Still, she added, many girls who develop early are not overweight. Central precocious puberty (CPP) is diagnosed when premature activation of the hypothalamic-pituitary axis occurs. Abstract Precocious puberty is defined as pubertal development occurring more than 2.5 standard deviations earlier than the average age. Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2018. Other factors may also be involved in earlier puberty, at least in girls. Bisphenol A (BPA) is another widely used chemical found in cups, water bottles, food storage containers and food cans. In central precocious puberty, the HPG axis is activated, resulting in early but normal development, symmetric progression of secondary sexual characteristics, and increasing growth velocity.6,9,32 Central precocious puberty is approximately 10-fold more common in girls than in boys.33 Although usually idiopathic in girls, it can be incited by head trauma, neoplasm, radiation, or genetic conditions.5,6,9 Pathologic causes of central precocious puberty are more common in boys.5,6,9, Peripheral precocious puberty occurs when hormonal influences originating outside of the HPG axis produce incomplete, atypically sequenced or rapid pubertal progression.5,6,9 Quickly progressing or significant hyperandrogenic findings may warrant workup for congenital adrenal hyperplasia or an androgen-secreting tumor. 25.98% and 38.58% of boys with precocious puberty were respectively accompanied by obesity (OR=2.15, 95% CI=1.31 to 3.50) or central obesity (OR=2.10, 95% CI=1.46 to 3.03); meanwhile, 13.86% and 29.42% of girls with precocious puberty were respectively accompanied by obesity (OR=9.00, 95% CI=5.60 to 14.46) or central obesity (OR=5.40, 95% CI=4.10 to 7.12). Isolated prepubertal vaginal bleeding not caused by trauma, abuse, a foreign body, infection, or an exceedingly rare tumor is usually benign.6,28, Premature adrenarche, driven by adrenal androgens rather than activation of the HPG axis, leads to slowly progressive appearance of pubic and axillary hair, body odor, sweating, and/or mild acne without change in linear growth velocity or enlargement of the testes, penis, breasts, ovaries, or clitoris. This site needs JavaScript to work properly. A tumor in the cells that make sperm (germ cells) or in the cells that make testosterone (Leydig cells). Evid Based Complement Alternat Med. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. No commercial use is permitted unless otherwise expressly granted. In this study, the results regarding body shape awareness and satisfaction showed that childrens dissatisfaction with overweight or obesity was lower than the results reported by Cho et al. Other causes may include central nervous system problems, family history of the disease, or certain rare genetic syndromes. Abnormal pubertal timing can adversely affect a child's physical and psychosocial well-being and may be caused by a range of generally benign or pathologic etiologies. History and physical examination should be followed by measurements of serum follicle-stimulating hormone, luteinizing hormone, and testosterone (boys) or estradiol (girls); and bone age radiography. Girls achieve peak height velocity during sexual maturity ratings 2 and 3 (mean: 8.3 cm per year, age 11 or 12 years) and boys during sexual maturity ratings 3 and 4 (mean: 9.5 cm per year, age 13 or 14 years). When the factors that make up the scale were considered separately, the score for moderation was the lowest overall, at 45.9 3.7, and was regularly the highest at 66.8 5.6 points. Treatment for precocious puberty typically includes medication to delay further development. https://www.nytimes.com/2022/05/19/science/early-puberty-medical-reason.html, endocrine disrupters affect puberty in boys. Chen C., Chen Y., Zhang Y., Sun W., Jiang Y., Song Y., Zhu Q., Mei H., Wang X., Liu S., et al. Sparse, long, slightly pigmented, straight or slightly curled, along the medial labia, Breasts and areolae are further enlarged with a continuous rounded contour, Darker, coarser, more curled, spread sparsely over the mons pubis, Areola and nipple form a secondary mound above the contour of the breast, Adult type, but the area covered is smaller and there is no extension to the medial thighs, Mature adult stage, nipple projection without the secondary mound, Adult type and quantity, sometimes extending to the medial thighs, Enlargement of the testes (more than 4 mL in volume and more than 2.5 cm in length) and scrotum, but not the penis, Sparse, long, slightly pigmented, straight or slightly curled, at the base of the penis, Continued testicular and scrotal enlargement with penile growth, Darker, coarser, more curled, spread sparsely over the pubis, Continued testicular, scrotal, and penile growth with enlargement of the glans, Adult type but the area covered is smaller and there is no extension to the medial thighs or linea alba, Peak height velocity, spermarche, facial hair, voice change, Adult quality and distribution with spread to the medial thighs, Body mass index and weight (growth charts), High: may be associated with precocious puberty, McCune-Albright syndrome, neurofibromatosis, Pubertal growth spurt, pathologic growth due to an underlying condition, Hyperandrogenism: premature adrenarche, peripheral precocious puberty, Neurologic assessment (abnormal examination findings, or symptoms such as headaches or vision