenyltrichloroethane (DDT) and the metabolite dichlorodiphenyl dichloroethane (DDE) were banned in the United States in the 1970s, countries around the world are still using these pesticides. Studies found that adolescents reached early menarche or thelarche when exposed to DDT and DDE.[13][14] It was determined that women with high exposure reached menarche earlier than women who had low exposure. There were also studies that refuted findings mentioned above, showing that DDT exposure had no correlation with early menarche. Serum DDE levels were studied in females in urban areas as well as places in New York, and cities in Canada, including findings in animals with serum DDE levels exceeding the upper limit determined by the FDA.[13][15] In New York specifically, there was no link between DDE levels and breast development in 9-year-old girls.[16]
Geographical location and zones also plays a part in the timing of pubarche. A study was done in different zones in Nigeria and found that males in the Northeast, Northwest, and Southwest had an earlier timing of pubarche compared to the males in the Southeast, whereas females had delayed pubarche in the Southeast regions of Nigeria.[17] Within these regions, scocio-economic classes were also taken into consideration. They found that households with a higher economic status posed an increased risk of premature, or an early onset of pubarche, possibly related to food being easily accessible. Nutrition is vital in adolescent development. Failure to meeting average nutritional needs, such as calcium and vitamin D for bone growth[18], may result in growth stunt. Over-nourishment and/or living a sedentary lifestyle can lead to obesity which can also affect adolescent pubarche. [18] The Dietary Guidelines for Americans 2010 declared that females between the ages of 9 to 13 years should meet a caloric intake of 1400 to 2200, while females between the ages of 14 to 18 years should meet a caloric intake of 1800 to 2400 calories a day.[19]
Delayed Pubarche and Its Treatment edit
[Treatment] - no articles found on PubMed directly linking to the treatment of delayed pubarche -- but there are articles linked with the treatment of delayed puberty...
Another cause of delayed puberty in both males and females is hypogonadotropic hypogonadism[20], which is a condition in which the male and female genitalia produce little to none of sex hormones. This is a temporary condition in adolescents, usually caused by various stresses, including disease states such as persistent asthma, ulcerative colitis, and sickle cell anemia.[20]
In males diagnosed with constitutional delay in puberty and growth (CDPG), a short-course of testosterone in low doses is used to initiate puberty. In females diagnosed with CDPG, a short-course of estrogen in low doses is used to initiate puberty.[20] Testosterone is available via oral route or intramuscular injection (IM), with IM being the preferred method of administration because oral testosterone has been shown to have liver toxicity side effects. Estrogen is available via oral route and IM, however oral estrogen is the preferred method of administration.[20] Upon initiation of treatment and thereafter, the adolescent must be monitored for pubertal development, which includes breast development in females and enlargement of the testicles in males.[20] A provider can make a cinical judgement to stop treatment and monitor development while an adolescent is off therapy.
References edit
- ^ Dietrich, Jennifer E., ed. (2014). Female Puberty: A Comprehensive Guide for Clinicians. New York, NY: Springer New York. doi:10.1007/978-1-4939-0912-4. ISBN 978-1-4939-0911-7.
- ^ Rosenfield, Robert L (2021). "Normal and Premature Adrenarche". Endocrine Reviews. 42 (6): 783–814. doi:10.1210/endrev/bnab009. ISSN 0163-769X. PMC 8599200. PMID 33788946.
- ^ a b Latronico, Ana Claudia; Brito, Vinicius Nahime; Carel, Jean-Claude (2016). "Causes, diagnosis, and treatment of central precocious puberty". The Lancet Diabetes & Endocrinology. 4 (3): 265–274. doi:10.1016/S2213-8587(15)00380-0.
- ^ "Medical Definition of PUBARCHE". www.merriam-webster.com. Retrieved 2023-07-25.
- ^ "UpToDate". www.uptodate.com. Retrieved 2023-07-25.
- ^ Avila, Jonathan T. (2023-01-01), Halpern-Felsher, Bonnie (ed.), "Normal adolescent growth and development", Encyclopedia of Child and Adolescent Health (First Edition), Oxford: Academic Press, pp. 735–745, doi:10.1016/b978-0-12-818872-9.00011-x, ISBN 978-0-12-818873-6, retrieved 2023-07-26
- ^ Biro, Frank M.; Huang, Bin; Daniels, Stephen R.; Lucky, Anne W. (2008-12). "PUBARCHE AS WELL AS THELARCHE MAY BE A MARKER FOR THE ONSET OF PUBERTY". Journal of pediatric and adolescent gynecology. 21 (6): 323–328. doi:10.1016/j.jpag.2007.09.008. ISSN 1083-3188. PMC 3576862. PMID 19064225.
