Homocysteine levels correlate with velocimetric parameters in patients with erectile dysfunction undergoing penile duplex ultrasound.

INTRODUCTION: Hyperhomocysteinemia may contribute to the development of endothelial dysfunction and, consequently, atherosclerosis, a systemic disease involving the vessels that may affect the cavernous arteries leading to vasculogenic erectile dysfunction. Our study aims therefore to explore the relationship between homocysteine levels and velocimetric parameters detected by basal penile duplex ultrasound such as peak systolic velocity and flaccid penile acceleration in patients with erectile dysfunction. METHODS: A cross-sectional study was conducted collecting clinical, metabolic, hormonal, and instrumental (basal penile duplex ultrasound) data in patients affected by vasculogenic erectile dysfunction. RESULTS: Data of 126 subjects affected by erectile dysfunction were collected. Mean age was 52.1 ± 12.6 years, whereas mean body mass index was 25.6 ± 4.0 kg/m2 . Basal penile duplex ultrasound showed peak systolic velocity values of 13.1 ± 2.9 cm/s and mean flaccid penile acceleration of 2.28 ± 0.70 m/s2 , with a strong correlation among these two parameters (r = 0.690; p < 0.001). Frankly pathological values of peak systolic velocity and flaccid penile acceleration were detected in 39.7% and 4.8% of the subjects examined, respectively. Mean homocysteine levels were 14.9 ± 9.5 µmol/l. Homocysteine values >15 µmol/l were found in 26% of the subjects with erectile dysfunction. Peak systolic velocity values and homocysteine levels showed an inverse correlation (r = -0.213; p = 0.03). Similarly, flaccid penile acceleration values were inversely correlated to homocysteine levels (r = -0.199; p = 0.05). In addition, an inverse correlation was found between both peak systolic velocity and flaccid penile acceleration and body mass index, atherogenic lipid pattern, and age. Homocysteine and metabolic parameters showed no significant correlations. CONCLUSION: Hyperhomocysteinemia is highly prevalent in erectile dysfunction patients. The results of our study show that homocysteine levels correlate with velocimetric parameters assessed by basal penile duplex ultrasound, confirming the role of hyperhomocysteinemia in the genesis of erectile dysfunction of arterial origin.

Coenzyme Q10 and Male Infertility: A Systematic Review.

Infertility affects 15% of couples worldwide. A male factor is involved in 50% of cases. The etiology of male infertility is poorly understood, but there is evidence for a strong association between oxidative stress (OS) and poor seminal fluid quality. For this reason, therapy with antioxidants is one of the cornerstones of empirical treatment of male infertility. Coenzyme Q10 (CoQ10)-an essential cofactor for energy production with major antioxidant properties-is commonly used to support spermatogenesis in idiopathic male infertility. This systematic review aims to elucidate the usefulness of CoQ10 supplementation in the treatment of male infertility, particularly with regard to semen quality assessed by conventional and advanced methods, and pregnancy rates. All studies report a beneficial effect of CoQ10 supplementation on semen parameters, although randomized controlled trials are a minority. Moreover, the optimal dosage of CoQ10 or how it can be combined with other antioxidant molecules to maximize its effect is unknown. However, CoQ10 is still one of the most promising molecules to treat idiopathic male infertility and warrants further investigation.

Impact of adult growth hormone deficiency on metabolic profile and cardiovascular risk [Review].

Adult growth hormone deficiency (GHD) is a well defined clinical condition, which is characterized by abnormal body composition, impaired physical activity and decreased quality of life. In addition, in recent years, growing interest has been shown towards cardiovascular risks in adult patients affected by GHD. In this regard, GHD is widely known to be associated with increased mortality, likely due to the increase of risk factors, such as central obesity, impaired lipid and glucose profiles and other less-known risk factors, such as inflammatory cytokines, endothelial dysfunction and oxidative stress. However, very few papers have recently discussed this topic. In this review, the aim is to clarify this issue by discussing evidence regarding the effects of adult GHD on metabolic and cardiovascular profiles.

Testosterone and cardiovascular risk.

Cardiovascular (CV) disease is one of the most common causes of death in the western populations and, nowadays, its incidence is increasing even in the developing countries; although CV disease affects both sexes, it is more frequent in males in whom it shortens the average life expectancy. In this regard, this difference has been wrongly attributed for many years to the negative effects of testosterone (T); however, nowadays, a large amount of evidence suggests that this hormone may have protective effects on the CV system and that, indeed, the low levels of T could be associated with an increased CV risk and with an augmentation of morbidity and mortality in males. Such an aspect gains great relevance in light of the consideration that T decrease, besides occurring as a consequence of rare pathological conditions, can often take place with natural aging, causing a state of "male menopause", also called late-onset hypogonadism. In this review, we aimed to summarize the present state of the art concerning the association between T deficit and CV disease by analyzing the protective role of T on CV system and the relationship of this hormonal lack with metabolic syndrome, CV morbidity and mortality, and with the CV complications, such as ischemic heart disease, heart failure and stroke, that frequently occur in T deficiency.