Del Castillo syndrome or male infertility. Male infertility - consultation health potential Leydig cell dysfunction

XX syndrome in men

This is a type of Klinefelter syndrome in which mental retardation is much less common. The frequency of XX syndrome is 1-10% of cases of Klinefelter syndrome. Histological examination of testicular tissue in patients with XX syndrome after a period of pubertal development reveals the same changes as in Klinefelter syndrome. When studying sex chromatin in scrapings of the mucous membranes of the cheeks, the contours of Barr bodies are unclear, the karyotype is 46 XX.

Treatment for such patients is prescribed only if there are signs of insufficient androgenization.

Del Castillo syndrome (germinal aplasia)

This syndrome is also known as “single Sertoli cell” syndrome.

It is caused by the congenital absence of germ cells- gonocytes, occurs as a result of the death of germinal cells in a normally formed gonad. Similar conditions are described in the literature with radiation exposure and some other diseases.

Main signs of the syndrome: small testicles, normal sizes of the penis and scrotum, sufficient development of male secondary sexual characteristics, normal physical status, azoospermia in the ejaculate.

On histological examination: small size of seminiferous tubules, complete absence of spermatogenic epithelium in the presence of sustentocytes, normal basement membrane, Leydig cells.

In the described syndrome, unlike Klinefelter's syndrome, there is no gynecomastia, a normal male genotype of 46 XY is noted, and the sex chromatin test is negative.

Copulatory functions, spontaneous and adequate erections, ejaculations, orgasm, sexual desire are preserved, patients do not experience difficulties in sexual activity, complaining only of infertility. Hormone treatment is not needed. The prognosis for fertility is unfavorable.

“Sexopathology”, G.S. Vasilchenko

Intrauterine disorders of the morphogenesis of the gonads, reproductive tract and genital organs are divided into the following groups I. Gonadal agenesis: “pure” gonadal agenesis (without somatic deformities); gonadal agenesis in Turner syndrome (with somatic deformities); intrauterine anorchism. II. Gonadal dysgenesis: bisexual gonad syndrome (true hermaphroditism); testicular dysgenesis syndrome; ovarian dysgenesis syndrome. III. Embryogenetic forms of functional (endocrine) pathology of the gonads: syndrome...

Proper treatment, begun even in adulthood, makes it possible to achieve normal sexual development, pregnancy and childbirth. When monitoring patients during pregnancy, it is necessary to take into account that they suffer from glucocorticoid insufficiency of the adrenal cortex. Along with this, even a slight increase in androgen levels with an insufficient dosage of prednisolone interferes with the normal course of pregnancy and often leads to spontaneous pregnancy...

The disease is expressed in pathologically prolonged lactation in combination with amenorrhea and atrophy of the genital organs. PPA syndrome is divided into the following forms: postpartum (Chiari-Frommel syndrome); idiopathic, not related to childbirth (Aumada - del Castillo triad); tumor (Forbes-Albright syndrome - pituitary adenoma); medicinal (iatrogenic). Identification of various forms of PPA syndrome allows us to develop more accurate indications for...

Gonadal agenesis is the lack of differentiation of gonads in early ontogenesis. In these cases, regardless of the karyotype, the formation of the reproductive system occurs without any participation of the gonads. According to the laws of embryogenesis, in such patients the Müllerian canals persist, forming into rudimentary tubes, uterus, and vagina. The external genitalia have an infantile female structure. Secondary sexual characteristics do not develop. “Pure” gonadal agenesis “Pure” gonadal agenesis...

The most important link in the neurohumoral component of the copulatory cycle is the hypothalamic region. It regulates the endocrine support of sexual functions, and through the target cells of the hypothalamus, sensitive to sex steroids, the eroticizing effect of sex hormones on the brain is carried out. Disorders of the functions of the hypothalamus occur under the influence of various exogenous hazards: traumatic brain injuries, infections (flu, tonsillitis, rheumatism, etc.), intoxications (alcohol, organic solvents, long-term use of large...

Sertoli cell syndrome is a disease in which the embryonic anlage of testicular tissue is disrupted.

Germ cell aplasia is not a diagnosis but a characteristic histopathological phenotype first described by Del Castillo in 1947 and sometimes named after him.

Species

• full
• focal

In complete germ cell aplasia, tubules reduced in diameter contain only Sertoli cells and are completely devoid of spermatogenic cells, hence Sertoli cell syndrome; such patients are infertile.

In focal Sertoli cell syndrome, one or another percentage of the tubules contain germ cells, but even in these tubules, spermatogenesis is often impaired both qualitatively and quantitatively.

Focal or complete Sertoli cell syndrome was found in approximately 30% of patients undergoing testicular biopsy. 8% of them had bilateral Sertoli cell syndrome.

Considering the possibility of selecting sperm from the testicles for subsequent artificial insemination, it is necessary to know how accurately the biopsy results allow us to judge the presence of germ cells. Be that as it may, a confident diagnosis of complete Sertoli cell syndrome requires the most scrupulous examination of biopsy specimens. In such cases, multiple tissue samples should be collected and examined.

The production of Leydig cells remains almost unchanged, so patients, as a rule, are normally androgenized, and only infertility forces them to see a doctor.

In congenital germ cell aplasia, for some reason they do not migrate into the tubular epithelium or do not survive there. Microdeletions of the Y chromosome are an important genetic cause of Sertoli cell syndrome. Severe endo- and exogenous damage, associated, for example, with defects in testicular descent, radiation, the action of cytostatic agents and viral infections, also lead to germ cell aplasia.

Symptoms and diagnosis

When complete germ cell aplasia occurs, the result is always azoospermia.

Focal Sertoli cell syndrome is characterized by oligo-astheno-teratospermia of varying degrees, but even in such cases azoospermia may occur. Testicular volume is usually reduced, although sometimes it remains at the lower limit of normal. Ultrasound of the testicles reveals the heterogeneity of their tissue. Serum levels are usually elevated and correlate with the degree of germ cell aplasia. Inhibin B levels show an inverse correlation with the severity of testicular damage. Determining this indicator, although it increases the sensitivity of diagnosis, does not predict the presence or absence of sperm in biopsy specimens.

Diagnosis can only be made by testicular biopsy; at the same time, the possibility of ICSI is also determined, differentiating complete and focal Sertoli cell syndrome. Therefore, testicular biopsy should be planned as a diagnostic and therapeutic measure with a TESE perspective.

Treatment

In complete Sertoli cell syndrome, there is no possibility of improving spermatogenesis. At present, it is impossible to increase the number of spermatozoa formed in the foci of intact tubules. Pregnancy can be induced by insemination with homologous sperm using IVF. With severe oligo-astheno-teratospermia, the likelihood of pregnancy is very low. Therefore, in most cases, the only method of symptomatic therapy remains ICSI, possibly in combination with TESE.

Sertoli cell syndrome was last modified: October 12th, 2017 by Maria Saletskaya

In traditional literature, male infertility is divided into secretory, excretory and mixed. At the same time, secretory infertility associated with insufficient testicular function accounts for 20% in the structure of all male infertility, where hypergonadotropic hypogonadism is 98%, and hypogonadotropic hypogonadism is only 2%. Excretory infertility associated with obstruction of the vas deferens is detected in 3-7.4% of infertile men. However, male factor infertility goes beyond just these forms. In particular, which form of infertility includes the influence of infections on fertility, antisperm immune factors, anejaculatory syndrome. Therefore, we accept the division of male infertility into pretesticular, testicular and posttesticular.

I. Pretesticular infertility.

Pretesticular causes of infertility include all syndromes of hypogonadotropic and normogonadotropic hypogonadism (hyperprolactinemia) associated with dysfunction of the hypothalamic-pituitary complex and, as a result, insufficient stimulation by gonadotropic hormones of the hormone-producing and sperm-forming functions of the testicles.

