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Sperm abnormalities

 

Infertility and Sperm Abnormalities

Hypogonadism

Male hypogonadism can be caused by a disease of the testicles, or an altercation of the pituitary gland, which results in insufficient production of gonadotrophic hormone. Changes in the pituitary can be congenital (eg Kallman syndrome) or may be acquired as a result of a pituitary adenoma (eg prolactinoma, craniopharyngioma) or as a result of radiation treatment.

In men, hypogonadism causes the symptoms and signs of deficiency of the hormone androgen. Their effects vary with the development of disability before or after puberty. Typical effects include the lack of growth of body hair and beard, soft skin, a high-pitched voice, sexual drive and performance reduced, underdevelopment of the genitalia and poor muscular development.


Hypothalamic-pituitary disease

Hyper-and / or hypo-secretion of hormones or hypothalamic pituitary is a rare cause of infertility. When this is the cause of infertility, the results of pro-fertility treatment are often excellent. Two syndromes are recognized:
  • Hypergonadotropic hypogonadism

  • Hypogonadism

Hypergonadotropic hypogonadism

This altercation is characterized by very high levels of circulating gonadotropins, but the testes do not respond to stimulation. These findings usually occur in patients with primary testicular failure. The chances of fertility are remote, but the empirical hormonal treatment with testosterone is rarely effective.

Hypogonadism

In these patients, the secretion of pituitary gonadotropins is insufficient to stimulate the normal testes. The defect may be at the level of the pituitary gland itself, or at the hypothalamic level. A very large number of endocrine disorders, most of them rare, such as trauma, infections or tumours, can result in levels of gonadotropins absent or reduced.


Is possible to differentiate between primary failure of pituitary secretion or pituitary insufficiency secondary to a hypothalamic defect, with reduced secretion of GnRH. In the case of primary pituitary insufficiency, the treatment is replacement therapy by administration of exogenous gonadotropins. When the defect is at the hypothalamus, specific treatment is by administration of GnRH.

Chromosomal

An abnormal numbers of sex chromosomes may result in changes in the male reproductive system. For example, infertility often follows the Klinefelter syndrome. This condition occurs due to a chromosomal abnormality in which a male subject has one or more extra X chromosomes in their cells. Klinefelter's syndrome affects about one in every 500 male children born and the likelihood of a baby having the condition increase with age of the mother.

Klinefelter's syndrome is almost always associated with azoospermia. The extra X chromosome appears to have little effect on the structure of the seminiferous tubules before puberty, but puberty appears progressive and devastating destruction of the seminiferous epithelium. Some patients with Klinefelter syndrome, in fact, have significant growth of the testes in early puberty, followed by a subsequent decrease in size. Also there is an increase volume of the breasts
There is no cure for Klinefelter syndrome, although hormone therapy can be used to induce secondary sexual characteristics, such as growth of facial hair.

Men with an extra Y chromosome have various degrees of spermatogenic impairment, ranging from normal spermatogenesis to stop spermatogenesis. There are some other rare chromosomal changes that also result in inability to produce sperm.


Defects in sperm-egg fusion

  It has been shown that additional adhesion molecules are located on the surface of the oocyte and sperm. These molecules interact and lead to fusion (fertilization). The function of this system seems to be important not only for fusion but also for the prevention of polyspermy (the fertilization of an egg by more than one sperm). Changes in adhesion molecules on the surface of gametes, or other disabilities that affect sperm-egg fusion, are recognized causes of infertility

 

Last updated: 10/02/2012

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