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Biomedical subjects

Robert I McLachlan

Publications and source records attributed to Robert I McLachlan.

At least 19 recordsLinked to original sources
PubMed2007

Primary testicular failure in Klinefelter's syndrome: the use of bivariate luteinizing hormone-testosterone reference charts.

BACKGROUND: The diagnosis of androgen deficiency is based on clinical features and confirmatory low serum testosterone levels. In early primary testicular failure, a rise in serum LH levels suggests inadequate androgen action for the individual's physiological requirements despite a serum testosterone level within the normal range. The combined evaluation of serum LH and testosterone levels in the evaluation of testicular failure has not been widely advocated. PATIENTS: Seven hundred and six healthy males and 39 patients with known primary hypogonadism due to Klinefelter's syndrome and SRY-positive 46,XX karyotypes were included in the study. DESIGN: Testosterone, oestradiol and LH serum concentrations were measured in all individuals. Based on the 706 healthy males two-dimensional bivariate LH-testosterone reference charts were constructed. RESULTS: Despite a median serum total and free testosterone and oestradiol levels being reduced (P < 0.001) and LH levels elevated (P < 0.001) in Klinefelter's syndrome and 46,XX-males, many subjects (69%) had total testosterone within the reference range. However, using the bivariate charts all subjects lay outside the 97.5 percentile. CONCLUSION: Bivariate LH and testosterone charts are useful in the evaluation of men with known primary testicular failure due to sex chromosomal aneuploidy in whom evaluation based on testosterone measurement in isolation underestimates the prevalence of hypogonadism. It is, however, important to emphasize that isolated use of the bivariate evaluation should not form the basis for androgen substitution therapy. Further studies are needed in order to evaluate the use of bivariate LH and testosterone charts in the assessment of any younger man with possible primary testicular failure.

Adult↗
PubMed2006

Men in Australia Telephone Survey (MATeS): predictors of men's help-seeking behaviour for reproductive health disorders.

OBJECTIVE: To identify sociodemographic factors associated with help-seeking behaviour for reproductive health disorders in middle-aged and older Australian men. DESIGN: A cross-sectional, population-based, computer-assisted telephone interview exploring sociodemographic factors and general and reproductive health. PARTICIPANTS AND SETTING: Analysis of data from the Men in Australia Telephone Survey (MATeS) of 5990 Australian men aged 40 years and older interviewed between September and December 2003. MAIN OUTCOME MEASURES: Self-reported diagnosis of prostate disease and erectile dysfunction (ED), help-seeking behaviour (including visiting a doctor, prostate-specific antigen testing, treatment of prostate disease, speaking to a health professional about ED and treatment of ED). RESULTS: Age was a significant predictor of all help-seeking behaviour studied, other than treatment for ED. Controlling for all predictor variables, never-married status predicted a lower likelihood of visiting a doctor (odds ratio [OR], 0.68 [95% CI, 0.48-0.97]) or speaking to a health professional about ED (OR, 0.44 [95% CI, 0.21-0.93]), while divorced/separated status predicted lower likelihood of having a prostate-specific antigen test (OR, 0.63 [95% CI, 0.50-0.79]). Living in a regional or remote area or being from a non-English-speaking background predicted lower likelihood of receiving treatment for ED (ORs, 0.62 [95% CI, 0.42-0.92] and 0.41 [95% CI, 0.24-0.72], respectively), but did not influence screening for prostate disease. CONCLUSION: Seeking advice or treatment for male reproductive health disorders is predicted by sociodemographic factors specific to different reproductive health problems. As middle-aged and older men do attend doctors, opportunities exist for health professionals to optimise their consultations by routinely discussing reproductive health with all men, to identify under-reported male reproductive health disorders.

Adult↗
PubMed2006

The association between obesity and the diagnosis of androgen deficiency in symptomatic ageing men.