Insufficient stimulation of the hormone-producing and sperm-forming functions of the testicles
. Suppression of the function of the hypothalamic-pituitary system and testicular functions by high levels of prolactin

II. Testicular infertility.

Testicular infertility includes all syndromes of congenital and acquired hypergonadotropic hypogonadism, which develops as a result of congenital or acquired failure of the testicles, both sperm-forming and hormone-producing. Testicular infertility also includes isolated disorders of the sperm-forming function of the testicles, which result in azoospermia, pathospermia, as well as ultrastructural disorders of the structure of sperm, which leads to the occurrence of male factor infertility.

Congenital primary hypogonadism
. Acquired primary hypogonadism
. Isolated disorders of sperm-forming function of primary and secondary origin
It is necessary to dwell in more detail on the syndromes of primary hypogonadism and isolated disorders of sperm-forming function, which have a predominant effect on male fertility.

Germinal epithelial aplasia (Sertoli cell syndrome, Del Castilio syndrome)

First described in 1947 by Del Castilio in infertile men with azoospermia, with a normal male phenotype and karyotype and with preserved sexual function.
Aplasia of the germinal epithelium is not a diagnosis, but only characterizes the histopathological phenotype. This condition of the testicular parenchyma is described as a syndrome that includes slightly reduced testicles of normal consistency, azoospermia and increased levels of follicle-stimulating hormone.
Most researchers attribute this syndrome to a congenital primary hypergonadotropic form of hypogonadism with early atrophy of the germinal epithelium. In complete germ cell aplasia, the tubules are reduced in diameter and contain only Sertoli cells and are completely devoid of spermatogenic cells.
In the focal form, one or another percentage of the tubules contain germ cells, but even in these tubules, spermatogenesis is often impaired both qualitatively and quantitatively.
G.M. Bere, I. Nishlag reported in 2005 that Sertoli cell syndrome, focal or complete, was found in approximately 30% of patients who underwent a biopsy and only 8% had a bilateral process.
Histological examination of the testicle shows a reduced size of the seminiferous tubules, but no sclerosis or hyalinization. Spermatogenic epithelial cells are completely absent; only Sertoli cells are detected in the seminiferous tubules. Leydig cells preserved
Data from electron microscopic studies of testicular biopsies showed that in 40-80% of cases there are normal Leydig cells, in 20-60% they are either pathologically differentiated or at various stages of development.
It should be noted that in other diseases of the testicles, only Sertoli cells can be observed in the seminiferous tubules (cryptorchidism, Klinefelter syndrome, orchitis). However, in contrast to Sertoli cell syndrome, the testes are usually small, and on histological examination the predominant feature is severe sclerosis and hyalinization of the seminiferous tubules.
An important genetic cause of Sertoli cell syndrome is microdeletion of the Y chromosome. Sertoli cell syndrome is caused by severe endogenous and exogenous damage associated with defects in testicular descent, radiation, the effects of cytostatics and viral infections.
Patients correspond to normal male parameters in physical and sexual development. Usually they complain of infertility. Sexual function is not affected. When assessing the andrological status, no significant differences are revealed.
In childhood, the syndrome does not manifest itself in any way. Puberty is not delayed, the degree of masculinization and the rate of pubertal development are without deviations. Features of eunuchoidism are extremely rarely observed. When assessing the andrological status of an adult, no significant deviations are noted.
Sex chromatin is positive, karyotype 46XY. Against the background of normal testosterone levels in the blood, a high level of follicle-stimulating hormone is detected, the concentration of luteinizing hormone is not changed. Inhibin B levels show an inverse correlation with the severity of testicular damage. Determining this indicator, although it increases the sensitivity of diagnosis, does not predict the presence or absence of sperm in biopsy specimens. In complete Sertoli cell syndrome, azoospermia is always observed. Focal is characterized by oligo-astheno-teratozoospermia of varying degrees, but even in such cases azoospermia can occur. The final arbiter in making a diagnosis is a testicular biopsy, and the possibility of ICSI is also determined, differentiating complete or partial Sertoli cell syndrome.

Blockade of spermatogenesis.

Blockade of spermatogenesis is a stop in the maturation of germ cells.
Like Sertoli cell syndrome, blockade of spermatogenesis is a histopathological phenomenon of polyetiological nature.
Spermatogenesis can be blocked at the level of spermatogonia, primary and secondary spermatocytes or round spermatids.
According to summary data, testicular biopsy reveals blockage of spermatogenesis in 4-30% of cases. G.M. Bere, I. Nishlag 2005 reported on 23% of patients with blockade of spermatogenesis who underwent a biopsy, mainly at the stage of primary spermatocytes. In a third of cases this blockade was bilateral.
This condition may be genetically determined or associated with exogenous influences. Primary genetic causes occur with trisomy, with balanced autosomal abnormalities (translocations, inversions), with deletion of the Y chromosome (Yq11).
Toxic factors (radiation and chemotherapy, antibacterial therapy), exposure to high temperatures and systemic diseases (liver and renal failure, sickle cell anemia).

Fixed cilia syndrome

The complete absence of motile sperm in the ejaculate may indicate immotile cilia syndrome. At the same time, spermatozoa lack dynein handles that connect microtubules to each other, which leads to immobility of the flagellum.
It is known that the cilia of the ciliated epithelium of the upper respiratory tract and the tails of spermatozoa in patients with immotile cilia syndrome are affected almost equally. This gives grounds to consider the syndrome of immobile cilia as one of the manifestations of primary ciliary dyskinesia, which is characterized by weakened or absent motility of cilia in respiratory tract, which is accompanied by recurrent upper respiratory tract infections.
The classic manifestation of this disease is Kartagener's syndrome, which includes a triad of symptoms: situs inversus (reverse arrangement internal organs), bronchiectasis and rhinosinusitis.
The so-called “incomplete Kartagener syndrome”, represented by the last two signs, is much more common. Clinically, ciliary dyskinesia manifests itself already in childhood: chronic sinusitis and rhinitis, chronic cough with expectoration of sputum. Most patients with fixed cilia syndrome exhibit severe asthenozoospermia.
When examining ejaculate, volume and morphology are usually within normal limits, but sperm motility is sharply reduced or absent.
Analysis of pedigrees convincingly indicates the genetic nature of the syndrome of immotile cilia, including Kartagener's syndrome. Given that many genes are involved in the creation of eyelashes, damage to any of them can lead to structural or functional disorders. Therefore, so far attempts to map a single gene for Kartagener syndrome have not been successful.

Syndrome 9+0

This syndrome is characterized by a structural defect in the sperm tails. The central pair of microtubules is missing, which leads to cell immobility. Only a few such cases have been described so far. With this syndrome, all sperm are usually affected and remain immobile. The discovery of this syndrome in brothers indicates its genetic basis.

Globulozoospermia.

Round head syndrome and complete agenesis of the acrosome (globulozoospermia). Data from electron microscopic studies of ejaculate cells from patients with rounded sperm head syndrome indicate that there are two subtypes of sperm heads.
One subtype is sperm with true round head syndrome, characterized by complete loss of the acrosome and decondensed chromatin. In the axoneme and flagellum of such spermatozoa, microtubules and mitochondria are often abnormal.
In the second subtype of round spermatozoa, an abnormal distribution of chromatin is also determined, but an acrosome is formed. In these cases, the acrosome reaction may not be impaired.
Since there are publications about familial cases of round head sperm syndrome, the genetic nature of this pathology is assumed to be of an autosomal dominant type. The nature of the anomaly depends on the type of mutation of the corresponding genes and the degree of their expression. Acrosome agenesis leads to irreversible infertility. Pregnancy can occur in sexual partners of patients with globulozoospermia only when intracytoplasmic sperm injection (ICSI) is used. Since there is no selection of gametes with ICSI, it is important to determine the degree of risk of transferring a genetic defect to offspring. It has been shown that in patients with globulozoospermia the frequency of aneuploidy in germ cells is higher compared to the control group. These data make us cautious about including patients with globulozoospermia due to acrosome agenesis in the ICSI program.

