Adolescent Development and Tanner Staging
Ajuah Davis
NORMAL PUBERTAL DEVELOPMENT
Puberty is the period of transition from sexual immaturity to potential fertility, during which secondary sexual characteristics develop. It begins with decreasing sensitivity of the hypothalamic-pituitary-gonadal (HPG) axis and increasing pulsatile release of gonadotropin-releasing hormone (GnRH), and the gonadotropins luteinizing hormone (LH), and follicle-stimulating hormone (FSH). The hormonal changes begin years before the physical changes are noted. Breast development is the first sign of puberty in girls. In boys, puberty is heralded by an increase in testicular size to a volume of 4 cc or a length >2.5 cm in the long axis. Pubertal events usually follow a sequence, with a mean age at onset of 11.2 years in girls and 11.6 years in boys. However, the onset of puberty in healthy children varies widely.
Tanner staging is used to correlate pubertal events and their typical ages at presentation (Tables 44.1 and 44.2). Along with height velocity, it provides a good measure of growth and physical maturation. Peak height velocity occurs early in girls, at Tanner stage II/III. In boys, it is a late pubertal event, occurring at Tanner stage IV. The appearance of acne occurs in late puberty in both boys and girls, as does the growth of axillary hair in girls and of axillary and facial hair in boys. Most girls experience menarche at the age of 12.8 ± 1.0 year, when they are at Tanner stage III/IV.
Two extreme variations of normal development are premature thelarche and premature adrenarche. Premature thelarche is characterized by early breast development without other signs of puberty. It occurs most often within the first 2 years of life, with a second peak noted after the age of 6 years. Premature adrenarche, characterized by the early development of pubic hair, usually occurs between the ages of 6 and 8 years. These conditions are not associated with other pubertal changes. No height acceleration or advancement in the bone age takes place. Follow-up of these patients is indicated every 4 to 6 months to confirm the benign, nonprogressive nature of their condition. In some cases, what was initially thought to be a benign condition evolves into precocious puberty. Pubertal gynecomastia is another normal variant that occurs in as many as 75% of boys during the teenage years. The problem typically resolves within 2 years, but in cases of prolonged or excessive breast development surgery is indicated. Some pathologic conditions can also be associated with gynecomastia.
The onset of puberty before the age of 8 years in girls and 9 years in boys is unusual and deserves evaluation. If puberty is caused by reactivation of the HPG axis, the condition is called central precocious puberty. The hormonal interactions are normal, but the timing is early. Central precocious puberty is five times more common in girls than in boys, and in most cases no cause is identified. In boys, neurological causes are seen in >60% of cases, so that a thorough search for central nervous system (CNS) pathology is especially important.
When puberty is not mediated by pituitary gona-dotropin secretion, it is called peripheral precocious puberty. The source of the sex hormones may be exogenous or endogenous, gonadal or extragonadal. Maturation may be incomplete, with only one type of secondary sexual characteristic developing early. In some children the pubertal development can be contrasexual (characteristics of the opposite sex develop).
TABLE 44.1 MEAN AGES FOR TANNER STAGES IN U.S. GIRLS | ||||||||||||||||||||||||||||||
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PRECOCIOUS PUBERTY
When a girl younger than 8 years or a boy younger than 9 years presents with one or more of the features of breast development, growth of pubic hair, accelerated linear growth, menstruation, or acne development, an evaluation for possible precocious puberty is warranted. The goals of the evaluation are to:
Document whether precocious puberty is taking place
Differentiate central from peripheral precocious puberty
Identify and appropriately treat the cause of the precocious puberty
The diagnosis of precocious puberty should be established by the physical examination. The normal variants, premature thelarche and premature adrenarche, usually can be distinguished on the basis of the examination and confirmed by careful medical follow-up.
The differential diagnosis for precocious puberty includes the following.
TABLE 44.2 MEAN AGES FOR TANNER STAGES IN U.S. BOYS | ||||||||||||||||||||||||||||||
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Central Precocious Puberty
Idiopathic
CNS lesions
Hypothalamic hamartoma
Tumors (neurofibroma, craniopharyngioma)
Malformations (septo-optic dysplasia, hydrocephalus, arachnoid cyst)
Infection (brain abscess, meningitis)
Trauma (surgery, irradiation, injury)
States of peripheral precocious puberty
Peripheral Precocious Puberty
Congenital adrenal hyperplasia
Ovarian cysts
Autonomous (McCune-Albright syndrome, testotoxicosis)
Exogenous hormones
Severe primary hypothyroidism
Adrenal or gonadal tumors
The pubertal changes, and their duration and progression, should be determined. Slowly progressive or minimal physical changes are often benign in nature, whereas multiple changes in the same child are of concern. An assessment of the patient’s general health, medications, and nutrition is required. It is important to obtain previous heights so that the patient’s growth pattern can be determined. An increase in the growth velocity is seen during puberty. Prior to puberty the child’s growth rate is approximately 2.5 in. or 6 cm per year. Any type of CNS dysfunction can cause central precocious puberty. A history of CNS trauma or infection, headaches, and visual changes should be elicited. Precocious puberty may develop in survivors of childhood cancers and CNS tumors as a result of their treatment. The age at onset of puberty in other family members should be noted because children often follow family patterns. The physician should also inquire about possible exposure to exogenous hormones.
During the physical examination, the physician should pay particular attention to Tanner staging and the presence of other pubertal changes, such as acne, adult body odor, and axillary hair. The skin should be carefully inspected for pigmented lesions (McCune-Albright syndrome or neurofibromatosis). A neurologic assessment should be performed. The ophthalmologic examination should include funduscopic and visual field evaluations.
The development of true breast tissue versus fatty tissue is assessed by palpation with the child in a supine position. In addition to the development of pubic hair, the color of the vaginal mucosa should be noted in girls. Visual inspection is adequate to assess the presence of estrogen stimulation. A glistening red appearance is consistent with a non-estrogen-stimulated mucosa, whereas a pinkish mucosa is suggestive of estrogen stimulation.
A bone age roentgenogram for skeletal maturation should be obtained immediately. In children with precocious puberty, the bone age is usually advanced, but advancement in the bone age may not be apparent if the pubertal changes have occurred rapidly. Children with premature thelarche or adrenarche do not have an advanced bone age. In many children with central precocious puberty, physical maturation progresses more rapidly than the normal pattern. A skeletal survey should be requested in suspected cases of McCune-Albright syndrome to look for polyostotic fibrous dysplasia.
Because of the episodic nature of gonadotropin secretion, random LH and FSH levels may not be elevated. A GnRH stimulation test should be performed to determine whether the gonadotropin response is consistent with maturation of the HPG axis. Children with central precocious puberty exhibit a brisk rise in FSH levels, and an even greater rise in LH levels. Prepubertal children or those with peripheral precocious puberty do not show a rise in LH and FSH levels. Measurement of the plasma estradiol or testosterone level can support the suspected diagnosis.
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