OBJECTIVE: To determine the influence of obesity on the diagnosis of age-related androgen deficiency (AD) in symptomatic men according to current Australian guidelines. DESIGN, SETTING AND PARTICIPANTS: A community-based cohort of healthy ageing men with symptoms suggestive of AD was studied between May 2001 and February 2003. Men were classified as obese or non-obese according to body mass index (BMI) or waist circumference (WC). MAIN OUTCOME MEASURE: Diagnosis of AD according to Endocrine Society of Australia (ESA) guidelines. RESULTS: 223 men aged 54-86 years with mean BMI 27.3 +/- 0.2 kg/m2 (range 20.5-36.2 kg/m2) were recruited; 99 men were obese (BMI > or = 30.0 kg/m2 or WC > or = 102 cm) and 124 men were non-obese. Obese men had lower total testosterone (TT) (12.7 +/- 0.4 v 15.0 +/- 0.4 nmol/L); P < 0.001) and calculated free testosterone (275.7 +/- 7.8 v 299.3 +/- 7.4 pmol/L); P = 0.03) levels than non-obese men. TT levels < 8 nmol/L were recorded in 12% of obese men and 1% of non-obese men. Applying the ESA guidelines for the diagnosis of age-related AD, 15 obese men (15%) and 4 non-obese men (3%) were classified as being eligible for androgen therapy supported by the Pharmaceutical Benefits Scheme (PBS); the relative risk in obese men was 1.92 (95% CI, 1.44-2.55; P < 0.001). CONCLUSION: Obesity is an important determinant of serum TT levels in ageing men. Almost one in seven obese men but only one in 30 non-obese men in our study were eligible for PBS-supported androgen therapy according to Australian guidelines. Although obese men are more likely to have biochemical hypoandrogenism, the clinical implications of this remain uncertain. Studies of testosterone therapy in this group of ageing men are needed to determine whether androgen replacement is beneficial.

Aged↗
PubMed2006

The relative roles of follicle-stimulating hormone and luteinizing hormone in maintaining spermatogonial maturation and spermiation in normal men.

CONTEXT: Male hormonal contraception via gonadotropin and intratesticular androgen withdrawal disrupts spermatogenesis at two principal sites: 1) spermatogonial maturation, and 2) spermiation. OBJECTIVE: The objective of this study was to explore the relative dependence of each stage of germ cell development on FSH and LH/intratesticular androgen action. DESIGN, SETTING, AND PARTICIPANTS: Eighteen men enrolled in this prospective, randomized 14-wk study at Prince Henry's Institute. INTERVENTIONS: Subjects (n = 6/group) were assigned to 6 wk of 1) testosterone (T) implant (4 x 200 mg sc once)+depot medroxy progesterone acetate (DMPA; 150 mg im once); 2) T implant+DMPA+FSH (300 IU sc twice weekly); and 3) T implant+DMPA+human chorionic gonadotropin (hCG; 1000 IU sc twice weekly as an LH substitute). Men then underwent a vasectomy and testicular biopsy with previously reported control data used for comparison. MAIN OUTCOME MEASURES: Germ cell number (assessed by the optical disector stereological approach) and intratesticular androgen levels were determined. RESULTS: T+DMPA alone significantly suppressed type B spermatogonia, preleptotene through to pachytene spermatocytes, and round spermatids from control (P < 0.05). All germ cell subtypes were maintained at control levels by either FSH or LH activity, except pachytene spermatocytes, which were found to be lower in the hCG vs. FSH (P < 0.01) and control groups (P < 0.05). CONCLUSIONS: FSH and LH maintained spermatogenesis independently in this gonadotropin-suppressed model. Compared with LH, FSH showed better maintenance of pachytene spermatocyte number, whereas improved conversion to round spermatids was suggested with hCG treatment. Future contraceptive treatment strategies must consider independent regulation of spermatogenesis by both FSH and LH/intratesticular androgens for maximum efficacy.

Adult↗
PubMed2006

Male hormonal contraception: concept proven, product in sight?

Current male hormonal contraceptive (MHC) regimens act at various levels within the hypothalamic pituitary testicular axis, principally to induce the withdrawal of the pituitary gonadotrophins and in turn intratesticular androgen production and spermatogenesis. Azoospermia or severe oligozoospermia result from the inhibition of spermatogonial maturation and sperm release (spermiation). All regimens include an androgen to maintain virilization, while in many the suppression of gonadotrophins/spermatogenesis is augmented by the addition of another anti-gonadotrophic agent (progestin, GnRH antagonist). The suppression of sperm concentration to 1 x 10(6)/ml appears to provide comparable contraceptive efficacy to female hormonal methods, but the confidence intervals around these estimates remain relatively large, reflecting the limited number of exposure years reported. Also, inconsistencies in the rapidity and depth of spermatogenic suppression, potential for secondary escape of sperm into the ejaculate and onset of fertility return not readily explainable by analysis of subject serum hormone levels, germ cell number or intratesticular steroidogenesis, are apparent. As such, a better understanding of the endocrine and genetic regulation of spermatogenesis is necessary and may allow for new treatment paradigms. The development of an effective, consumer-friendly male contraceptive remains challenging, as it requires strong translational cooperation not only between basic scientists and clinicians but also between public and private sectors. At present, a prototype MHC product using a long-acting injectable testosterone and depot progestin is well advanced.