Microdeletions of the AZF locus of the Y chromosome.

The cause of genetically determined male infertility associated with impaired spermatogenesis is a mutation in one of the loci of the Y chromosome. This locus is called the azoospermia factor (AZF). The localization of AZF to the Yq11 region was confirmed by molecular studies. Since 1976, intensive studies of the Y chromosome began and its cytogenetic, physical and pathological map was built.

Normally, chromosome Y is one of the smallest in length in the human karyotype. The Y chromosome is divided into three regions: the euchromatic short arm Yp11, the euchromatic proximal long arm Yq11, and the heterochromatic distal long arm Yq12. The human Y chromosome includes about 50 million nucleotide pairs, with 60% of the DNA located in the heterochromatic region Yq12. The physical length of the short arm of Yp11 is estimated at approximately 13 million nucleotide pairs. The euchromatic part of the long arm of Yq11 does not exceed 7 million nucleotide pairs. More than 100 genes and DNA sequences are localized on the Y chromosome, the functions of 16 of them have been determined.
The genes of the short arm of the Yp11 chromosome are transcribed at different stages of the formation of organs of the reproductive system and during spermatogenesis. In this region, using molecular methods, 2 genes were discovered that are transcribed in testicular cells, called ZFY (zinc finger protein) and TSPY (testis specific protein). Mutations of these genes in sterile men have not yet been described, and their role in spermatogenesis is not clear. A gene called SRY (sex-determining region) is localized on the short arm of chromosome Yp11. It has a conservative structure and is responsible for the development of the testes. Its fragment of 35 thousand 13 million nucleotide pairs represents the minimum DNA sequence of the Y chromosome sufficient for the formation of a male phenotype.

The long arm of the Y chromosome contains genes responsible for reproductive function. In addition to AZF (azoospermia factor), a gene was discovered encoding a male-specific membrane cellular protein - H-Y antigen, which has long been considered the primary factor in the regulation of sex. The H-Y antigen is localized in close proximity to the AZF locus. Obviously, the function of this protein is associated with the formation of seminiferous tubules. The GBY (gonadoblastoma) gene is considered an oncogene that provokes tumors in dysgenetic gonads developing with 45,X/46,XY mosaicism. Another gene, GCY, which controls growth, is localized in the proximal part of Yq11. Its deletion or disruption of the DNA sequence in it causes short stature.
Currently, the main focus is on the gene that controls gametogenesis in men. It is located in the euchromatic part of the long arm of the Y chromosome and is called azoospermia factor (AZF).
Although AZF is present in all cells except red blood cells, it is active only in Sertoli cells. In 1996, using molecular methods, the heterogeneous structure of this gene was established. Microdeletions causing disorders reproductive function in men, were mapped to three different Yq11 subregions. One of the subregions corresponding to the AZF locus is located in the distal part of Yq11, the second and third are mapped proximal to the first. Patients with microdeletions of these loci showed impaired spermatogenesis at various stages, depending on the loss of a specific region of AZF. The consequence of a violation in each of these sequences is azoospermia or severe oligozoospermia, therefore these loci are named AZFa, AZFb and AZFc. Their role in the process of spermatogenesis is being studied. With azoospermia they occur with a frequency of 5-10%, and with severe oligospermia with a frequency of 2-5%.
Deletions of the AZFc locus are found significantly more often than AZFa and AZFb. The most important gene of the AZFc locus is DAZ (Deleted in Azoospermia) - deleted in azoospermia.
Clinically, such patients exhibit a pronounced disturbance of spermatogenesis. The endocrine function of the testicle is not affected. The histological picture varies from complete or focal Sertoli cell syndrome to blockade of spermatogenesis, or qualitatively intact, but quantitatively sharply weakened spermatogenesis. FSH levels are normal or elevated.

Testicular tumors and infertility.

Testicular tumors are the most common malignant diseases of men 25-40 years of age. Their prevalence has increased 3-4 times over the past 50 years.
More frequent detection of tumors in infertility is associated with the following factors:
. These tumors most often develop at an age when a man notices the absence of children.
. Defects in testicular descent that lead to infertility simultaneously increase the risk of developing cancer in them.
. Testicular tumors affect fertility more than diseases and tumors of any other location.
In 50% of patients with germ cell tumors, the sperm concentration was below 10-15 million/ml. After the introduction of ultrasound into routine diagnostic practice, the detection of testicular tumors in patients with infertility is 1:200 and in the general structure of infertility it accounts for 0.3% of patients.
In most patients, the first symptom of the disease is the appearance of a tumor in the testicle. A delay in the diagnosis of germ cell tumors of the testicle may be associated with ignoring the symptoms of the disease by the patient himself or the doctor, who mistakenly mistakes a tumor node in the testicle for epididymitis, and back pain for problems with the spine.
In a small number of patients, the primary tumor is localized extragonadally - retroperitoneally or in the mediastinum. About a third of patients with extragonadal retroperitoneal germ cell tumors have intraductal carcinoma (carcinoma in situ).
In another third of patients, an ultrasound examination of the testicles reveals a scar, indicating an existing primary testicular tumor that has “burnt out.” This testicle must also be removed. And only a third of patients have a true extragonadal germ cell tumor. In all young men with tumor involvement of the supraclavicular, retroperitoneal or mediastinal lymph nodes, testicular germ cell tumor must be excluded.
Increased levels alpha-fetoprotein and/or beta-human chorionic gonadotropin also support the diagnosis of testicular germ cell tumor. If tumor marker levels are normal and a testicular tumor is suspected, the final diagnosis should be confirmed by tumor biopsy. Histological variants such as poorly or undifferentiated carcinoma or poorly differentiated adenocarcinoma are highly suspicious for a possible testicular germ cell tumor. In this case, an immunohistochemical study with germ cell tumor-specific markers is indicated. Determining the expression of isochromosome I(12p) characteristic of testicular germ cell tumors can definitively confirm or reject the diagnosis.
When collecting an anamnesis, emphasis is placed on the following risk factors for developing a testicular tumor: a history of a contralateral testicular tumor, cryptorchidism, and a testicular tumor in first-degree relatives, especially the father or brothers.
Mandatory diagnostic procedures are palpation and determination of tumor markers alpha-fetoprotein and human chorionic gonadotropin. Lactate dehydrogenase levels are an important prognostic factor and should also be known before starting therapy
As a rule, orchofuniculectomy is the first medical procedure. In patients in serious condition caused by a metastatic process, as well as high level AFP or hCG is indicated for starting chemotherapy for health reasons without morphological verification of the diagnosis. In this situation, orchofuniculectomy is performed after completion of chemotherapy. Orchofuniculectomy is performed through an inguinal incision. The testicle affected by the tumor is removed along with the spermatic cord to the level of the internal inguinal ring. If the level of tumor markers is normal and the testicular tumor is small, an urgent intraoperative biopsy is necessary to determine the extent of surgical intervention. For a benign tumor, resection of the testicle can be limited.
Intraductal carcinoma is a precancerous disease.
In patients with intraductal carcinoma, the cumulative risk of developing a testicular germ cell tumor over 7 years is 70%. In 5% of patients with testicular germ cell tumor, the contralateral “healthy” testicle has intraductal carcinoma, which is detected by open biopsy in 99% of cases.
In an atrophic testicle (volume<12 мл) в возрасте до 30 лет риск обнаружения внутрипротоковой карциномы составляет более 34%.
In approximately one third of patients with extragonadal (retroperitoneal) germ cell tumors, biopsy reveals intraductal carcinoma in one or both testicles. The risk of developing a testicular tumor in a patient with an extragonadal germ cell tumor over the next 10 years is about 10% and higher for nonseminoma tumors and retroperitoneal localization compared to seminoma (1.4%) or a primary mediastinal tumor (6.2%). Intraductal carcinoma may be discovered incidentally during testicular biopsy for infertility. If the contralateral testis is normal, orchofuniculectomy is optimal, since radiation therapy may damage the healthy testicle with scattered radiation and impair fertility. In particular, this is applicable for patients with a testicular tumor that has developed in an atrophic testicle.

