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André T Guay

Publications and source records attributed to André T Guay.

7 recordsLinked to original sources
PubMed2006

Testosterone and erectile physiology.

The role of testosterone deficiency in sexual dysfunction is an important aspect of aging, because it affects such a large proportion of men over 50 years old. A number of age-related factors can cause sexual dysfunction (in particular erectile dysfunction) and testosterone deficiency, such as chronic illness and multiple medications, and the causative link between hypogonadism and erectile dysfunction is still debated. However, studies in castrated animals have proven that addition of testosterone, and its conversion to dihydrotestosterone, can restore erectile function. It appears that testosterone achieves this by peripheral mechanisms (endothelial dependent and independent) and central mechanisms. Testosterone replacement therapy is therefore effective for erectile dysfunction in men with hypogonadism, with success rates of 35-40%. Testosterone supplementation is also important in men who fail on phosphodiesterase type-5 inhibitors, because a minimum plasma concentration of testosterone is required for the successful restoration of erectile function with these agents. Testosterone gels are now the preferred formulation for testosterone supplementation and they can be highly beneficial in a proportion of men with erectile dysfunction.

Adult↗
PubMed2006

Are androgens critical for penile erections in humans? Examining the clinical and preclinical evidence.

Androgens are deemed critical for penile-tissue development, growth, and maintenance of erectile function, however, their role in erection, especially in humans, remains controversial. In this review, we summarize information from clinical and animal model studies to provide a comprehensive and rational argument for the role of androgens, or lack thereof, on penile erection ability in humans. The goal of this review is to present the clinical and preclinical evidence available in the literature with regard to testosterone and erectile physiology and engage the reader in this discussion. Ultimately, each reader will have to form his or her own conclusions based on the existing evidence. In humans, androgen-deficiency manifestations are noted in clinical situations such as: (i) inadequate development of the penis; and (ii) loss of erectile function in prostate cancer and benign prostatic hyperplasia patients managed with medical or surgical castration or antiandrogen therapy. Androgen treatment causes: (i) improvement in sexual function in hypogonadal patients treated with androgen supplementation; (ii) improvement in nocturnal penile tumescence in hypogonadal patients treated with androgens; (iii) improvement in erectile function with androgen supplementation in patients who did not respond to phosphodiesterase type 5 inhibitor therapy initially; and (iv) improvement in the well-being, mood, energy, and sexual function in aging men who have testosterone deficiency treated with androgen therapy. In contrast to animals, especially rodents in which the adrenal cortex does not synthesize androgens, the human adrenal is a source of peripherally circulating androgen precursors, thus, complete androgen insufficiency may not be observed in men at a younger age. Furthermore, in light of the concept that a threshold of androgen levels exists in animals and humans below which sexual function is diminished, further contributes to the complexity of understanding androgens role in erections, especially in humans. Nevertheless, based on the preclinical and clinical data available in the literature, to date, we infer that androgens play a critical role in maintaining erectile physiology in humans.

Androgens↗
PubMed2005

Relation of endothelial cell function to erectile dysfunction: implications for treatment.

The prevalence of both cardiovascular disease (CVD) and erectile dysfunction (ED) increases with advancing age. These conditions share the common risk factors of diabetes mellitus, hypertension, hyperlipidemia, smoking, and obesity. They also share a pathophysiologic mechanism of decreased vascular blood flow via endothelial dysfunction. There are several lines of evidence that endothelial dysfunction in men with ED can be detected well before overt manifestations of vascular damage, including atherosclerotic effects. Some evidence shows that ED can be improved not only with phosphodiesterase 5 inhibitors but also by treating the risk factors directly. This includes cessation of smoking, correction of hyperlipidemia, and amelioration of obesity through weight loss. Conversely, ED may be prevented through maintenance of lean body mass, consistency of physical activity, and smoking abstinence, similar to other risk factors for CVD.

Endothelial Cells↗
PubMed2005

Incidence of metabolic syndrome and insulin resistance in a population with organic erectile dysfunction.

