Erectile dysfunction in infertility

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Erectile dysfunction in infertility: The generally recognized “gold standard” of first-line pharmacotherapy of erectile dysfunction are phosphodiesterase inhibitors of the fifth type (PDE-5). The clinical efficacy and possible side effects of PDE-5 inhibitors may vary in each case. This is due to the individual features of the expression of all PDE-5 isoforms, on which PDE-5 inhibitors exert their potential influence. We believe that there may come a time when PDE-5 inhibitors will be selected individually based on genetic examination (pharmacogenetics), but for now it is necessary to focus on the known pharmacokinetic properties of PDE-5 inhibitors.

Currently, it has been established that only one PDE-5 inhibitor does not have an inhibitory effect on PDE-11, which is located in the gonads, and therefore this drug does not have testicular toxicity. Less selectivity to PDE-11 leads to greater safety in relation to the heart, pituitary gland, gonads. The absence of manifestations of testicular toxicity against the background of taking sildenafil has until recently been a pharmacokinetic fact that has not been confirmed in studies analyzing the clinical experience of using the drug. In this regard, there is a need to evaluate this advantage of sildenafil in routine practice.

Consider a clinical observation – the experience of using udenafil, instead of sildenafil, in a patient with severe oligoasthenospermia. Note: if a patient with infertility has oligoastenospermia with an increased level of follicle-stimulating hormone, then he is sent to the in vitro fertilization (IVF) clinic without preparation, which subsequently leads to a rather low effectiveness of the procedure. Meanwhile, the effectiveness of IVF increases significantly after simple drug preparation aimed at leveling oxidative stress and improving blood flow.

Erectile dysfunction in infertility: Clinical example

The patient went to the clinic about infertility in marriage for five years, erectile dysfunction, obesity.

Anamnesis For five years, the patient was monitored by a urologist for azoospermia. A testicular biopsy was performed on him, no spermatozoa were found during morphological examination of the material. The couple was offered insemination with donor sperm, which the patient and his wife refused.

During examination at the clinic Erectile dysfunction according to the hardness scale of the erection, the hardness of the penis is of the second degree (the penis is hard, but not hard enough for penetration). Waist circumference 106 cm (norm up to 93 cm), body weight 111 kg. By the method of bioimpedance measurement, it was found that the amount of fat exceeds the permissible norms by two times. This can serve as an independent cause of oxidative stress, and aggravate oxidative stress of another etiology.

The patient also had androgen deficiency – testosterone deficiency, which leads to metabolic disorders in all organs and tissues, including in the tissue of the spermatogenic epithelium, necessary for the proliferation and kinesis of germ cells. In addition, the patient had increased free triiodothyronine due to a deficiency of a metabolically important trace element – iodine involved in the synthesis of thyroid hormones, and therefore the patient was additionally examined by an endocrinologist.

Diagnosis Hypergonadotropic hypogonadism (isolated increase in follicle-stimulating hormone). Androgen deficiency on the background of obesity. Erectile dysfunction of organic origin. Iodine deficiency.

ED in infertility: Treatment

The possibility of drug-induced effects on elevated follicle-stimulating hormone in men with azoospermia is questioned. The approach to each patient should be individual and pathogenetically justified. It is necessary to exclude the risk of side effects in relation to spermatogenesis, including azoospermia with an increase in follicle-stimulating hormone.

erectile dysfunction in infertility

Based on the diagnosis and pathogenesis of the disease in this case, the main directions of therapy included the fight against endothelial dysfunction, testosterone and nitric oxide deficiency, as well as oxidative stress. To normalize testosterone levels, such patients must be prescribed stimulating therapy with the use of chorionic gonadotropin preparations at a dose of 3000 to 5000 IU weekly.

This therapy can be combined with the use of transdermal testosterone, which accelerates the process of burning adipose tissue. Chorionic gonadotropin, being an analogue of luteinizing hormone, stimulates the production of testosterone by Leydig cells (interstitial testicular cells). Under the influence of testosterone, nitric oxide is released in intact endothelial cells, which positively affects the overall vascular tone of tissues, including the testicle. All of the above leads to the activation of neuronal nitric oxide synthase by non-cholinergic non-adrenergic nerve endings, which are rich in the genitourinary system.

It is worth considering the fact that in this group of patients, endothelial and neuronal dysfunction are noted with varying degrees of severity and compensation for nitric oxide deficiency occurs slowly, in parallel with repair. In order to eliminate nitric oxide deficiency and accelerate repair, it is pathogenetically correct to prescribe PDE-5 inhibitors. However, not all inhibitors are devoid of a negative effect on spermatogenesis, and even more so are able to improve the prognosis of infertility treatment in patients with elevated levels of follicle-stimulating hormone.

Over the past 15 years, since the introduction of the first PDE-5 inhibitor into clinical practice, significant progress has been made in the treatment of erectile dysfunction. However, today the requirements for pharmacotherapy of erectile dysfunction, including PDE-5 inhibitors, are increasing.

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