Varicocele and infertility.

Varicocele is an enlargement of the testicular veins due to reflux of blood through the testicular vein system. Varicocele is observed in 15% of the general male population. In 80-98% of cases, varicocele is localized on the left, in 3-8% - on the right, and in 2-12% of cases - varicocele is bilateral.
“Varicocele and infertility” is one of the most controversial topics nowadays.
Arguments in favor of the negative impact of infertility on male fertility.
The World Health Organization recognizes varicocele as a disease that can cause infertility in men. In 60% of patients with varicocele, a violation of the spermatogenic function of the testicles is noted; in 40% of men examined for infertility, a varicocele is detected.
The influence of venous reflux with varicocele on the maturation of sperm in the testicle is realized in the following main ways:
. Increase in temperature in the testicles to body temperature. Normally, testicular temperature is lower than body temperature, which is necessary for normal spermatogenesis. For the same reason, the testicles are “moved” outside the abdominal cavity into the scrotum.
. Reverse flow of venous blood in the central vein of the left adrenal gland into the cortex of the organ, with activation and release into the general bloodstream of an increased amount of adrenal hormones, which inhibits the maturation of sperm in the testicle.
. Hypoxia of testicular tissue as a result of insufficient outflow of venous blood through the affected vessels, accumulation of “under-oxidized” compounds in spermatogenic tissue, which are strong cellular poisons.
As a result, there is a decrease in sperm production, testosterone production, as well as the formation of antisperm antibodies due to disruption of the blood-testis barrier.
Arguments against the negative impact of varicocele on male fertility.
“However, there is little evidence that surgical treatment will increase the likelihood of conceiving a child,” said Dr. Johannes L. H. Evers of Maastricht University in the Netherlands and Dr. John A. Collins of McMaster University in London. Hamilton (Canada).
During the study, Dr. Evers and Dr. Collins analyzed seven previously published study results to see if treating varicoceles increased the likelihood of conception. After pooling data from the studies, the researchers identified 61 pregnancies in 281 couples in which the men had undergone surgery to remove varicoceles and 50 pregnancies in 259 couples in which the men had not undergone this treatment. “Men who received the treatment increased their chance of conceiving a child with their partner by only 1 percent compared with men who did not receive the treatment,” the authors write. “We did not obtain sufficient evidence to conclude that treating clinical varicoceles in couples with subfertile men increases the likelihood of conception,” Dr. Evers and Dr. Collins concluded.
"Continued research into the treatment of varicoceles is needed," says Dr. Allan Templeton from the University of Aberdeen. Dr. Ellen writes that continued research on this issue "seems unlikely" due to the increasing availability of IVF, in which a single sperm is injected directly into the egg.
E. Nischlag and G. M. Bere (Institute of Reproductive Medicine at the Wesfaldian Wilhelm University) concluded, based on the treatment and observation of 125 couples, that regular counseling of married couples is as effective in terms of pregnancy rates as active treatment of varicocele
The Royal Society of Obstetricians and Gynecologists of the United Kingdom considers that there is insufficient evidence to recommend left spermatic vein occlusion for impaired fertility or oligospermia in patients with varicocele.
In our opinion, the most reasonable approach to treating infertility is offered by the American Urological Association.
The results of clinical and experimental data conducted on animals have demonstrated the detrimental effect of varicocele on spermatogenesis. Increased body temperature and venous reflux appear to play an important role in the development of varicocele-induced testicular dysfunction, although the full pathophysiological picture of the lesion is not clear.
When determining indications for the treatment of varicocele in a male sexual partner of a couple who is planning a pregnancy, all of the following conditions must be present:
. varicocele detected during external examination,


. a man has pathological changes in sperm tests.
Treatment of varicocele is not indicated if semen analysis is normal or if varicocele is subclinical.
Adult men who are not currently trying to have children, but are planning to do so in the future, and who have palpable varicoceles and abnormal sperm are also candidates for varicocele treatment.
Young adult men with varicoceles who have normal semen parameters are at risk for testicular dysfunction. They should be offered semen testing every 2 years to detect early changes in spermatogenesis.
Young men who have unilateral or bilateral varicocele and an objectively proven decrease in testicular size on the affected side should be considered as candidates for varicocele treatment. If these men have not been objectively proven to have decreased testicular size, they should undergo an annual examination with testicular size measurement and/or semen testing for early detection of changes in the testicles or sperm.
It is necessary to offer treatment for varicocele to the male sexual partner of a couple who is planning a pregnancy if all of the following conditions are present:
. palpable varicocele,
. couple diagnosed with infertility,
. the woman is fertile or has a potentially treatable infertility problem,
. a man has pathological changes in sperm tests
Adult men who have a palpable varicocele, pathological changes in sperm and who are planning a future pregnancy should also be offered treatment for varicocele.
Young men who have varicocele and normal sperm counts should undergo a sperm examination once every 2 years.
Adolescents with varicocele who have a proven decrease in the size of the testicle on the affected side should be offered treatment for varicocele.
Adolescents with varicoceles and normal testicular size should be offered annual testicular monitoring and/or semen testing.
Treatment of varicocele can be considered as primary treatment when a man with varicocele has suboptimal sperm quality and a normal female partner. In vitro fertilization with or without intracytoplasmic sperm injection can be considered as a primary treatment when used for a woman's pathology, regardless of whether there is a varicocele or suboptimal sperm quality.

Posttesticular infertility.

Excretory infertility

Antisperm immunity

Male infertility and inflammatory diseases of the genital organs.

Sperm secretion disorders
1. Somatic obstacles to sperm transport - stricture of the urethra, hypospadias, epispadias, phimosis, genital curvature (see section of the site “Diseases”)
2. Erectile dysfunction (see section of the site “Erectile dysfunction”)
3. Ejaculatory dysfunction (see section of the site “Orgasm disorders”)
4. Vaginismus in a woman and violations of sexual technique to achieve pregnancy (rare sexual activity, the practice of predominantly non-vaginal coitus, inability to make frictional movements)

Excretory infertility.

Excretory infertility is understood as azoospermia or clinically significant oligozoospemia in a man in an infertile marriage due to complete or partial, one or two-sided obstruction of the vas deferens. Excretory infertility can be primary or secondary and is classified according to the level of obstruction.

Congenital obstruction of the vas deferens due to cystic fibrosis.