Androgens↗
PubMed2006

The effects of gonadotropin suppression and selective replacement on insulin-like factor 3 secretion in normal adult men.

CONTEXT: Gonadotropic regulation of the testicular Leydig cell hormone insulin-like factor 3 (INSL3) is incompletely characterized. OBJECTIVE: The objective of this study was to assess the effects of gonadotropin suppression and induced or spontaneous recovery on serum INSL3. DESIGN AND PARTICIPANTS: Serum samples from 15 men enrolled in a short-term study of gonadotropin stimulation, suppression, and recovery and 11 men in a long-term study of gonadotropin suppression and spontaneous recovery were analyzed for INSL3. INTERVENTION: Gonadotropins were suppressed by exogenous testosterone and progestin. Recovery was spontaneous or induced with exogenous gonadotropins. OUTCOME MEASURE: The outcome measure was serum INSL3 in relation to other reproductive hormones. RESULTS: Serum INSL3 was not acutely sensitive to gonadotropins. In both studies, INSL3 declined markedly with gonadotropin suppression (6-13.5% of baseline; P < 0.05). In the short-term study, human chorionic gonadotropin partially restored suppressed serum INSL3 within 4 d of administration (from 7.5 to 38.3% baseline; P < 0.05); the increase correlated with the corresponding increase in serum pro-alphaC (r = 0.82; P < 0.01). FSH did not stimulate the suppressed INSL3. In the long-term study, serum testosterone recovered significantly better (80% baseline) compared with serum INSL3 (38.9% baseline; P < 0.01) in the presence of fully recovered serum LH. CONCLUSIONS: INSL3 is not sensitive to gonadotropin stimulation in normal men, but declines markedly in response to gonadotropin deprivation. After suppression, INSL3 was responsive to hCG 4 d after administration. After long-term suppression, INSL3 did not recover to the same degree as testosterone, suggesting that INSL3 is more sensitive to Leydig cell impairment than testosterone.

Adult↗
PubMed2006

A double exponential model for biochemical oxygen demand.

Biochemical oxygen demand (BOD) exertion patterns in anaerobically treated farm dairy wastewater were investigated on a laboratory scale. Oxygen uptake was typically characterised by a period of rapid oxygen exertion, a transitional "shoulder" phase and a period of slower activity. A multi-species model, involving rapidly degradable and slowly degradable material, was developed, leading to a double exponential model of BOD exertion as follows:where t is time, BOD(u1)(') and BOD(u2)(') are apparent ultimate BOD (BOD(u)) values, and k(1) and k(2) are rate constants. The model provided an improved description of BOD exertion patterns in anaerobically treated farm dairy wastewater in comparison to a conventional single exponential model, with rapidly degradable rate constant values (k(1)) ranging from 2.74 to 17.36d(-1), whilst slowly degradable rate constant values (k(2)) averaged 0.25d(-1) (range 0.20-0.29). Rapidly and slowly degradable apparent BOD(u) estimates ranged from 20 to 140g/m(3) and 225 to 500g/m(3), respectively, giving total BOD(u) levels of 265-620g/m(3). The mean square error in the curve fitting procedure ranged between 20 and 60g(2)/m(6), with values on average 70% lower (range 31-91%) than those obtained for the single exponential model. When applied to existing data for a range of other wastewaters, the double exponential model demonstrated a superior fit to the conventional single exponential model and provided a marginally better fit than a mixed order model. It is proposed that the presence of rapidly degradable material may be indicated from the value of the first rate constant (k1) and the time to 95% saturation of the first exponential function. Further model development is required to describe observed transitional and lag phases.

Anaerobiosis↗
PubMed2006

Hypogonadotropism with elevated serum testosterone: reversible causes of secondary infertility.

