OAT syndrome

The OAT syndrome (oligo-Astheno teratozoospermia syndrome) is a pathological change of sperm. Here, too little (oligo) to small portable (astheno) and multiply malformed (terato) sperm to see. It is often accompanied by male infertility.

index

    1 Causes
        1.1 malposition of the testicles
        1.2 varicocele
        1.3 chromosomal abnormality
        1.4 Disorders of hormonal
        1.5 Infections
        1.6 Other causes
    2 diagnosis
        2.1 severities
    3 Prevention
    4 therapy
    5 Literature
    6 References

root causes

The causes lie either in the spermatogenesis (sperm production) or in transport in the seeds ways.
Malposition of the testicles

The testicles are formed approximately at the level of Nierenunterpols and hike up to the birth, but no later than by the end of the first year, in the scrotum (the scrotum). When disturbances of this so-called descent of the testis the testicles in the abdomen or elsewhere may remain. This is called positional anomalies of the testicles, as strips testicles sliding testis etc.

By malposition occurs a temperature rise and to damage of sperm formation through to their complete absence, of the so-called azoospermia.
Varicocele

In a varicocele is a palpable and visible extension of the vein network around the spermatic cord. In about 15% of men with a varicocele suffer from infertility, the relationship is still understood to be incomplete.
Chromosomal abnormality

Disorders of sex chromosomes can be the cause of an OAT syndrome. They may relate to both the X- and the Y-chromosome. The most common X-linked disorder is Klinefelter syndrome. This involves the 47, XXY. In these patients, there is almost always an azoospermia, however, there are also cases with a single OCT syndrome. In the region of the Y chromosome so-called microdeletions are responsible for a malfunction of fertility. Depending on the type of disorder can be present here azoospermia or OAT syndrome.
Disorders of the hormonal system

For spermatogenesis two hormones are critical in the first place. Firstly, follicle stimulating hormone (FSH) and the male sex hormone testosterone.

The release of these hormones is controlled by the gonadotropin-releasing hormone GnRH from the hypothalamus (in the brain). This hormone causes the pituitary gland, the pituitary, the release of FSH and LH hormone the luteotrophic. LH acts on the Leydig cells in the testes and stimulates them to to produce testosterone. In disorders of this axis by tumors, inflammation or congenital anomalies sperm production is impaired.
Infections

    Orchitis after mumps (mumps orchitis): A Mumpsorchitis after puberty occurs in 30% of cases on and in 10% of cases on both sides. It leads to a hardening of testicles with limitation of sperm production.
    Epididymitis (epididymitis): In an epididymitis may lead to a partial or total closure of the seminiferous tubules.
    Prostate inflammation (prostatitis): An inflammation of the prostate and seminal vesicles may also lead to a partial or complete closure of the seminal tract.

Other causes

    Chemotherapy and radiation can temporarily sometimes permanently affect sperm production.
    Drugs or stimulants can affect sperm production. Thus, for example anabolic steroids lead to an OAT syndrome or for azoospermia. The effects of nicotine and alcohol remains controversial.
    Heat or overheating leads temporarily to a slight impairment of spermatogenesis.

Diagnostic

In addition to careful medical history is an accurate physical examination in the first place. Further investigations are ultrasound, semen analysis and hormone diagnostics. The sperm study consists of the sperm, which is ideally carried out several times in order to obtain a clear statement. Moreover, here, additional special tests such as penetration test (how well the sperm can wander through mucus), membrane stability test and determination of sugar (fructose) and others (how stable the sperm) are performed. Examination of hormone levels in the blood is also part of the basic examination. When abnormalities other special tests may also be carried out here. For the diagnosis of genetic abnormalities of chromosomes an investigation is necessary. One can find no clear cause a biopsy of testicular tissue is required.
Severities

Often the OAT syndrome is divided into three levels of severity [1], which indicate how much the quality of the sperm is limited.
OAT OAT I II III OAT
Concentration <20-10 million sperm / ml <10-5 million / ml <5 million / ml
Motility <50-30% <30-20% <20%
Morphology <30-10% <10% <10%
prevention

    Undescended testicles: This should be treated until the end of the second year. Recent recommendations say that he should already be dealt with until the end of the first year.
    Routine mumps immunization in childhood (in combination with measles and rubella vaccine)

therapy

Treatment depends on the cause of the malfunction.

    Inflammation: first treatment of inflammation and control after the completion of treatment.
    Hormone deficiency: administration of appropriate hormones.
    Varicocele: surgery with sclerotherapy or ligation of the testicular vein (the blood can flow through other veins).
    Closure of the seminal tract
        Test the operational restoration of patency
        Direct extraction of sperm by testicular biopsy (TESE)
    Drugs and tobacco: renunciation of the relevant substances.
    Genetic anomaly as Klinefelter: possibly TESE possible.

Đăng bởi: ycantho - Ngày đăng: 23/01/2016
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