Congenital absence of the vas deferens occurs in 1-2% of men with infertility. This aplasia occurs due to congenital anomalies of the Wolffian duct, as a result of a mutation in the cystic fibrosis gene.
Cystic fibrosis is one of the most common autosomal recessive diseases in whites, affecting one in 2,500 children. Due to the improvement of treatment for cystic fibrosis, the life expectancy of patients is now 30 years or more. And in this regard, their fertility and the possibility of marriage have acquired important clinical significance.
The main cause of cystic fibrosis is mutations in the protein gene CFTR (cystic fibrosis transmembrane regulator) - the transmembrane regulator of cystic fibrosis. Since its cloning in 1989, more than 800 different mutations have been described. In the Central European population, among the genetic variants, the share of the AF 508 allele is 70%. There is a very weak relationship between the nature of the mutation and clinical manifestations.
The CFTR protein is actively expressed by the epithelium of the respiratory tract and some other organs, where it acts as a regulator of electrolyte transport. If the structure or function of this protein is disrupted due to mutations, the secretion becomes excessively viscous. Clinical manifestations of the usual form of cystic fibrosis are quite characteristic. Excessive secretion of chlorides, characteristic of cystic fibrosis, leads to hypersecretion of thick mucus in the cells of the endocrine pancreas, bronchial epithelium, and gastrointestinal mucosa. Clinically, this is manifested by intestinal obstruction due to meconium stagnation in newborns, chronic pancreatitis in 85% of children, chronic purulent-obstructive bronchitis and severe pneumonia.
The leading laboratory sign of cystic fibrosis is an increased concentration of chloride in sweat. Sweating should be stimulated by local electrophoresis of pilocarpine. A chloride concentration in sweat exceeding 60 mmol/l has a diagnostic value for cystic fibrosis.
More than 95% of men with cystic fibrosis have obstructive azoospermia. Most have bilateral congenital obstruction of the proximal vas deferens or epididymis. In typical cases, the intrascrotal part of the canal is either completely absent or reduced to a ribbon structure without a lumen. The body and tail of the appendage are usually hypoplastic, the heads of the appendages are usually preserved and noticeably expanded. Testicular histology usually shows preserved spermatogenesis. Seminal vesicles in cystic fibrosis are usually either aplastic or hypoplastic, characterized by occlusion, dilation and cystic degeneration. These abnormalities of the seminal vesicles explain the almost constant decrease in ejaculate volume.
Fertility is preserved in only a few men with cystic fibrosis. However, the disease itself, as a rule, is relatively mild. The function of the pancreas does not suffer, and destructive processes in the lung tissue develop more slowly than usual.
With obstructive azoospermia, the method of choice in the treatment of infertility in these patients is ICSI.

Congenital bilateral absence of the vas deferens (CDOS).

(Congenital bilateral absence of the vas deferens -CBAVD)
Congenital bilateral absence of the vas deferens (BCD) can be either an isolated anomaly or a manifestation of the systemic disease cystic fibrosis.
Molecular studies clearly show that most VDOSP variants represent a minor variant of cystic fibrosis and are caused by mutations in the CFTR protein gene. In the most general terms, we can say that CFTR gene mutations are divided into two large groups - “severe” and “mild”. “Severe” mutations underlie classical cystic fibrosis. “Mild” mutations are associated with less pronounced clinical abnormalities, for example, chronic bronchitis. In addition, VDOSP is characterized by the presence of polymorphism in intron 8 of the CFTR gene with alleles 5T, 7T and 9T. The 7T and 9T alleles are functionally neutral, and the 5T allele interferes with CFTR mRNA splicing. A significant amount of mRNA is deprived of exon 9 and the ability to be translated into active CFTR protein. From a functional point of view, the presence of the 5T allele is equivalent to a “mild” mutation. It is generally accepted that patients with classical cystic fibrosis are carriers of two severe mutations in the CFTR protein gene.
The most common genotype of men with VDOSP is the presence of one severe and one mild mutation or one severe mutation and the 5T allele. This situation is detected in 75% of those examined with VDOSP.
Mutations of the CFTR gene can lead not only to VDOSP, but also to idiopathic obstruction of the epididymis when the vas deferens is present. At least 47% of apparently healthy people with idiopathic epididymal obstruction also have various mutations in the CFTR gene. In 10-20% of cases, molecular studies do not detect any mutations or 5T alleles.
Changes in the anatomy of the reproductive tract and ejaculate parameters in VDOSP and cystic fibrosis are similar. In azoospermia associated with CFTR mutations, semen volume, pH, and fructose concentrations are much lower than in fertile men and patients with azoospermia but without a CFTR mutation.
Urinary tract abnormalities in patients with VDOSP are more common and indicate a variant of the disease not associated with CFTR mutations. Mutations are absent in almost every patient with VDOSP and concomitant renal pathology (unilateral aplasia, ectopia, horseshoe kidney). Ultrasound examination should be performed in all patients with VDOSP. If a disruption in the development of the meso-nephrotic duct occurs in the 4th week of embryonic development, then this leads not only to aplasia of the vas deferens, but also to aplasia of the kidney and ureter.
In cystic fibrosis, agenesis of the vas deferens occurs at 13-14 weeks of embryonic development. By this time, the urinary and reproductive systems are already separated. Therefore, mutations of the CFTR gene in its pure form are not accompanied by abnormalities in the development of the urinary system.
Every second patient with VDOSP complains of diseases of the upper respiratory tract. Recurrent bronchitis and sinusitis are characteristic. Bronchopulmonary diseases usually do not progress. Sometimes patients have symptoms of digestive disorders, which can be associated with mild pancreatic dysfunction. Sweat chloride concentrations may exceed the upper burrow limit of 60 mmol/L, but this is not always the case.
Agenesis of the vas deferens is always accompanied by partial underdevelopment of the epididymis. Congenital unilateral absence of the vas deferens (CAUD) has virtually no effect on fertility and is detected incidentally during a vasectomy or during examination of patients with reduced ejaculate parameters.
VDOSP and VOOSP are sometimes accompanied by cryptorchidism, and the cause of this condition has not yet been determined. The method of choice in the treatment of infertility in these patients is ICSI.

Young's syndrome

This syndrome with azoospermia occurs quite often - 3/100. Young's syndrome has a prevalence comparable to Klinefelter's syndrome and higher than that of cystic fibrosis and fixed cilia syndrome.
A distinctive feature of Young's syndrome is the combination of obstructive azoospermia with damage to the sinuses and bronchi. Despite some similarities in its manifestations with cystic fibrosis and congenital bilateral absence of the vas deferens, this syndrome is clinically and etiologically different from these diseases. Azoospermia in Young's syndrome is associated with obstruction of the middle segment of the epididymis. During histological examination of the epididymis, the secretion of the tubules is very thick and dense, in the form of amorphous masses. Azoospermia in Young's syndrome can occur in patients who already have children. This suggests that occlusion develops gradually in the initially patent epididymis, probably due to the production of thickened secretions. Young's syndrome is characterized by the absence of structural abnormalities of the vas deferens, epididymis and seminal vesicles. The volume of ejaculate and the fructose content in it remain normal, which is another difference from cystic fibrosis and VDOSP. A testicular biopsy reveals a picture of preserved spermatogenesis. Levels of sex and gonadotropic hormones are within normal limits.
Quantitative electron microscopy shows that in Young's syndrome, sperm tails are more likely to lack the central pair of microtubules, radial spokes, or denein “handles.” This can lead to dysfunction of the ciliated cilia and sperm tail. It is still unknown whether Jung's syndrome has a genetic basis.
Patients often suffer from bronchitis in childhood, but by adolescence their health status improves significantly. Bronchiectasis is often detected, but unlike cystic fibrosis, the lungs are not involved in the pathological process and, unlike cystic fibrosis, sweat and pancreatic functions remain unaffected - the level of chlorides in sweat remains normal.
Attempts to surgically restore the patency of the epididymis were unsuccessful. The method of choice in the treatment of infertility in these patients is ICSI.

Polycystic kidney disease.

At first glance, polycystic kidney disease has nothing to do with male infertility. However, such a disease is often systemic in nature and, along with numerous kidney cysts, cystic formations can be found in other organs - in the liver, spleen, pancreas, lung, ovary, testicle, epididymis and seminal vesicle. In men, polycystic kidney disease can be accompanied by infertility. In this case, multiple dilated cysts are found in the epididymis and seminal vesicles. Cysts compress the seminal ducts, which leads to obstructive azoospermia.