BACKGROUND: A 33-year-old man presented with secondary infertility, increased libido, and extreme oligospermia. Testicular volumes were reduced, but no gynecomastia was apparent and androgen abuse was denied. INVESTIGATIONS: Physical examination, semen-volume and sperm-density assessment, laboratory tests for serum levels of luteinizing hormone, follicle-stimulating hormone, testosterone, and dehydroepiandrosterone sulfate, karyotyping, testicular ultrasound, pelvic and abdominal CT, assessment for serum testicular tumor markers (alpha-fetoprotein and human chorionic gonadotropin), and histologic examination of testicular tissue. DIAGNOSIS: Benign Leydig-cell adenoma. MANAGEMENT: Left orchidectomy.

Adult↗
PubMed2005

Reproductive hormone reference intervals for healthy fertile young men: evaluation of automated platform assays.

CONTEXT: Management of male infertility and/or androgen deficiency requires accurate hormonal measurements with valid reference intervals. OBJECTIVE: The objective of this study was to develop a valid reference panel of blood samples from healthy eugonadal young men with verified normal reproductive function and to use this panel to evaluate the performance of seven fully automated, commercial multiplex immunoassay platforms used to measure serum total testosterone (T), LH, and FSH. DESIGN: This was an observational study of consistency among seven different automated immunoassays for each of total T, LH, and FSH. Each method was implemented in two laboratories, with each repeating the analysis of the full reference panel samples twice. Serum T concentrations were also measured by gas chromatography/mass spectrometry (GC/MS), and serum inhibin B levels were determined by an ELISA. SETTING: The study was performed at commercial, high-volume, clinical pathology laboratories. PARTICIPANTS: From 147 men screened, sera from 124 healthy, reproductively normal men (age, 21-35 yr) with normal sperm output were used as a reference panel. All laboratories selected for elite performance in the national immunoassay quality assurance program agreed to participate. MAIN OUTCOME MEASURE(S): For each of the 868 assays, descriptive statistics were calculated in the natural and log-transformed scales and were analyzed by nested, repeated measures ANOVA after log transformation. Reference intervals, defined as 95% confidence limits, were calculated using arithmetic (natural scale), geometric (log scale) and nonparametric methods. RESULTS: Descriptive statistics and reference intervals for serum T, LH, and FSH differed widely and significantly between methods, but variation between laboratories for the same assay was negligible. All T methods showed significant differences in regression slope and intercept in deviance plots as well as in estimated reference ranges compared with the independent GC/MS reference method. Although similar between-method differences existed for gonadotropin assays, the smaller quantitative discrepancies allowed assignment of consensus reference intervals for serum FSH (1.3-8.4 IU/liter) and LH (1.6-8.0 IU/liter), although these differed from manufacturers' currently quoted expected values. CONCLUSIONS: Using a reference panel of sera from healthy eugonadal young men with verified normal reproductive function, major differences exist between commercial T immunoassays as well as divergence from the GC/MS standard. This impairs their clinical diagnostic utility and requires substantial improvements in automated T immunoassay technologies or a switch to GC/MS methods. Gonadotropin assays showed less variability, but current high-throughput immunoassays remain suboptimal to confirm accurate diagnosis of azoospermia or androgen deficiency.

Adult↗
PubMed2005

Effects of testosterone and levonorgestrel combined with a 5alpha-reductase inhibitor or gonadotropin-releasing hormone antagonist on spermatogenesis and intratesticular steroid levels in normal men.

