Delayed puberty - Wikipedia, the free encyclopedia
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http://en.wikipedia.org/wiki/Delayed_puberty
From Wikipedia, the free encyclopedia
Puberty is described as delayed puberty with exceptions
when an organism has passed the usual age of onset of
puberty with no physical or hormonal signs that it is
beginning. Puberty may be delayed for several years and still
occur normally, in which case it is considered constitutional
delay, a variation of healthy physical development. Delay of
puberty may also occur due to malnutrition, many forms of
systemic disease, or to defects of the reproductive system
(hypogonadism) or the body's responsiveness to sex
hormones.
Delayed puberty
Classification and external resources
ICD-10
E30.0 (http://apps.who.int
/classifications/icd10/browse/2010/en#
/E30.0)
ICD-9
259.0 (http://www.icd9data.com
/getICD9Code.ashx?icd9=259.0)
DiseasesDB 17462
(http://www.diseasesdatabase.com
/ddb17462.htm)
MeSH
1 Normal timing
2 Evaluation
2.1 Lateness
2.2 Discordance
2.3 Indications of specific disorders
3 Possible causes
4 Constitutional delay
5 Medical evaluation
6 Management
7 See also
8 References
D011628 (http://www.nlm.nih.gov
/cgi/mesh/2012/MB_cgi?field=uid&
term=D011628)
Approximate mean ages for the onset of various pubertal changes are as follows. Ages in parentheses are the
approximate 3rd and 97th percentiles for attainment. For example, less than 3% of girls have not yet achieved
thelarche by 13 years of age. Developmental changes during puberty in girls occur over a period of 3 – 5 years,
usually between 10 and 15 years of age. They include the occurrence of secondary characteristics beginning
with breast development, the adolescent growth spurt, the onset of menarche – which does not correspond to
the end of puberty – and the acquisition of fertility, as well as profound psychological modifications.
The normal variation in the age at which adolescent changes occur is so wide that puberty cannot be considered
to be pathologically delayed until the menarche has failed to occur by the age of 18 or testicular development by
the age of 20.
For North American, Indo-Iranian (India, Iran)
and European girls
For North American, Indo-Iranian (India, Iran)
and European boys
Thelarche (breast development) 10.0y5m
Gonadarche (testicular enlargement) 11.5y
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(8y–13y)
Pubarche (pubic hair) 11y (8.5–13.5y)
Growth spurt 11.25y (10–12.5y)
Menarche (first menstrual bleeding) 12.5y
(10.5–14.5y)
Adult height reached 15.5y (?-?)
http://en.wikipedia.org/wiki/Delayed_puberty
(9.5–13.5y)
Pubarche (pubic hair) 12y (10–14y)
Growth spurt 14y (11-17y)
Completion of growth 17y (15-20y)
The sources of the data, and a fuller description of normal timing and sequence of pubertal events, as well as the
hormonal changes that drive them, are provided in the principal article on puberty.
There are three indications that pubertal delay may be due to an abnormal cause.
Lateness
The first is simply degree of lateness: although no recommended age of evaluation cleanly separates pathologic
from physiologic delay, a delay of 2–3 years or more warrants evaluation.
In girls, no breast development by 13 years, or no menarche by 3 years after breast development (or by
16).
In boys, no testicular enlargement by 14 years, or delay in development for 5 years or more after onset of
genitalia enlargement.
A delay of two standard deviations has been proposed as a standard.[1]
Discordance
The second indicator is discordance of development. In most children, puberty proceeds as a predictable series
of changes in specific order. In children with ordinary constitutional delay, all aspects of physical maturation
typically remain concordant but a few years later than average. If some aspects of physical development are
delayed, and others are not, it is likely that something is wrong.
For instance, in most girls, the beginning stages of breast development precede pubic hair. If a 12 year old
girl were to reach Tanner stage 3 pubic hair for a year or more without breast development, it would be
unusual enough to suggest an abnormality such as defective ovaries.
Similarly, if a 13 year old boy had reached stage 3 or 4 pubic hair with testes that still remained
prepubertal in size, it would be unusual and suggestive of a testicular abnormality.
Indications of specific disorders
The third indicator is the presence of clues to specific disorders of the reproductive system.
Malnutrition or anorexia nervosa severe enough to delay puberty will give other clues as well.
Poor growth would suggest the possibility of hypopituitarism or Turner syndrome.
Reduced sense of smell (hyposmia) suggests Kallmann syndrome.
