[Normal and deviating puberty in boys].
BACKGROUND
Onset of puberty in boys is more complex than in girls, and delayed onset is the most common puberty complication in boys. This article presents the physiology of normal development of male puberty and the background for commonly associated disturbances.


METHODS
The article builds on clinical experience and relevant publications within pediatric endocrinology.


CONCLUSIONS
Mechanisms involved in pubertal development of gonads remain unclear despite intensive research. Height growth as well as the age for onset of puberty are influenced by environmental factors. Genetic factors are however more important determinants within a defined population and one usually inherits the probability for both early and delayed puberty. Gonadotropin releasing hormone (GnRH) neurons in the hypothalamus secrete GnRH in intermittent pulses to the pituitary glands that respond with pulsatile LH and FSH production. These neurons are thus decisive for testicle activity and therefore puberty development. GnRH-neurons are inactive during childhood because many types of hypothalamic neurons suppress them. Puberty starts when this suppression is reduced and kisspeptin-producing neurons stimulate GnRH neuron activity. At a testicle volume of 4 mL the Leydig cells' testosterone production has reached such a level that pubertal changes become apparent. Delayed or incomplete puberty sometimes occurs in certain syndromes, and complete lack of puberty can also be syndrome-related. Klinefelter's syndrome is associated with gonad dysgenesis expressed as gradual reduction of gonadal function starting after puberty. Cancer treatment during childhood; especially radiation therapy of the gonads, may cause hypogonadism and infertility. It is therefore essential to follow gonad function closely in these patients. In conclusion, each doctor treating children should be able to evaluate the degree of puberty development and when needed request adequate laboratory tests.
Barnendokrinologiska Enheten, Astrid Lindgrens Barnklinik, Karolinska Sjukhuset, S-171 76 Stockholm.
Lars
L
Hagenäs
D000293:Adolescent; D050499:Adrenarche / Q000502:physiology; D002648:Child; D012734:Disorders of Sex Development / Q000503:physiopathology; D007987:Gonadotropin-Releasing Hormone / Q000502:physiology; D013006:Growth Hormone / Q000502:physiology; D006801:Humans; D007006:Hypogonadism / Q000503:physiopathology; D008297:Male; D011627:Puberty / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D025064:Sex Chromosome Disorders / Q000503:physiopathology; D013737:Testis / Q000033:anatomy & histology / Q000166:cytology / Q000254:growth & development
D007987:Gonadotropin-Releasing Hormone; D013006:Growth Hormone