CONTEXT: Combination of a GnRH antagonist (acyline), types I and II, 5alpha-reductase inhibitor (dutasteride) or levonorgestrel (LNG) with testosterone (T) treatment may augment the suppression of spermatogenesis and intratesticular (iT) steroids. OBJECTIVE: The objective of this study was to assess the effects of combined hormonal contraceptive regimens on germ cell populations and iT steroids. DESIGN, SETTING, AND PARTICIPANTS: Twenty-nine normal health men enrolled in this prospective, randomized, 14-wk study at the University of Washington. INTERVENTION(S): Twenty-two men (n = 5-6/group) received 8 wk of T enanthate (TE; 100 mg, i.m., weekly) combined with 1) 125 microg LNG daily, orally; 2) 125 microg LNG plus 0.5 mg dutasteride daily, orally; 3) 300 microg/kg acyline twice weekly, s.c.; or 4) 125 microg LNG daily, orally, plus 300 microg/kg acyline twice weekly, s.c. Subjects then underwent a vasectomy and testicular biopsy. Control men (n = 7) proceeded directly to surgery. MAIN OUTCOME MEASURE(S): The main outcome measures were germ cells and iT steroids [T, dihydrotestosterone, 3alpha- and beta-androstanediol (Adiol), and estradiol (E2)]. RESULTS: High iT levels of all androgens (6- to 123-fold serum levels) and E2 (407-fold serum levels) were found in control men. iTT (1.9-2.6% control; P < 0.001) and iT3betaAdiol (16-34% control; P < 0.05) levels decreased with all treatments. iT dihydrotestosterone (13-29% control; P < 0.05) and iT3alphaAdiol (44-47% control; P < 0.05) levels decreased with all but the TE plus LNG treatment. iTE2 levels decreased only in the TE plus acyline group (28% control; P = 0.01). Germ cells from type B spermatogonia onward were suppressed, with no differences between groups found. Variable sites of impairment of germ cell progression were evident between men (spermagonial maturation, meiosis 1 entry, and spermiation). Other than a negative correlation between iT3alphaAdiol and haploid germ cell number (P < 0.006), no correlations between germ cell number and gonadotropins, sperm concentration, or iT steroids were found. CONCLUSIONS: A similar high testicular:serum gradient exists for E2 and T in normal men, and 8 wk of gonadotropin suppression markedly reduces iTT, with 5alpha-reduced androgens and E2 levels decreasing to a much lesser degree. The heterogeneity of the germ cell response, regardless of treatment, gonadotropins or iT steroids, points to the individual sensitivity of sites in germ cell development, which is worthy of additional exploration.

5-alpha Reductase Inhibitors↗
PubMed2005

Oestrogen does not affect the restoration of spermatogenesis in the gonadotrophin-releasing hormone-immunised adult rat.

Oestrogen is a metabolite of testosterone, but its role in spermatogenesis is ill-defined. Oestrogen may exert its effects on spermatogenesis, as oestrogen receptor (ER)-beta has been localised to both germ and somatic cells. This study sought to establish whether the restoration of early germ cell numbers in spermatogenesis by high-dose exogenous testosterone was influenced by its metabolite, oestrogen. The ER antagonist (ICI 182780) was administered, at a dose known to impair oestrogen action in the male reproductive tract, during testosterone treatment of gonadotrophin-releasing hormone (GnRH)-immunised rats, and germ cell numbers were determined. GnRH-immunised adult Sprague-Dawley rats (n=7-8 per group) received two doses of testosterone, either as a Silastic implant (24 cm (T24 cm)) or an injectable ester for 10 days alone or in combination with ICI 182780 (2 mg/kg, s.c. injection daily). Control rats received vehicle alone. Testes were perfusion-fixed and germ cells were quantified by the optical disector technique. GnRH-immunisation reduced (P<0.001) both type A/ intermediate spermatogonial and type B spermatogonial/ preleptotene spermatocyte number (56% of control) and leptotene/zygotene spermatocyte number (63% of control). Pachytene spermatocyte and round spermatids were reduced to 12% and l% (P<0.01) of control respectively. Testosterone treatment did not increase type A/intermediate spermatogonial number compared with GnRH-immunised controls over the 10-day study period. Treatment with testosterone-esters increased type B spermatogonial/preleptotene spermatocytes and leptotene/zygotene spermatocyte numbers (both being ~83% of control, P<0.05), while T24 cm treatment did not significantly increase their numbers (~73% of control) compared with GnRH-immunised controls. Both treatments increased pachytene spermatocyte and round spermatid numbers to 55% and 8% of control respectively. Co-administration of ICI 182780 had no effect on any of these germ cell numbers. We conclude that oestrogen action plays no role in the short-term restoration of spermatogenesis by testosterone in the GnRH-immunised rat.

Animals↗
PubMed2005

Management of the infertile couple.

BACKGROUND: With the further development of reproductive technology over the past 2 decades, options for subfertile couples have greatly increased. OBJECTIVE: This article discusses the assessment of common male and female causes of infertility and describes a logical routine for the investigation and treatment of the subfertile couple using a flow chart approach. DISCUSSION: We suggest an approach to assessment for general practitioners, and outline the likely course of more sophisticated testing and treatments that their patients may then experience.

Coitus↗
PubMed2004

Novel male hormonal contraceptive combinations: the hormonal and spermatogenic effects of testosterone and levonorgestrel combined with a 5alpha-reductase inhibitor or gonadotropin-releasing hormone antagonist.