Müllerian cyst and urogenital sinus cyst.

Obstruction of the ejaculatory ducts occurs in 1-3% of cases of obstructive azoospermia. The presence of congenital cysts of the Müllerian duct or urogenital sinus is the cause of obstructive azoospermia. The cyst is located midway in the prostate and in the first case, displaces the ejaculatory ducts laterally, squeezing them, and in the second case, the ducts empty directly into the cyst.

Some clinical forms of acquired forms of obstructive infertility

Bilateral epididymitis.
Inflammation of the epididymis is often complicated by scarring of the epididymal tissue.
Newly formed scar tissue leads to narrowing or complete obliteration of the epididymal canal. In this regard, the most unfavorable localization of the inflammatory process is in the tail, which occurs more often than in the head of the appendage.
In the head of the epididymis, due to the presence of many seminiferous tubules, there are still some chances that obliteration will not affect all the tubules and some of them will retain their patency. There is only one tubule in the tail of the epididymis and the likelihood of its patency remaining intact after inflammation is extremely low.

Male sterilization.

In the last two decades, in many countries, for the purpose of contraception, male sterilization - bilateral intersection of the vas deferens - has been widely performed. About 5% of sterilized men eventually decide to restore their fertility. It turned out that during the first two years after sterilization, vaso-vasoanastomosis can restore patency in 80-90% of cases, and the ability to fertilize in 40-50%. The more time passes after a vasectomy, the worse the treatment results. If more than 5 years pass after sterilization, then, despite the restoration of the patency of the vas deferens, the ability of sperm to fertilize is practically absent. This is due to the development of antisperm immunity, which develops against the background of chronic obstruction and stagnation of sperm in the epididymis.

Obstructive vesiculitis.

Sometimes inflammation of the seminal vesicles is accompanied by a gradual decrease in sperm concentration, up to oligozoospermia and azoospermia. This is not a sign of spermatogenesis deficiency, but is due to the involvement of the vas deferens ampullae in the inflammatory process. It is known that during embryogenesis, seminal vesicles develop from the ampullae of the vas deferens, and these structures are anatomically and functionally a single organ. Therefore, the inflammatory process in the seminal vesicles is usually accompanied by inflammation of the ampullae of the vas deferens, leading to their partial or complete obstruction. Incomplete obstruction of the ampullary ducts is manifested by functional oligozoospermia and is characterized by a decrease in ejaculate volume of less than 1 ml and a decrease in the concentration of fructose in the ejaculate.
In case of complete obstruction, ultrasound examination, including transrectal one, is not always sufficiently informative. Therefore, for diagnostic purposes, puncture of the seminal vesicles and aspiration of their contents are performed. If in a patient with azoospermia numerous spermatozoa are detected in the seminal vesicles, this indicates obstruction of the ampullary ducts.

Antisperm immunity

One of the immunological factors leading to infertility is the formation of antisperm antibodies. Antisperm antibodies are found in 9-36% of infertile couples, compared with 0.9-4% of couples having children.
Antisperm antibodies are immunoglobulins of the IgG, IgA and/or IgM isotypes, which are directed against sperm membrane antigens.
Antisperm antibodies are diverse, which is determined by the presence of different target antigens (various antigens have now been identified, such as YWK II, BE-20, rSMP-B, BS-63,BS-17, HED-2 and 75-kDa) and, Thus, immunological infertility is a consequence of the combined effects of various antisperm antibodies.
Antisperm antibodies are formed in various parts of the reproductive tract in men - the testicles, epididymis, vas deferens, they are directed against different parts of the sperm - the head of the sperm, the tail, the middle part or a combination thereof, can be present in different quantities and affect the reproductive processes in different ways.
Because sperm is not produced in the body until puberty, specific sperm antigens are not recognized as “self” by the immune system. However, sperm are not attacked by the immune system, since they are protected from contact with cells of the immune system circulating in the bloodstream by several physiological mechanisms.
The first mechanism is the existence of a biological barrier between the seminiferous tubules and blood vessels, the so-called blood-testis barrier. It is formed by tight junctions between Sertoli cells and the basement membrane. The blood-testis barrier protects testicular cells from immune cells entering the spermatic cord.
However, a small number of sperm and their precursors can cross the blood-testis barrier and enter the blood, thereby triggering an immune response against sperm, so there are immunological defense mechanisms:
. Immunological tolerance due to a low threshold for the penetration of sperm antigens.
. Immunomodulatory mechanisms within the testes, such as steroids, macrophages, suppressor cells, which can prevent activation of immunological recognition.
. Peripheral testicular immunomodulation: T-suppressor cells in the epididymis and immunosuppressive activity of seminal fluid. There is a component in sperm called Immunoglobulin binding factor (IBF) that is thought to reduce the activation of B lymphocytes or suppress the activity of T helper cells, thereby preventing the production of antisperm antibodies in the reproductive tract.
Disturbances of the blood-testis barrier, such as injury, infection, or surgery, can trigger the entry of circulating immune cells into the male genital tract and expose sperm to the immune system. When this occurs, the suppressive activity of T cells may be suppressed primarily by the production of antibodies to sperm. Men who have had a vasectomy are an example of this problem. Many of them have antisperm antibodies (more than 65%).
Risk factors for the development of antisperm antibodies in men are:
. Injury
. Varicocele (enlargement of the veins surrounding the spermatic cord)
. Blockage of the vas deferens
. Infections
. Oncology
. Cryptorchidism
. Surgical operations on the reproductive organs

For a long time, it was unclear how antisperm antibodies affect reproductive processes. Currently, numerous studies have shown that the effect of antisperm antibodies is quite diverse; the following mechanisms are known:
. decreased sperm motility, disruption of their functional activity,
. blockade of sperm penetration into cervical mucus,
. influence on such important stages of sperm preparation for fertilization as capacitation and acrosomal reaction
. impact on the process of fertilization of an egg by a sperm (interaction between a sperm and an egg),
. influence on the blastocyst implantation process,
. inhibition of embryo growth and development.

Antisperm antibodies, fixing on the sperm membrane in various areas (sperm head, middle part, tail) have an inhibitory effect on sperm, both during their movement in the male reproductive tract and in the female.
Antisperm antibodies can cause agglutination (“gluing”) and immobilization (immobilization) of sperm. The extent to which sperm motility will be reduced will depend on the amount of antisperm antibodies (there must be a high titer of antibodies), as well as on the place of their fixation. The most unfavorable site for fixation of antisperm antibodies is the head of the sperm.
Antisperm antibodies interfere with the interaction of gametes (sex cells). They prevent sperm from penetrating the zona pellucida of the egg. Although the mechanisms of this have not been fully elucidated, it is reliably known that antisperm antibodies suppress the acrosomal reaction of sperm, which is a necessary condition for successful fertilization. If a husband or wife has antisperm antibodies, the quality of the resulting embryos deteriorates, which reduces the likelihood of success in infertility treatment using in vitro fertilization.
Illustration of the mechanisms of development of antisperm immunity from the abstract of the dissertation by D.V. Sizyakin “PATHOGENESIS OF INFERTILITY IN MEN DUE TO CIRCULATION DISORDERS”

Male infertility due to inflammatory diseases of the genital organs.