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Variation of normal (constitutional delay)
In females, prolonged high level of physical exertion, e.g. from being an athlete
Systemic disease, e.g. Inflammatory bowel disease, chronic renal failure
Undernutrition e.g. anorexia nervosa, zinc deficiency
Hypothalamic defects and diseases e.g. Prader-Willi syndrome, Kallmann syndrome
Pituitary defects and diseases e.g. hypopituitarism
Gonadal defects and diseases e.g. Turner syndrome, Klinefelter syndrome, Testicular failure due to
mumps orchitis, Coxsackievirus B, irradiation, chemotherapy, or trauma. Testicular failure is treated with
testosterone replacement,[2] Ovarian failure.[2]
Absence or unresponsiveness of target organs e.g. androgen insensitivity syndrome, mullerian agenesis
Other hormone deficiencies and imbalances, Endocrine disorders.[3] e.g. hypothyroidism, Cushing's
syndrome
Cystic fibrosis[4]
Mutations in FSHB[5]
Frasier syndrome[6]
Various forms of congenital adrenal hyperplasia.[3]
Gonadotropin, a deficiency resulting from a number of congenital and acquired abnormalities of the
central nervous system
Biedl-Bardet syndrome
Brain tumors e.g. craniopharyngioma, prolactinoma, germinoma, glioma; diseases of hypothalamus,
irradiation and trauma.
Children who are healthy but have a slower rate of physical development than average have constitutional delay
in growth and adolescence. These children have a history of stature shorter than their age-matched peers
throughout childhood, but their height is appropriate for bone age, and skeletal development is delayed more
than 2.5 SD. They usually are thin and often have a family history of delayed puberty. Children with a
combination of a family tendency toward short stature and constitutional delay are the most likely to seek
evaluation. They quite often seek evaluation when classmates or friends undergo pubertal development and
growth, thereby accentuating their delay.
Pediatric endocrinologists are the physicians with the most training and experience evaluating delayed puberty.
A complete medical history, review of systems, growth pattern, and physical examination will reveal most of the
systemic diseases and conditions capable of arresting development or delaying puberty, as well as providing
clues to some of the recognizable syndromes affecting the reproductive system.
Since bone maturation is a good indicator of overall physical maturation, an x-ray of the hand to assess bone age
usually reveals whether the child has reached a stage of physical maturation at which puberty should be
occurring. Visible secondary sexual development usually begins when girls achieve a bone age of 10.5 to 11
years, and boys achieve a bone age of 11.5 to 12 years.
The most valuable blood tests are the gonadotropins, because elevation confirms immediately a defect of the
gonads or deficiency of the sex steroids. In many instances, screening tests such as a complete blood count,
general chemistry screens, thyroid tests, and urinalysis may be worthwhile.
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More expensive and complicated tests, such as a karyotype or magnetic resonance imaging of the head, are
usually obtained only when specific evidence suggests they may be useful.
Use of gonadotropin releasing hormone can be of value in the differential diagnosis.[7]
If delayed puberty is accompanied with a lack of sense of smell (anosmia) or a history of un-descended testicles
(cryptorchidism) when born then a diagnosis of Kallmann syndrome could be considered.[8][9]
If a child is healthy but simply late, reassurance and prediction based on the bone age can be provided. No other
intervention is usually necessary. In more extreme cases of delay, or cases where the delay is more extremely
distressing to the child, a low dose of testosterone or estrogen for a few months may bring the first reassuring
changes of normal puberty.
If the delay is due to systemic disease or undernutrition, the therapeutic intervention is likely to focus mainly on
those conditions.
If it becomes clear that there is a permanent defect of the reproductive system, treatment usually involves
replacement of the appropriate hormones (testosterone/dihydrotestosterone for boys,[10] estradiol and
progesterone for girls).
Pubertal delay due to gonadotropin deficiency is treated with testosterone replacement or with HCG [2]
Growth hormone is another option that has been described.[11][12]
Subnormal vitamin A intake is one of the aetiological factors in delayed pubertal maturation. Supplementation of
both vitamin A and iron to normal constitutionally delayed children with subnormal vitamin A intake is as
efficacious as hormonal therapy in the induction of growth and puberty.[13]
Endocrinology
Menarche
Precocious puberty
Tanner stage
Developmental milestones
Hypogonadism
Kallmann syndrome
1. ^ Traggiai C, Stanhope R (2003). "Disorders of
pubertal development". Best Pract Res Clin Obstet
Gynaecol 17 (1): 41–56.
doi:10.1053/ybeog.2003.0360 (http://dx.doi.org
/10.1053%2Fybeog.2003.0360) . PMID 12758225
(//www.ncbi.nlm.nih.gov/pubmed/12758225) .
2. ^ a b c Marianne J. Legato, ed. (2004) "Principles of
Gender-Specific Medicine, Volume 1-2", ISBN
0-12-440905-9, p. 22
3. ^ a b Greenspan, FS; Gardner DG (2004). "Puberty".
Basic & Clinical Endocrinology. pp. 617–627.
ISBN 0-07-140297-7.
4. ^ Johannesson M, Gottlieb C, Hjelte L (1997).
"Delayed puberty in girls with cystic fibrosis despite
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5.
