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Semelhante a J buvat paris sfa sfms t & santés métab & cv 01 09
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- 1. La Dysfonction Erectile en 2010 Nouvelles perspectives et attitudes pratiques
- 4. Testostérone et santés métabolique et vasculaire de l’homme: quelles preuves en 2010? Jacques BUVAT, CETPARP, LILLE [email_address] Symposium des Société Française d’Angéiologie (SFA) et Société Francophone de Médecine Sexuelle (SFMS), Paris, 8 Janvier 2010
- 5. Déficit en Testostérone (DT) « lié à l’age » Prevalence des taux abaissés T totale et libre selon l’age (Vermeulen et Kaufman 1997) Déclin longitudinal des T totale et libre dans la Baltimore Longitudinal Study on Aging (2001)
- 6. Quelle est la signification du DT chez l’homme avec DE? p < 0.0001 2,3 ng/ml 3,46 ng/ml 41% 42% 12% 4% Bacon et al 2006 (étude prospective de 14 ans): Obesité significativement risque de DE (RR 1.9) tandis que l’activ. physique le significativt (RR 0.7) Prevalence du DT chez 2435 patients avc DE selon leur degré d’obésité : 59% avaient un excés de poids (Corona et al 2008)
- 16. TESTOST É RONE ET SANT É CARDIOVASCULAIRE La testostérone a été longtemps considérée nocive pour le coeur
- 24. Quels sont le risques des traitements par la testostérone pour la fonction cardiovasculaire
- 26. Evènements cardiovasculaires associés au traitement par la testostérone chez les hommes de plus de 45 years Meta-Analyse de 19 essais randomisés contre placebo (Odd-Ratios poulés) (Calof et al 2005) 0.38,1.95 0.86 11.1 5.5 Cerebrovasc evts 0.32,1.93 0.78 5.5 0 Death 0.59,2.20 1.14 44.3 33.2 All cardiovasc evts 0.35,1.79 0.74 13.9 3.76 Coronary procedur 0.44,2.26 0.99 8.3 7.4 Myocardial infarct. 0.39,2.26 0.93 8.3 7.4 Chest pain, ischem 1.82,7.51 3.69 ** 2.8 64.5 Hematocrit > 50% 95% Confidence Interval Pooled Odd Ratio Taux EI/1000 années-patient Placebo Taux EI/1000 années-patient Testosterone
- 27. Testosterone and cardiovascular risk in men: a systematic review and meta-analysis of 30 RCTs in men of any age (27/30 > 50y) (Haddad et al 2007) Six RCTs reported on cardiovascular events with consistent results. No signific increase in the risk: pooled OR 1.82, 0.78-4.23 « Currently available evidence weakly supports the inference that testosterone use in men is not associated with important cardiovascular effects. Patients and clinicians need large randomized trials of men at risk for cardiovascular disease to better inform the safety of long-term testosterone use »
Notas do Editor
- Vermeulen & Kaufman: healthy
- % according to BMI: 41.5, 42 OW, 12 OB, 4 morb OB. IN ED PATIENTS TD DEFICIENCY IS SIGNIFICANTLY CORRELATED TO OBESITY, AND PROBABLY THE CONSEQUENCE OF IT; IN THIS STUDY OB SIGNIF ASSOC WITH HTA AND DYSLIPIDEMIA Bacon: prospective study in 22800 american 40-75 y old with 14 years FU. Other studies ob predicts ED: Heidler 2007, Riedner 2006 (central ob)
- A cluster of risk factors for cardiovascular disease and type 2 diabetes mellitus, which occur together more often than by chance alone, have become known as the metabolic syndrome. A Joint Interim Statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation;International Atherosclerosis Society; and International Association for the Study of Obesity. Three abnormal findings out of 5 would qualify a person for the metabolic Sd (alors que dans def précédentes obésité viscérale était une composante obligatoire syndrome. A single set of cut points would be used for all components except waist circumference, for which further work is required. In the interim, national or regional cut points for waist circumference can be used
- (TT < 3-3.5 ng/ml ou 10.4-12 nmol/l)
- Cancer prostate évolué. Prospectives uniqut à court terme, cross sectionnelles pour les autres. Manque d’études prospectives. Venant contrebalancer la diminution de la mortalité par K. Au total cette situation expérimentale ne permet pas non plus d’affirmer un risque vasculaire lié à l’hypogonadisme
- stiffness
- Chronic administration of low physiological doses of T has also been beneficial. Four RPCTs (Jaffe 1977, Wu et Wang 1993, English et al 2000, Malkin et al 2004) reported short-term improvements in ECG changes of CHD with respect to placebo, including longer exercise time to ischemia, after a maximum of 12 weeks of T supplementation. T therapy also substantially improved cardiac condition in 2 RPCTs of men with heart failure (including 1 till 12 months Malkin (Pugh et al 2004, Malkin et al 2006). Direct effects of T on male vasculature could explain these acute and chronic findings.