More than 65% of patients show a deterioration in sperm parameters with clinical symptoms of chronic prostatitis.
The effect of inflammatory diseases of the genital organs and urogenital infections on male fertility is as follows:
. Extreme forms of the inflammatory process in the genital organs, especially associated with tuberculosis, gonorrhea, urogenital trichomoniasis and chlamydia, form partial or complete obstruction of the spermatic ducts (epididymis, seminal vesicles and ejaculatory duct, prostate gland) with the development of an obstructive form of male infertility with azoospermia or severe oligozoospermia.
. The inflammatory process in the genital organs triggers autoimmune mechanisms of antisperm immunity, which affects the sperm themselves, causing astheno- and teratozoospermia, as well as the interaction of sperm with the female reproductive tract, the egg and subsequent stages of development of the fertilized egg.
. Inflammatory diseases of the genital organs and associated leukocytospermia are characterized by a high rate of lipid peroxidation. In mild cases, this leads to premature capacitation and acrosomal reaction of sperm, and in extreme cases to direct damage to sperm with the development of asthenozoospermia, necrospermia and teratozoospermia.
. Inflammatory diseases of the prostate gland and seminal vesicles change the physical properties of seminal plasma, in particular viscosity, which prevents the full activity of sperm.
. Causative agents of inflammatory diseases of the genital organs and sexually transmitted infections can directly affect the seminal cells, reducing sperm fertility.

Leukocytospermia.

The number of leukocytes in normal ejaculate should not exceed I.0x l0x6/l. Among sperm leukocytes, granulocytes (50 - 60%), macrophages (20 - 30%), T-lymphocytes (2 - 5%) prevail. Among men in infertile marriages, leukocytospermia is found in 10-20% of cases.
The presence of leukocytes in the ejaculate is an important indicator of inflammatory diseases of the genital organs. However, a clear pattern between the presence of leukocytes and the severity of symptoms or the degree of changes in the prostate gland is not always visible. It is known that leukocytes adversely affect the functional parameters of seminal fluid and can play a role in the development of male infertility:
. The number of leukocytes in seminal plasma in infertile patients is higher than in fertile men.
. A decrease in the number of sperm, deterioration in their motility and morphology is associated with the presence of leukocytospermia. After antibiotic therapy, the leukocyte count and morphological characteristics of seminal fluid most often return to normal.
. The presence of leukocytes worsens the performance of functional tests (hamster oocyte penetration test, etc.) and serves as an unfavorable prognostic factor for in vitro fertilization
Lipid peroxidation reactions.
Research in recent years has made it possible to clarify the nature of the effect of leukocytospermia on sperm function. The main reason for the damaging effect of leukocytes on sperm is associated with oxygen radicals of leukocytes (ROS, reactive oxigen species), which are products of oxygen metabolism - superoxide anion (O2-), hydrogen peroxide H2O2 and hydroxyl radical OH-.
It has been shown that the content of superoxide anions O2- is significantly higher in patients with leukocytospermia compared to normal fertile men. There was a direct correlation between the superoxide anion content and the level of leukocytes and the number of immotile sperm.
The main damaging factor for sperm is hydrogen peroxide. Low concentrations of hydrogen peroxide do not affect sperm viability, but cause a decrease in motility, mainly due to inhibition of intracellular ATP and a subsequent decrease in phosphorylation of flagellar kinematic proteins. High concentrations of hydrogen peroxide react with phospholipids in cell membranes, inducing fatty acid peroxidation and other degradation products leading to cell death.
In vitro experiments found that neutrophils at a concentration of 0.6 million/ml (3 times less than normal values ​​according to WHO instructions) cause a 35% decrease in sperm motility and produce ROS 100 times more than in semen samples from infertile men. The absence of a pronounced damaging effect in vivo is explained by the presence in sperm and seminal plasma of a protective system that regulates the concentration of ROS, which includes enzymes such as superoxide dismutase, catalase, glutathione peroxide reductase, as well as a number of antioxidants (albumin, glutathione, pyruvate, vitamins E and C). The protective abilities of seminal plasma have significant individual variations. The levels of antioxidants in the seminal plasma of infertile men are significantly lower than in fertile men. In case of infertility associated with increased levels of oxygen radicals in sperm, there is a therapeutic effect of antioxidants affecting the level of ROS. Thus, after oral administration of vitamin E and an increase in its level in the blood, the functional test of attachment to the zona pellucida of an unfertilized human egg became positive.
The capacitation and acrosomal reaction of sperm occurs through lipid peroxidation and ROS production, but there is a delicate balance between ROS production and the system that ensures their destruction. An excess of ROS-producing leukocytes disrupts this balanced system, triggering capacitation and the acrosomal reaction at an earlier time, thereby impairing their fertilizing ability.

Prostatitis and male infertility.

The most common symptom of chronic bacterial prostatitis is oligoasthenozoospermia.
The function of prostate secretion products depends not only on the transport of sperm. It has been established that from 2 to 67% of prostatic zinc is associated with spermatozoa through ligand proteins with high molecular weight. A decrease in the amount of chromatin-bound zinc leads to a decrease in chromatin stability, which may cause failure of fertilization and fetal development.

Vesiculitis and male infertility.

According to a number of authors, a feature of vesiculitis is its long asymptomatic course, when the initial stages of the disease manifest themselves in the form of pathological changes in the ejaculate - a decrease in sperm motility, an increase in the viscosity of the ejaculate, an increase in the number of pathological forms and a decrease in the number of living sperm.
As inflammation of the seminal vesicles progresses, clinical manifestations arise: a feeling of heaviness in the perineum, constipation and pain during bowel movements; weakening of erections, painful orgasm. Advanced forms of vesiculitis are characterized by obstructive pathospermia, up to azoospermia.

Urogenital infections and male infertility.

“Microorganisms or their secretion products damage the seminal tract directly, while an increase in the number of activated leukocytes and increased secretion of lymphokines and monokines causes their secondary inflammation. In addition, increased formation of oxygen free radicals can reduce the fertilizing ability of sperm.” G.M Bere, I.Nishlag 2005
Before the widespread use of antibiotic therapy, gonorrhea was a common cause of obstructive azoospermia. Currently, seminal tract infections are caused by microorganisms such as chlamydia (Chlamydia trachomatis), mycoplasmas, especially Ureaplasma urealiticum, as well as gram-negative flora typical of the genitourinary tract, such as Escherichia coli.
Chlamydia (Clamydia trachomatis) and ureaplasma (Ureaplasma urealiticum) are detected in patients with idiopathic infertility much more often than in the control group.
A study of ejaculate in patients with chlamydial infection reveals a decrease in sperm concentration of varying degrees, an increase in the number of dead and pathologically altered forms of sperm. Typical for chlamydial infection is a decrease in sperm motility, which is due to the ability of chlamydia to adhere tightly to sperm.
Antichlamydial IgA to Chlamydia trachomatis is determined in the secretion of the prostate gland and in seminal plasma. At the same time, there is a statistically significant increase in the IgA titer in seminal plasma compared to the titer in blood serum.
Antichlamydial antibodies in sperm appear due to the activation of T-helper lymphocytes in the male reproductive tract, which predisposes to the formation of antisperm autoantibodies and immune infertility. Asymptomatic Chlamydia trachomatis infection in men with idiopathic infertility is detected quite often (according to some authors in 25% of cases) and correlates with the presence of antisperm antibodies.
Mycoplasmas (especially Ureaplasma urealiticum) also reduce sperm motility and cause disturbances in the process of their penetration into the egg.
Adhesion of ureaplasmas to the heads of spermatozoa has been described, which leads to damage to their membranes. A sperm with such disorders is no longer capable of fertilization, even if it maintains good mobility.
The damaging effects of other microorganisms on the male reproductive tract and male seminal cells have also been described.

