EAU Pocket Guidelines on Male Infertility 2003

EAU GUIDELINES POCKET EDITION 1 CONTENTS: INFERTILITY ERECTILE DYSFUNCTION MANAGEMENT of URINARY and MALE GENITAL TRACT INFECTIONS 2 3 EAU POCKET GUIDELINES EDITION 1 Introduction This is one of a series of convenient pocket size books (currently 3) offering a comprised version of several EAU guidelines. These short texts are based on the currently avai- lable extended guidelines texts and can serve as a quick refe- rence guide for medical professionals. The EAU considers it to be of paramount importance to con- tinuously update its guidelines texts and introduce new data and the latest versions can be viewed online at http://www.uroweb.nl. All EAU members will automatically receive a printed version. Board EAU Healthcare Office March 2003 EAU POCKET GUIDELINES EDITION 1 Introduction Introduction 4 GUIDELINES FOR THE INVESTIGATION 2 Diagnosis 5 2.1 Introduction AND TREATMENT OF MALE INFERTILITY The diagnosis of male fertility must focus on a number of prevalent disorders, such as varicocele, testicular and epididymal abnormalities, obstructions of the genital tract, and anom- G. Dohle and the members of the guidelines working party alies of prostate and seminal vesicles (Table 1). Simultaneous on Male Infertility. assessment of the female partner is preferable, even if abnormalities are found in the male. GUIDELINES ON INFERTILITY 1. INTRODUCTION 1.1 Definition Table 1: The main cause of male infertility “Infertility is the inability of a sexually active, non-contracept- Testicular insufficiency ing couple to achieve pregnancy in one year” (WHO, 1995). ¼ Cryptorchidism About 25% of couples do not achieve pregnancy within 1 ¼ Orchitis (viral) year. Of these couples, 15% seek medical treatment for infer- ¼ Testicular torsion tility and less than 5% remain unwillingly childless. ¼ Cytotoxic therapy (chemotherapy) ¼ Radiotherapy 1.2 Prognostic factors ¼ Genetic causes (Klinefelter’s syndrome, Y deletions) The main factors influencing the prognosis in infertility are: Endocrine disorders ¼ Duration of infertility ¼ Kallmann’s syndrome GUIDELINES ON INFERTILITY ¼ Primary or secondary infertility ¼ Prader-Willy syndrome ¼ Results of semen analysis ¼ Pituitary gland disorders (adenoma, infection) ¼ Age and fertility status of the female partner Obstructions of the male genital tract ¼ Congenital absence of the vas deferens/epididymis As a urogenital expert, the urologist should examine any male ¼ Müllerian prostatic cysts with fertility problems for urogenital abnormalities. This ¼ Epididymal obstructions (infections, congenital) applies to all males diagnosed with reduced sperm quality. A ¼ After groin or scrotal surgery diagnosis is mandatory to initiate appropriate therapy (Drugs, Sperm antibodies Surgery, Assisted reproduction) Medication, environment, stress, illness Varicocele Sexual problems/ejaculation disorders Idiopathic Infertility Infertility 6 2.2 Semen analysis spermatozoa) and teratozoospermia (< 14% normal forms). 7 Andrological examination is indicated if semen analysis shows Quite often, all three pathologies occur simultaneously as abnormalities (Table 2). Since semen analysis still forms the oligo-asteno-teratozoospermia (OAT) syndrome. In extreme basis of important decisions concerning appropriate treatment, cases of OAT syndrome (< 1 million spermatozoa/ml), just as standardization of the complete laboratory work-up is highly with azoospermia, there is an increased incidence of obstruc- desirable. tion of the male genital tract and genetic abnormalities. Table 2: Overview of standard values for semen analy- 2.3 Hormonal investigation GUIDELINES ON INFERTILITY sis according to the 1992 WHO criteria Endocrine malfunctions are more prevalent in infertile men Volume ≥ 2.0 ml than in the general population, but are still quite uncommon. pH 7.0-8.0 Hormonal screening can be limited to determining follicle- Sperm concentration ≥ 20 million/ml stimulating hormone (FSH), luteinizing hormone (LH) and Total no. of spermatozoa ≥ 40 million/ejaculate testosterone levels. In men diagnosed with azoospermia or Motility ≥ 50% with progressive motility or extreme OAT, it is important to distinguish between obstruc- 25% with rapid motility within 60 tive and non-obstructive causes. A criterion with reasonable minutes after ejaculation predictive value for obstruction is a normal FSH with bilater- Morphology ≥ 14% of normal shape and form* ally a normal testicular volume. However, 29% of men with a Leucocytes < 1 million/ml normal FSH appear to have defective spermatogenesis. Immunobaed test < 20% spermatozoa with adherent GUIDELINES ON INFERTILITY particles 2.3.1 Hypergonadotrophic hypogonadism (elevated FSH/LH) MAR-test** < 10% spermatozoa with adherent Primary testicular developmental disorder with an elevated particles