We postulated that the addition of a combined types I and II, 5alpha-reductase inhibitor (dutasteride) or long-acting GnRH antagonist (acyline) to combination testosterone plus levonorgestrel treatment may be advantageous in the suppression of spermatogenesis for male contraception. This study aimed to examine effects of novel combination contraceptive regimens on serum gonadotropins and androgens and sperm concentration.This study was divided into three phases: screening (2 wk), treatment (8 wk), and recovery (4 wk). Twenty-two men (n = 5-6/group) received 8 wk of treatment with testosterone enanthate (TE, 100 mg im weekly) combined with one of the following: 1) levonorgestrel (LNG) 125 mug orally daily; 2) LNG 125 microg plus dutasteride 0.5 mg orally daily; 3) acyline 300 microg/kg sc every 2 wk (as a comparator for any additional progestin effects); or 4) LNG 125 microg orally daily plus acyline 300 microg/kg sc every 2 wk. Serum gonadotropin levels were similarly suppressed by all treatments, falling to a nadir between 1.2 and 3.4% and 0.5 and 0.8% baseline for FSH and LH, respectively (P < 0.05). Serum dihydrotestosterone levels were significantly (P < 0.05) decreased in the dutasteride group throughout the treatment period to a nadir of 31% baseline (wk 7). No significant differences in sperm concentrations among treatment groups were seen. Severe oligospermia (0.1-3 million/ml) or azoospermia was seen in none of five and four of five in TE + LNG; two of six and four of six in TE + LNG + dutasteride; two of six and four of six in TE + acyline; and one of five and three of five in TE + LNG + acyline groups, respectively. There was one nonresponder in each of the TE + LNG and TE + LNG + acyline groups.We conclude that the addition of a combined types I and II, 5alpha-reductase inhibitor or long-acting GnRH antagonist to a testosterone plus LNG regimen provides no additional suppression of gonadotropins or sperm concentration over an 8-wk treatment period. However, further evaluation of the effects of these regimens on the testis (including testicular steroid levels and germ cell maturation) and the treatment of larger numbers of men (and for longer periods) may provide data to support their place in contraceptive development.

Adult↗
PubMed2004

Stereological analysis of the human testis after vasectomy indicates impairment of spermatogenic efficiency with increasing obstructive interval.

OBJECTIVE: To quantify germ cell loss and the extent of testicular fibrosis in vasectomized patients of varying obstructive intervals. DESIGN: Retrospective study. SETTING: Specialized male reproductive surgery and endocrinology service. PATIENT(S): Thirty-four vasectomized patients 1-20 years after surgery and 10 normal subjects. INTERVENTION(S): Thirty-four testicular biopsies taken at the time of vasectomy reversal (vasovasostomy). Control biopsies taken from 10 normal men at the time of vasectomy. MAIN OUTCOME MEASURE(S): Stereological assessment of testicular germ cell populations and testicular fibrosis. RESULT(S): Vasectomy caused a significant decrease in germ cells in the later stages of spermatogenesis, with significant reductions in pachytene spermatocytes (by 18%), round spermatids (by 40%), elongating spermatids (by 23%), and elongated spermatids (by 39%). The loss of spermatids showed a significant relationship with obstructive interval. A significant 2.7-fold increase in total (peritubular plus interstitial) fibrosis was observed, which showed a positive relationship with obstructive interval. Decreased germ cell populations and fibrosis did not seem to be related to sperm antibody levels nor to sperm counts obtained up to 2 years after vasovasostomy. CONCLUSION(S): Vasal obstruction results in significant reductions in germ cells in the later stages of spermatogenesis and increases in testicular fibrosis, both worsening with an increasing obstructive interval. Testicular damage after vasectomy might impact upon the prospects for reversal.

Adult↗
PubMed2004

Genetic screening of infertile men.

Male infertility is an extraordinarily common medical condition, affecting 1 in 20 men. According to the World Health Organization, this condition is now considered to be a complex disease involving physical, genetic and environmental factors. With continuing advances in our understanding of male reproductive physiology and endocrinology, together with the availability of the complete sequence of the human genome and powerful functional genomic techniques, the stage is now set to identify the genes that are essential for spermatogenesis. Given that the process of spermatogenesis, from the germ cell to mature sperm, is complex, the challenge for research is to develop the strategies for identifying new genetic causes of idiopathic male infertility and defining genotypes associated with specific defects in semen parameters and testicular pathologies. Such information will form the basis of new genetic tests that will allow the clinician to make an accurate diagnosis of the male partner and a more informed decision about treatment options for the couple.

Genetic Testing↗