6.
7.
8.
9.
good clinical status"
(http://pediatrics.aappublications.org
/cgi/pmidlookup?view=long&pmid=8989333) .
Pediatrics 99 (1): 29–34. doi:10.1542/peds.99.1.29
(http://dx.doi.org/10.1542%2Fpeds.99.1.29) .
PMID 8989333 (//www.ncbi.nlm.nih.gov/pubmed
/8989333) . http://pediatrics.aappublications.org
/cgi/pmidlookup?view=long&pmid=8989333.
^ Layman LC, Lee EJ, Peak DB, et al. (1997).
"Delayed puberty and hypogonadism caused by
mutations in the follicle-stimulating hormone
β-subunit gene" (http://content.nejm.org
/cgi/pmidlookup?view=short&pmid=9271483&
promo=ONFLNS19) . N. Engl. J. Med. 337 (9):
607–11. doi:10.1056/NEJM199708283370905
(http://dx.doi.org
/10.1056%2FNEJM199708283370905) .
PMID 9271483 (//www.ncbi.nlm.nih.gov/pubmed
/9271483) . http://content.nejm.org
/cgi/pmidlookup?view=short&pmid=9271483&
promo=ONFLNS19.
^ Chan WK, To KF, But WM, Lee KW (June 2006).
"Frasier syndrome: a rare cause of delayed puberty"
(http://www.hkmj.org/abstracts/v12n3/225.htm) .
Hong Kong Med J 12 (3): 225–7. PMID 16760553
(//www.ncbi.nlm.nih.gov/pubmed/16760553) .
http://www.hkmj.org/abstracts/v12n3/225.htm.
^ Jungmann E, Trautermann C (1994). "[The status
of the gonadotropin releasing hormone test in
differential diagnosis of delayed puberty in
adolescents over 14 years of age]" (in German).
Med. Klin. (Munich) 89 (10): 529–33.
PMID 7808353 (//www.ncbi.nlm.nih.gov/pubmed
/7808353) .
^ Oxford Endocrinology Library. Testosterone
Deficiency in Men. 2008. ISBN 978-0199545131
Editor: Hugh Jones. Chapter 9. Puberty & Fertility.
^ Male Hypogonadism. Friedrich Jockenhovel.
Uni-Med Science. 2004. ISBN 3-89599-748-X.
http://en.wikipedia.org/wiki/Delayed_puberty
Chapter 3. Diagnostic work up of hypogonadism.
10. ^ Saad RJ, Keenan BS, Danadian K, Lewy VD,
Arslanian SA (October 2001). "Dihydrotestosterone
treatment in adolescents with delayed puberty: does
it explain insulin resistance of puberty?"
(http://jcem.endojournals.org
/cgi/pmidlookup?view=long&pmid=11600557) . J.
Clin. Endocrinol. Metab. 86 (10): 4881–6.
doi:10.1210/jc.86.10.4881 (http://dx.doi.org
/10.1210%2Fjc.86.10.4881) . PMID 11600557
(//www.ncbi.nlm.nih.gov/pubmed/11600557) .
http://jcem.endojournals.org
/cgi/pmidlookup?view=long&pmid=11600557.
11. ^ Heinrichs C, Bourguignon JP (1991). "Treatment
of delayed puberty and hypogonadism in girls".
Horm. Res. 36 (3–4): 147–52.
doi:10.1159/000182149 (http://dx.doi.org
/10.1159%2F000182149) . PMID 1818011
(//www.ncbi.nlm.nih.gov/pubmed/1818011) .
12. ^ Massa G, Heinrichs C, Verlinde S, et al.
(September 2003). "Late or delayed induced or
spontaneous puberty in girls with Turner syndrome
treated with growth hormone does not affect final
height" (http://jcem.endojournals.org
/cgi/pmidlookup?view=long&pmid=12970282) . J.
Clin. Endocrinol. Metab. 88 (9): 4168–74.
doi:10.1210/jc.2002-022040 (http://dx.doi.org
/10.1210%2Fjc.2002-022040) . PMID 12970282
(//www.ncbi.nlm.nih.gov/pubmed/12970282) .
http://jcem.endojournals.org
/cgi/pmidlookup?view=long&pmid=12970282.
13. ^ Zadik Z, Sinai T, Zung A, Reifen R. (2004).
"Vitamin A and iron supplementation is as efficient
as hormonal therapy in constitutionally delayed
children." (http://www.ncbi.nlm.nih.gov/pubmed
/15163330) . Clin Endocrinol (Oxf). 60 (6): 682–7.
PMID 15163330 (//www.ncbi.nlm.nih.gov/pubmed
/15163330) . http://www.ncbi.nlm.nih.gov/pubmed
/15163330.
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Categories: Endocrine gonad disorders Gonadotropin-releasing hormone and gonadotropins Pediatrics
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