production of gonadotrophins is an isolated failure of sper- * Assessment according to Kruger and Menkfeld criteria. matogenesis and generally not caused by a disruption of the ** MAR = Mixed antiglobulin reaction endocrine system. Causes may be: ¼ Congenital - Klinefelter’s syndrome (sometimes accompa- Frequency semen analyses nied by gynaecomastia), anorchia, enzyme defects in If values are normal according to WHO criteria, one test androgen synthesis and cryptorchididsm should suffice. Only if the results are abnormal in at least two ¼ Acquired - after orchitis, testicular torsion, castration and tests are further andrological tests necessary. cytotoxic therapy It is important to distinguish between oligozoospermia (< 20 million spermatozoa/ml), astenozoospermia (< 50% motile Infertility Infertility 8 2.3.2 Hypogonadotrophic hypogonadism (deficient FSH/LH) used to be described as idiopathic male infertility will, in fact, 9 Low levels of gonadotrophins due to dysfunction of the pitu- have a genetic origin. By taking an extensive family history and itary gland or hypothalamus may occur as a result of: carrying out karyotype analysis, a number of these disorders ¼ Congenital anomalies - isolated arrest of FSH and LH secre- can be detected. This will not only yield a diagnosis, but also tion (Kallmann’s syndrome, accompanied by anosmia), iso- allow for appropriate genetic counselling. The latter may be lated arrest of LH secretion (fertile eunuch), idiopathic very important with the advent of intracytoplasmic sperm hypopituitarism and delayed puberty. injection (ICSI), because the fertility disorder and possibly the ¼ Acquired anomalies - generally as an expression of a more corresponding genetic defect may be transferred to the off- GUIDELINES ON INFERTILITY complex disorder of the pituitary gland or hypothalamus, spring. or iatrogenic (gonadotrophin-releasing hormone [GnRH] Chromosomal abnormalities are more common in men with agonists and anti-androgens) extreme OAT and with azoospermia. The most common sex chromosome abnormality is Klinefelter’s syndrome (47 XXY), If hypogonadotrophic hypogonadism is suspected, the medical which affects around 10% of men diagnosed with azoospermia. examination should include magnetic resonance imaging (MRI) Klinefelter’s syndrome is characterized by gynaecomastia and or a computed tomography (CT) scan of the pituitary gland hypergonadotrophic hypogonadism. Occasionally, a eunuchoid phenotype is found and sometimes psychological disorders. 2.4 Microbiological assessment Both testicles are very small and present with tubular sclerosis. Indications for microbiological assessment include abnormal In around 60% of all patients, testosterone levels decrease with urine samples, urinary tract infections, ‘male accessory gland age requiring androgen replacement. GUIDELINES ON INFERTILITY infections’ (MAGI) and sexually transmitted diseases (STDs). In men presenting with extremely poor quality semen, The clinical implications of white blood cells detected in a chromosome translocations and deletions can be found, which semen sample is as yet undetermined. However, in combina- may be hereditary and which may cause habitual abortion and tion with a small ejaculate volume, this may point to a (partial) congenital malformations in the offspring. It is recommended obstruction of the ejaculatory ducts caused by a (chronic) that karyotyping is performed in all men presenting with < 1 infection of the prostate or seminal vesicles. Genital infections million spermatozoa/ml and who are candidates for ICSI. may instigate the production of spermatotoxic free oxygen In cases of azoospermia or severe OAT, deletions in the radicals. Gonorrhoea and Chlamydia trachomatis can also azoospermic factor (AZF) region of the Y chromosome can cause obstruction of the genital tract . occur and testing is advised. The prevalence of Y deletions is considerable (around 5%) in this group of patients. Identifying 2.5 Genetic evaluation a Y deletion means that the defect will be passed on to sons A substantial number of andrological fertility disorders, which who will then also be infertile Infertility Infertility 10 When performing ICSI with surgically-retrieved sperm, ¼ Absence of seminiferous tubules (tubular sclerosis) 11 based on a diagnosis of congenital bilateral absence of the vas ¼ Presence of Sertoli cells only (Sertoli cell only syndrome) deferens (CBAVD), both the male and the female partners ¼ Maturation arrest - incomplete spermatogenesis, not should be checked for mutations in the cystic fibrosis trans- beyond the spermatocyte stage membrane regulator (CFTR) gene. Apart from causing cystic ¼ Hypospermatogenesis - all cell types up to spermatozoa are fibrosis (CF), this gene is also associated

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