{{cite journal}}: Check date values in:|date=(help) - ^ academic.oup.com. doi:10.1210/clinem/dgaa135 https://academic.oup.com/crawlprevention/governor?content=%2fjcem%2farticle%2f105%2f8%2f2846%2f5807960. Retrieved 2023-07-26.
{{cite web}}: Missing or empty|title=(help) - ^ a b "UpToDate". www.uptodate.com. Retrieved 2023-07-27.
- ^ "Pediatric Endocrinology". 2008. doi:10.1016/b978-1-4160-4090-3.x5001-7.
{{cite journal}}: Cite journal requires|journal=(help) - ^ Sultan, Charles; Gaspari, Laura; Maimoun, Laurent; Kalfa, Nicolas; Paris, Françoise (2018-04). "Disorders of puberty". Best Practice & Research. Clinical Obstetrics & Gynaecology. 48: 62–89. doi:10.1016/j.bpobgyn.2017.11.004. ISSN 1532-1932. PMID 29422239.
{{cite journal}}: Check date values in:|date=(help) - ^ a b Ibáñez, Lourdes; Díaz, Rubén; López-Bermejo, Abel; Marcos, Maria Victoria (2009-03). "Clinical spectrum of premature pubarche: links to metabolic syndrome and ovarian hyperandrogenism". Reviews in Endocrine & Metabolic Disorders. 10 (1): 63–76. doi:10.1007/s11154-008-9096-y. ISSN 1389-9155. PMID 18726694.
{{cite journal}}: Check date values in:|date=(help) - ^ a b c d Fisher, Marisa M.; Eugster, Erica A. (2014). "What is in our environment that effects puberty?". Reproductive toxicology (Elmsford, N.Y.). 44: 7–14. doi:10.1016/j.reprotox.2013.03.012. ISSN 0890-6238. PMC 4096833. PMID 23602892.
- ^ Deng, F.; Tao, F.-b.; Liu, D.-y.; Xu, Y.-y.; Hao, J.-h.; Sun, Y.; Su, P.-y. (2012). "Effects of growth environments and two environmental endocrine disruptors on children with idiopathic precocious puberty". European Journal of Endocrinology. 166 (5): 803–809. doi:10.1530/EJE-11-0876. ISSN 0804-4643.
- ^ Denham, Melinda; Schell, Lawrence M.; Deane, Glenn; Gallo, Mia V.; Ravenscroft, Julia; DeCaprio, Anthony P.; and the Akwesasne Task Force on the Environment (2005). "Relationship of Lead, Mercury, Mirex, Dichlorodiphenyldichloroethylene, Hexachlorobenzene, and Polychlorinated Biphenyls to Timing of Menarche Among Akwesasne Mohawk Girls". Pediatrics. 115 (2): e127–e134. doi:10.1542/peds.2004-1161. ISSN 0031-4005.
- ^ Wolff, Mary S.; Britton, Julie A.; Boguski, Lisa; Hochman, Sarah; Maloney, Nell; Serra, Nicole; Liu, Zhisong; Berkowitz, Gertrud; Larson, Signe; Forman, Joel (2008). "Environmental exposures and puberty in inner-city girls". Environmental Research. 107 (3): 393–400. doi:10.1016/j.envres.2008.03.006.
- ^ Fagbamigbe, Adeniyi Francis; Obiyan, Mary; Fawole, Olufunmilayo I. (2022). "Gender differentials in the timing and prognostic factors of pubarche in Nigeria". PLOS ONE. 17 (11): e0277844. doi:10.1371/journal.pone.0277844. ISSN 1932-6203. PMC 9678277. PMID 36409757.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ a b Das, Jai K.; Salam, Rehana A.; Thornburg, Kent L.; Prentice, Andrew M.; Campisi, Susan; Lassi, Zohra S.; Koletzko, Berthold; Bhutta, Zulfiqar A. (2017). "Nutrition in adolescents: physiology, metabolism, and nutritional needs: Adolescents: physiology, metabolism, and nutrition". Annals of the New York Academy of Sciences. 1393 (1): 21–33. doi:10.1111/nyas.13330.
- ^ Soliman, Ashraf; De Sanctis, Vincenzo; Elalaily, Rania (2014). "Nutrition and pubertal development". Indian Journal of Endocrinology and Metabolism. 18 (Suppl 1): S39. doi:10.4103/2230-8210.145073. PMC 4266867. PMID 25538876.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ a b c d e Tang, Christine; Zafar Gondal, Anoosh; Damian, Middey (2023), "Delayed Puberty", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31335042, retrieved 2023-07-26