A disease manifested by infertility in men with karyotype 46 XY. Described Del Castillo syndrome in 1947. Examination of the ejaculate reveals aspermia, less often azoospermia, and histological examination of testicular tissue reveals seminiferous tubules lined only with Sertoli cells.
The causes of the disease have not been sufficiently studied to date. Most authors consider the main cause of gonadal underdevelopment to be a low concentration of embryonic androgens in the fetal blood. The harmful factor selectively acts on the germinal elements of the testicles, which leads to atrophy of the seminiferous epithelium, while the Sertoli cells are not damaged. Similar changes are observed in severe diseases of the nervous system (multiple sclerosis), spinal fractures, skull injuries, and radiation injuries. Patients in sexual and physical development are no different from healthy men. They usually see a doctor about infertility. Histological examination of the testicles is of decisive importance in diagnosing the disease. The prognosis for fertility is unfavorable. Male sex hormones should be used only in cases of existing androgen deficiency.

(Source: Sexological Dictionary)

See what “Del Castillo syndrome” is in other dictionaries:

DEL CASTILLO SYNDROME- (described by the Argentine endocrinologist E. V. del Castillo, 1897–1969; synonyms - testicular dysgenesis syndrome, “Sertoli cell syndrome”) - primary hypogonadism. The main symptom is infertility. External signs of testicular... ...

- (E. V. del Castillo, Argentine doctor; synonym testicular dysgenesis syndrome) a combination of decreased testicular size and aspermia with normal or increased levels of gonadotropic hormones in the blood, observed with underdevelopment of the testicles ... Large medical dictionary

AUMAD – DEL CASTILLO SYNDROME- (described by the Argentine gynecologist J. C. Ahumada and endocrinologist E. B. del Castillo, 1897–1969) - one of the eponymous names for the galactorrhea amenorrhea syndrome: amenorrhea, galactorrhea and a decrease in gonadotropin in the urine in young non-pregnant and ... ... Encyclopedic Dictionary of Psychology and Pedagogy

del Castillo syndrome- GSD, a form of testicular dysgenesis, characterized by infertility as a result of underdevelopment of the germinal epithelium of the gonads (the structure of Sertoli and Ludwig cells is normal); is transmitted in a sex-linked recessive manner. [Arefyev V.A.,... ... Technical Translator's Guide

Sertoli cell syndrome only, del Castillo syndrome del Castillo syndrome. GSD, a form of testicular dysgenesis, characterized by infertility as a result of underdevelopment of the germinal epithelium of the gonads (the structure of Sertoli and Ludwig cells is normal); ... Molecular biology and genetics. Explanatory dictionary.

Argonnes–del Castillo syndrome- Amenorrhea, galactorrhea without previous pregnancy. Often uterine atrophy, abdominal pain, sacral pain, irritability, insomnia. It is regarded as a consequence of diencephalic hypothalamic pathology, provoked by a pituitary adenoma. Described... ... Encyclopedic Dictionary of Psychology and Pedagogy

The organs responsible for reproduction in men are called testes. They produce sex cells - sperm and hormones, for example, testosterone. The anatomical and histological structure of the testicles in men is complex, since these organs perform several functions at once. They carry out spermatogenesis - the formation and development of germ cells. The testicles also perform an endocrine function. They are located in a special skin sac - the scrotum. A special temperature is maintained there, which is slightly lower than in other parts of the body.

The testicles have the shape of an ellipse, their size is about 4 cm in length and 3 cm in width. Normally, slight asymmetry of the gonads may be observed. Each testicle is divided by membrane septa into many lobules. They contain convoluted seminal canals that form the testicular plexus. Its efferent ducts enter the epididymis. The main part of the sperm is formed there - the head. Later - the channels enter which is directed to the bladder. Further, they expand and penetrate through another organ of the male reproductive system - the prostate. Before this, the canal is formed into the ejaculatory duct, which has an outlet in the urethra.

Histological in men

The male gonads consist of spermatic cords and interstitial tissue. On the outside they are covered with a white membrane. It is represented by dense connective tissue. The tunica albuginea is fused with the organ. Laterally it thickens, forming the mediastinum of the testicle. At this point, the connective tissue is divided into many strands. They form lobules, inside of which there are convoluted tubules. They are represented by the following structural units:

1. Sertoli cell - sustentocyte. Together with other elements, it participates in the formation of the blood-testicular barrier.
2. Cells responsible for spermatogenesis.
3. Myofibroblasts. Another name for them is peritubular cells. The main function of myofibroblasts is to ensure the movement of seminal fluid through convoluted channels.

In addition, the testicular structure contains interstitial tissue. It is about 15%. Interstitial tissue is represented by elements such as Leydig cells, macrophages, capillaries, etc. If convoluted channels are responsible for the formation of germ cells, then the formation and production of male hormones occurs here.

Sertoli cell: structure

Sertoli cells have an elongated shape. Their size is about 20-40 microns. These are quite large structural units, which are otherwise called supporting cells. The cytoplasm of these elements contains many organelles. Among them:

1. Core. It has an irregular, sometimes pear-shaped shape. Chromatin in the nucleus is distributed unevenly.
2. Smooth and rough EPS. The first is responsible for production; the second ensures protein synthesis.
3. Thanks to this organelle, the final synthesis, storage and excretion of products occurs.
4. Lysosomes - participate in phagocytosis.
5. Microfilaments. These organelles are involved in sperm maturation.

In addition, each Sertoli cell contains fatty inclusions. The base of sustentocytes is located on the walls of the seminiferous tubules, and the apex faces into their lumen.

Sertoli cells: functions

The Sertoli cell is one of the constituent parts that form the convoluted seminiferous tubules. It is of great importance as it participates in the process of spermatogenesis and the synthesis of male hormones. The following functions of Sertoli cells are distinguished:

1. Trophic. These elements provide immature sperm with oxygen and nutrients.
2. Protective. Each cell has lysosomes in the cytoplasm - organelles involved in phagocytosis. They absorb and process decay products, for example, dead fragments of spermatids.
3. Providing a blood-testis barrier. This function is ensured thanks to the close barrier necessary to separate male reproductive cells from the blood and the substances it contains. In addition, it prevents the penetration of sperm antigens into the plasma. This reduces the risk of developing autoimmune inflammation.
4. Endocrine function. Sertoli cells are involved in the formation of sex hormones.

Sustentocytes are necessary for the formation and maintenance of a special environment in which spermatozoa develop favorably. It is known that the ionic composition of Sertoli cells differs from blood plasma. The sodium concentration in them is lower, and the potassium content, on the contrary, is increased. In addition, many biologically active substances are synthesized in Sertoli cells. Among them are prostaglandins, cytokines, follistatin, growth and division factors, opioids, etc.

Functions and structure of Leydig cells

Leydig cells are part of the interstitial tissue of the testicle. Their size is about 20 microns. In the male gonads there are more than 200 * 10 6 Leydig cells. The structural features of these elements are a large oval-shaped nucleus and foamy cytoplasm. It contains vacuoles containing the protein lipofuscin. It is formed during the breakdown of fats at the time of synthesis of steroid hormones. In addition, the cytoplasm contains 1 or 2 nucleoli containing RNA and protein. The main function of Leydig cells is the production of testosterone. In addition, they are involved in the synthesis of activin. This substance stimulates the production of FSH in the brain.

What is Sertoli cell syndrome?

One of the rare diseases of the male reproductive system is Sertoli cell syndrome. The main manifestation of this pathology is infertility. The disease is a congenital developmental anomaly, since it causes aplasia (significant reduction or absence) of the germinal tissue of the testicles. As a result of this disorder, the seminiferous tubules do not develop. The only element that is not damaged is the Sertoli cell. Another name for this pathology is del Castillo syndrome. Some Sertoli cells still undergo degeneration, however, most of them are normal. Despite this, the tubular epithelium is atrophied. Spermatozoa are not formed with this pathology.

Leydig cell dysfunction

When Leydig cells are damaged, their main function - testosterone synthesis - is disrupted. As a result, symptoms such as:

1. Decreased muscle mass.
2. Absence of secondary sexual characteristics (male hair growth, voice timbre).
3. Libido disturbance.
4. Decreased bone density.