INTRODUCTION: Advanced age in men is accompanied by an increased prevalence of cardiovascular disease (CVD) and erectile dysfunction (ED). Prior studies revealed that 56% of an ED population have asymptomatic myocardial ischemia, 75% of men with CAD have symptoms of ED, and 91% of our ED patients have cardiovascular risks. AIM: Because metabolic syndrome (MS) and insulin resistance (IR) are both predictors of CVD, we wished to evaluate these parameters in our population. METHODS: Our men (N = 154) were evaluated for multiple cardiovascular risk factors and graded on severity of ED. The severity of ED was evaluated by the Sexual Health Inventory for Men (SHIM) questionnaire. The prevalence of MS was determined by NCEP/ATP III criteria. Insulin resistance was measured by QUICKI. MAIN OUTCOME MEASURES: Bivariate associations among total cholesterol/high-density lipoprotein (HDL), triglyceride/HDL, and Quantitative Insulin Sensitivity Check Index (QUICKI) were compared. Chi-square analysis was used to evaluate the relation between the presence and severity of IR with the severity of ED. RESULTS: The total cholesterol/HDL ratio was moderately and negatively correlated with QUICKI (r = -0.33; P < 0.01) and similarly for the triglyceride/HDL ratio (r = -0.32; P < 0.01). Metabolic syndrome was present in 43% of our ED population as opposed to 24% in a matched patient population. Approximately 79.2% of our total population had IR and 73.3% of the nondiabetic portion (N = 120) had IR, compared to 26% in a general population study. Metabolic syndrome (P = 0.01), IR (P = 0.01), and fasting blood sugar (FBS) >110 mg/dL (P = 0.01) correlated positively and moderately with increasing severity of ED by SHIM score. CONCLUSION: Men with ED have a high incidence of MS and IR. Early detection of metabolic disease in patients with ED may be a gateway to the reduction endothelial dysfunction in younger men with increased cardiovascular risk but who present for treatment of ED alone.

Comorbidity↗
PubMed2004

Endocrine aspects of female sexual dysfunction.

INTRODUCTION: Various endogenous hormones, including estrogen, testosterone, progesterone and prolactin, may influence female sexual function. AIM: To provide recommendations for the diagnosis and treatment of women with endocrinologic sexual difficulties. METHODS: The Endocrine Aspects of Female Sexual Dysfunction Committee was part of a multidisciplinary International Consultation. It included four experts from two countries and several peer reviewers. MAIN OUTCOME MEASURE: Expert opinion was based on committee discussion, a comprehensive literature review and evidence-based grading of available publications. RESULTS: The impact of hormones on female sexual function and their etiological roles in dysfunction is complex. Research data are limited as studies have been hampered by lack of precise hormonal assays and validated measures of sexual function in women. Sex steroid insufficiency is associated with urogenital atrophy and may also adversely affect central sexual thought processes. Systemic estrogen/estrogen progestin therapy alleviates climacteric symptoms but there is no evidence that this therapy specifically improves hypoactive sexual desire disorder (HSDD) in premenopausal or postmenopausal women. Exogenous testosterone has been shown in small randomized controlled trials (RCT) to improve sexual desire, arousal and sexual satisfaction in both premenopausal and postmenopausal women. However, as there is no biochemical measure that clearly identifies who to treat, use of exogenous testosterone should be considered only after other causes of HSDD have been excluded, such as depression, relationship problems and ill health. The clinical assessment of HSDD should include detailed medical, gynecologic, sexual and psychosocial history and physical examination including the external/internal genitalia. Hormonal therapy should be individualized and risks/benefits fully discussed, and all treated women should be carefully followed up and monitored for therapeutic side effects. CONCLUSIONS: There is a need for prospective, multi-institutional clinical trials to define safe and effective endocrine treatments for female sexual dysfunction.

Age Factors↗
PubMed2002

Screening for androgen deficiency in women: methodological and interpretive issues.

OBJECTIVE: To appreciate the problems in obtaining and interpreting androgen levels in women. DESIGN: Review of the literature to compare various laboratories and methods of analysis of serum androgens. PATIENT(S): Normal control populations culled from the literature to compare with patients previously reported on by us; data from our laboratory quality control compared with data from the literature. RESULT(S): Investigators and laboratories disagree as to the best methods of measuring testosterone (T) levels in women. Measuring DHEAS levels is much less controversial. CONCLUSION(S): Serum T levels should be measured in the morning hours and during the middle third of the menstrual cycle in premenopausal women. DHEAS levels may be measured at any time. Androgens decrease with age, but age-related levels are not accurate because current control populations have never been screened for sexual dysfunction. Such control populations need to be obtained.

Adolescent↗