- LESS THAN ONE THIRD OF THE STUDIES CLEARLY SUPPORT A SIGNIFICANT ROLE OF HYPOGONADISM IN THE DEVELOPMENT OF CVD Seventeen prospective cohort or nested case controlled studies have also examined the relationship between T levels and cardiovascular morbidity and mortality. In 10 studies there was no correlation between baseline T levels and subsequent development of fatal or non fatal CHD, cerebro-vascular disease, or heart failure after adjustment for confounders, during observation periods of 5 to 31 years (Abbot et al 2007, Arnlov et al 2006, Barret-Connor et al 1988, Cauley et al 1987, Contoreggi et al 1990, Harman et al 2001, Hautanen et al 1994, Philips et al 1988, Vikan et al 2009, Yarnell et al 1993). Weak correlations of high androgen levels with cardiovascular mortality were observed in 2 studies (Araujo et al 2007, Maggio et al 2007). Conversely 2 studies reported significant correlations between low baseline T levels and cardiovascular deaths (Khaw et al 2007, Laughlin et al 2008), and 2 others between low baseline T and progression of carotid artery IMT (Muller et al 2004) or between low T and an increased incidence of stroke or transitory ischemic events (Yeap et al 2009). However, 2 other prospective studies were unable to confirm the correlations with IMT progression (Vikan et al 2009), and with an increased risk of stroke (Abbot et al 2007). Lastly, the Caerphilly study found a positive association of the cortisol/testosterone ratio with CHD incidence and mortality (Smith et al 2005). NB Laughlin: correlations signif à 20 ans dans la même Rancho-Bernardo study qui n’était pas significative à and in another between low T +low DHEA +low IGF1 and CV mortality Maggio 2007)
- In conclusion much data, especially including the inverse correlation of circulating T with most classical vascular risk factors, suggests the possibility of a detrimental effect of hypogonadism on cardiovascular health. However currently available results of the prospective observational studies cannot definitely confirm the role of low T in atherosclerosis, since a positive association was only found in a minority of these studies. Androgens have been shown to both promote and suppress pro-atherogenic and pro-inflammatory effects on all cell types involved in atherosclerosis. Given current evidence it would appear that androgen effects are dependent on cell type, dose, type of androgen, and type of exposure (McGrath et al 2008). A net effect of T on the arterial wall which would reduce or even delete the vascular benefit resulting from the improvement of the other vascular risk factors might explain the preceding discrepancy. More long term prospective epidemiological studies, as well as large scale, placebo-controlled, randomized trials of T therapy including vascular parameters among the primary end-points are urgently needed to resolve this issue.
- In conclusion much data, especially including the inverse correlation of circulating T with most classical vascular risk factors, suggests the possibility of a detrimental effect of hypogonadism on cardiovascular health. However currently available results of the prospective observational studies cannot definitely confirm the role of low T in atherosclerosis, since a positive association was only found in a minority of these studies. Androgens have been shown to both promote and suppress pro-atherogenic and pro-inflammatory effects on all cell types involved in atherosclerosis. Given current evidence it would appear that androgen effects are dependent on cell type, dose, type of androgen, and type of exposure (McGrath et al 2008). A net effect of T on the arterial wall which would reduce or even delete the vascular benefit resulting from the improvement of the other vascular risk factors might explain the preceding discrepancy. More long term prospective epidemiological studies, as well as large scale, placebo-controlled, randomized trials of T therapy including vascular parameters among the primary end-points are urgently needed to resolve this issue.
- Recommendation proposed by Graham Jackson. I have only added the first sentence to make it more explanatory. 17’’