OAT syndrome
| Classification according to ICD-10 | |
|---|---|
| N46 | Sterility in men Azoospermia NOS Oligozoospermia NOS |
| ICD-10 online (WHO version 2019) | |
The OAT syndrome (oligo-astheno-teratozoospermia syndrome) is a pathological change in the sperm . Too few (oligo), insufficiently mobile (astheno) and more malformed (terato) sperm are seen. It is often associated with male infertility .
causes
The causes lie either in spermiogenesis (sperm formation) or in transport in the seminal ducts.
Misalignment of the testicles
The testes arise approximately at the level of the lower pole of the kidney and migrate into the scrotum (the scrotum ) until birth , but no later than the end of the first year of life . If this so-called descensus testis is disturbed , the testicles can remain in the abdomen or elsewhere. One then speaks of anomalies in the position of the testicle , such as inguinal testicles , sliding hives, etc.
The incorrect position leads to an increase in temperature and damage to sperm formation , even to the point of complete absence, known as azoospermia .
Varicocele
A varicocele is a palpable and visible extension of the venous plexus around the spermatic cord . About 15% of men with a varicocele suffer from infertility, although the relationship is not fully understood here.
Chromosomal abnormality
Disorders of sex chromosomes may be cause of OAT syndrome. They can affect both the X and Y chromosomes. The most common X-linked disorder is Klinefelter syndrome . The karyotype is 47, XXY. Azoospermia is almost always present in these patients , but there are also isolated cases with OAT syndrome. In the area of the Y chromosome, so-called microdeletions are the cause of fertility disorders. Depending on the type of disorder, azoospermia or OAT syndrome can be present.
Disorders of the hormonal balance
Two hormones are primarily decisive for spermiogenesis. Firstly, the 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 and the pituitary to release FSH and the luteotropic hormone LH . LH acts on the Leydig cells in the testes and stimulates them to produce testosterone. If this axis is disturbed by tumors, inflammation or congenital anomalies, sperm formation is impaired.
Infections
- Inflammation of the testicles after mumps ( mumps orchitis ): Mumps orchitis after puberty occurs in 30% of cases and in 10% of cases on both sides. It leads to a hardening of the testicles with reduced sperm production.
- Inflammation of the epididymis ( epididymitis ): With inflammation of the epididymis, the seminiferous tubules can be partially or completely blocked.
- Prostate inflammation ( prostatitis ): Inflammation in the area of the prostate and seminal vesicles can also lead to partial or complete occlusion of the seminal ducts.
Other causes
- Chemotherapy and radiation can temporarily or occasionally permanently impair sperm formation.
- Medicines and stimulants can have an influence on sperm formation. For example, anabolic steroids can lead to OAT syndrome or azoospermia. The effects of nicotine and alcohol are still controversial.
- Warmth or overheating temporarily leads to a slight impairment of spermiogenesis.
Diagnosis
In addition to a careful medical history , a thorough physical examination is paramount. Further examinations are sonography , semen examination and hormone diagnostics. The semen examination consists of the spermiogram , which is ideally carried out several times in order to obtain a clear statement. In addition, additional special tests such as penetration test (how well can the sperm migrate through mucus), membrane stability test (how stable are the sperm) and determination of sugar ( fructose ) and others can be carried out here. The examination of the hormone level in the blood is also part of the basic examination. If there are any abnormalities, further special tests can also be carried out here. To diagnose genetic abnormalities, it is necessary to examine the chromosomes. If no clear cause is found, a biopsy of testicular tissue is required.
Degrees of severity
The OAT syndrome is often divided into three degrees of severity, which indicate how severely the quality of the sperm is impaired.
| OAT I | OAT II | OAT III | |
|---|---|---|---|
| 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 of life. Recent recommendations say that it should be treated by the end of the first year of life.
- Routine mumps vaccination in childhood (in combination with measles and rubella vaccination)
therapy
Therapy depends on the cause of the disorder.
- Inflammation : Initially, therapy of the inflammation and control after completion of the treatment.
- Hormone deficiency: administration of appropriate hormones.
- Varicose vein hernia : an operation that sclerosing or ligation of the testicular vein (the blood can drain through other veins ).
- Closure of the seminal ducts
- Attempt to operationally restore patency
- Direct collection of sperm by means of testicular biopsy ( TESE )
- Medicines and luxury foods: Avoid the corresponding substances.
- Genetic abnormality like Klinefelter: possibly TESE possible.
literature
- G. Cavallini: Male idiopathic oligoasthenoteratozoospermia. In: Asian J Androl. 2006 Mar; 8 (2), pp. 143-157. Review. PMID 16491265 .
- A. Taylor: ABC of Subfertility. Making a diagnosis. In: BMJ. 2003 Aug 30; 327 (7413), pp. 494-497. Review. PMID 12946973 .
- A. Hirsh: Male subfertility. In: BMJ. 2003 Sep 20; 327 (7416), pp. 669-672. Erratum in: BMJ. 2003 Nov 15; 327 (7424), p. 1165-a. PMID 14500443 .