changes), Temperature intolerance, gastrointestinal symptoms, tremor, depression, palpitations, Benign variant, genital trauma or abuse, foreign body, infection, McCune-Albright syndrome, Androgen-secreting tumor, congenital adrenal hyperplasia, Body mass index and weight (on growth charts), Low: eating disorder, caloric insufficiency, gastrointestinal or other systemic disease, Chemotherapy, radiation treatment, brain tumor, Dysmorphic features (webbed neck, short stature, low hairline), Constitutional delay of growth and puberty, Peripubertal growth slowing, pathologic growth due to underlying condition, Short stature: Turner syndrome, constitutional delay of growth and puberty, Neurologic assessment (abnormal examination findings or symptoms such as headaches, vision changes), Red (vs. dull pink) or thin vaginal mucosa, Delayed pubertal development (unspecified), Weight loss, stress, excessive exercise, inadequate nutrition, fatigue, Fat tissue but no glandular breast tissue on palpation; associated with obesity, Early but normal sequence of pubertal events that does not progress prematurely, Surveillance every 3 to 6 months to evaluate for progression of pubertal development, Pubic and axillary hair growth, body odor, sweating, and/or mild acne; may have mildly elevated dehydroepiandrosterone sulfate, but normal levels of FSH, LH, 17-hydroxyprogesterone, estradiol, and testosterone; no change in linear growth velocity or enlargement of the testes, penis, breasts, ovaries, or clitoris, Surveillance every 3 to 6 months to evaluate for progression of pubertal development; linear growth velocity should be normal (i.e., consistent with bone age), Glandular breast tissue on palpation (as opposed to lipomastia) without other secondary sexual characteristics, Absence of secondary sexual characteristics, genital trauma or abuse, foreign body, infection, evidence of McCune-Albright syndrome; possible ovarian enlargement on ultrasonography, Surveillance for heavy or recurrent bleeding, Central nervous system lesion (e.g., hypothalamic hamartoma), radiation, trauma, Early but normal sequence of pubertal events; possible magnetic resonance imaging abnormalities, Treatment of underlying cause, which may involve GnRH analogue, Early but normal sequence of pubertal events; possible reproductive organ enlargement on ultrasonography (unlike premature thelarche), Prior sex steroid exposure (e.g., peripheral precocious puberty), Early but normal sequence of pubertal events with suggestive history, Pubic or axillary hair growth, possibly acne and clitoromegaly; prepubertal testes; elevated adrenal hormone (e.g., dehydro-epiandrosterone sulfate); adrenal imaging abnormalities, Pubic or axillary hair growth, possibly acne and clitoromegaly; prepubertal testes; elevated adrenal hormone (e.g., 17-hydroxy-progesterone), Referral to a pediatric endocrinologist for multisystem treatment and surveillance, Exposure to contraceptives, testosterone preparations, phthalates, or lavender tree oil, Elevated thyroid-stimulating hormone, breast or testicular development, Multiple caf au lait spots and fibrous dysplasia of bones, ovarian enlargement or testicular abnormalities on ultrasonography; may have menstrual bleeding before other development, May be apparent on physical examination or imaging and accompanied by elevated serum testosterone or estradiol; human chorionic gonadotropinsecreting germ cell tumors activate testes in boys; may occur outside of the gonads, Treatment of the tumor; ovarian tumor should be differentiated from a benign ovarian cyst, Elevated (girls): estrogen exposure; if markedly elevated (> 100 pg per mL [367 pmol per L]), evaluate for ovarian tumor, especially if luteinizing hormone is suppressed, Low (girls): prepubertal, may suggest poor ovarian function in response to gonadotropins, Elevated: testicular (boys), adrenal, or exogenous source, Low (boys): prepubertal, poor response of testes to gonadotropin stimulation, Serum LH and follicle-stimulating hormone, Prepubertal levels: benign variant or peripheral precocious puberty, High: gonadal insufficiency, Turner syndrome, Klinefelter syndrome, Postpubertal levels > 0.3 mIU per mL (0.3 IU per L): central precocious puberty, Low: hypogonadotropic hypogonadism, constitutional delay of growth and puberty, Directed testing (e.g., for celiac disease; diabetes mellitus; or hepatic, renal, or inflammatory conditions), Functional hypogonadotropic hypogonadism, seek underlying cause, Gonadotropin-releasing hormone analogue stimulation test, Elevated LH: central precocious puberty (vs. benign variant) in complex clinical scenarios, Suppressed LH but elevated sex steroids: peripheral precocious puberty, Elevated: nonclassic (late onset) congenital adrenal hyperplasia, Elevated: adrenal source, premature adrenarche (mild elevation) vs. peripheral precocious puberty, Normal for age: may suggest persistent hypogonadotropic hypogonadism rather than constitutional delay of growth and puberty, Serum human chorionic gonadotropin (boys), Elevated: human chorionic gonadotropinsecreting germ cell tumor, Low: growth hormone deficiency (if low for both bone and chronologic age), High: prolactin-secreting tumor, hypothyroidism, other neoplasm, Serum thyroid-stimulating hormone and free thyroxine, Advanced (> 2 standard deviations): more likely to be central or peripheral precocious puberty, less likely to be benign pubertal variant, Delayed: constitutional delay of growth and puberty, underlying chronic disease, Magnetic resonance imaging (brain and pituitary), Ovarian or testicular tumor; greater ovarian volume may indicate central precocious puberty (vs. benign variant), Absence of the uterus (e.g., androgen insensitivity, Mllerian system abnormalities), Normal growth velocity, history of delayed puberty in parents, delayed bone age, Surveillance every 6 months to evaluate for progression of pubertal development, Abdominal pain, malabsorption, anemia, poor weight gain; short stature may be the only symptom; positive serology results, confirmed with endoscopic biopsy, Polyuria, polydipsia, polyphagia, weight loss, or known but poorly controlled disease; confirmed by serology, Weight loss, heat intolerance, insomnia, tachycardia, hypertension; confirmed with serology, Weight gain, cold intolerance, fatigue, bradycardia; confirmed with serology, Inadequate nutrition for metabolic needs (e.g., eating disorder), Weight loss or poor weight gain, excessive exercise, food restriction, purging, Weight restoration, treatment of underlying disorder, Abdominal pain, constipation, diarrhea, hematochezia, poor weight gain, elevated serum erythrocyte sedimentation rate and C-reactive protein; confirmed with endoscopic biopsy, Gonadotropin-releasing hormone deficiency, bilateral cryptorchidism, micropenis, unilateral renal agenesis, synkinesis (mirror movements), cleft lip or palate, hearing loss, dental agenesis, skeletal malformations, Referral to a pediatric endocrinologist for hormone therapy, Anosmia in addition to congenital hypogonadotropic hypogonadism presentation, History of trauma, surgery, or CNS radiation for prior malignancy; may present similarly to CNS tumor if acute, Referral to a pediatric endocrinologist for hormone therapy; other referrals as necessary for treatment of underlying disease, Headaches, vision changes, seizures, suggestive magnetic resonance imaging findings of the brain and pituitary, Referral for diagnosis and treatment of underlying disease (e.g., neurosurgeon, endocrinologist), Chemotherapy, radiation, or trauma to gonads, Tall stature, learning disabilities, relatively small testes (3 to 6 mL) for degree of androgenization; 47,XXY karyotype, Short stature, facial dysmorphism, webbed neck, brachydactyly, heart defects; in cases of mosaicism, short stature may be the only sign; 45,X or related karyotype, Referral to a pediatric endocrinologist for hormone therapy and other comprehensive care, Any pubertal changes before 6 years of age in girls and 9 years of age in boys, Pubertal changes with associated headaches, vision changes, new-onset seizures, Confirmed central or peripheral precocious puberty (not a generally benign variant), Known predisposing conditions (e.g., neurofibromatosis, previous irradiation, known neoplasm), Boys without testicular growth to at least 4 mL in volume or 2.5 cm in length by 14 years of age, Girls without breast development by 13 years of age. Obesity is reported to be closely relevant to early sexual development but the relationship between sexual precocity and obesity or central obesity is still inconsistent, especially in boys. All rights reserved. Drug and Therapeutics and Executive Committees of the Lawson Wilkins Pediatric Endocrine Society. Evaluation for chronic disease; hyperprolactinemia; testicular or adrenal neoplasm; use of prescription, recreational, or performance-enhancing drugs; or hypogonadism (e.g., Klinefelter syndrome) should be initiated if symptoms persist for 18 to 24 months or the patient has no pubertal changes.31, Precocious puberty can be characterized by the pathologic location. The associations between the BMI of the children and the parents were evaluated by Pearsons correlation coefficient analysis. In many cases, no cause can be found for the disorder. 8600 Rockville Pike nutrition obesity obstetrics oncology ophthalmology orthopaedics paediatrics . With shared decision making, parents can weigh the risks of sedation, intravenous contrast media, and follow-up imaging (leading to anxiety and high cost) against the low likelihood that imaging will show a new central nervous system malignancy (at most 1%).5,6,35, If started early in the course of central precocious puberty, gonadotropin-releasing hormone analogues (e.g., leuprolide [Lupron]) appear to safely prevent premature fusion of growth plates, thereby preserving height potential.36 Because of high annual costs, treatment may be most appropriate if bone age suggests impending short stature or if the patient exhibits aggression (boys) or profound emotionality in response to menses (girls).10,37, Delayed puberty is the absence of breast development by 13 years of age in girls or the absence of testicular growth to at least 4 mL in volume or 2.5 cm in length by 14 years of age in boys.79,25,38 Constitutional delay of growth and puberty is the most common cause of delayed puberty in boys (60%) and girls (30%).39,40 It represents an extreme of the normal spectrum of pubertal timing and is a diagnosis of exclusion.39,40 For more than 75% of patients with constitutional delay of growth and puberty, family history may reveal parental pubertal delay.41,42, Other etiologies of delayed puberty are categorized based on gonadotropin levels. 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