Avanafil (Stendra) for the treatment of erectile dysfunction

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*avanafil shows high efficacy in complicated patients (diabetes, hypertension, dyslipidemia)....daily administration can result in more effective outcomes
 

































 
Great information. Am I the only one that grinds and snorts it for quicker results and a lower effective dose? Only with clean dye-free pills and typically not viagra because it’s a bigger volume of product.
 
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Q&A - The Past,Present & Future of Erectile Dysfunction

1. so it was just interesting to know that uric acid or hyper gout is a risk factor for erectile dysfunction, so would you recommend screening for hyperuricemia for any patient visiting with erectile dysfunction?

2. what is the recommended startup dose for Avanafil? Would you start the patient with 200 mg right away or you will just startup with a 100 mg if failed and after how many trials will you go for 200 mg? Is the 50 mg daily something recommended or not?


1. we have a big population now of patients of the first-generation PDE5 that they are doing very well whether they are taking Tadalafil or Vardenafil, do you think that we should suggest for them to switch if they are doing well on their medication or to stick to what's working?

2. we all know from all data that erectile dysfunction is a window on a patient heart that you have to check him for diabetes, high uric acid, and triglycerides but also there is a lot of data that correcting high uric acid or correcting high triglyceride is better for the patient but does not affect his sexual dysfunction so correcting these comorbidities is good for the patient but does not reflect on the sexual part he still needs the medication for that, do you have any data opposite to this?


1. I want to ask about the physiological or cellular cause between HDL and testosterone, why do we get this testosterone with the HDL, what is the actual physiological event happening?

2. Can we combine PDE5 inhibitors with ICI prostaglandin just to give a more potent erection


1. How do the second-generation PDE5 inhibitors differ from the first generation?

2. Is there a role for Avanafil and treating LUTS symptoms like Tadalafil?


1. On a real-life daily basis how would we perfectly recommend the usage of Avanafil for the daily use or OND use and for combinations and even salvaging non-responders in your daily practice?

2. In your presentation in the comparison between step two and step three in the meta-analysis regarding the efficacy of 100 and 200 mg of Avanafil the step two odds ratio is lower than the step three which is unlogic?


1. How to counsel the patient about drugs and about food interaction, alcohol interaction things like that?

2. Avanafil has been here for 10-12 years, why it's so late to come on I mean internationally it was not very well represented in the major meetings, can you give us a backstage story about why Avanafil is a late boomer?


1. Sometimes we get the patients who have a blown picture of hypogonadism, he's weak he has poor libido his muscle is weak his mood is not right he's not responding well to PDE5 and you check his testosterone and it is low normal it is still within the normal limit but clinically he's manifesting with hypogonadism, do you treat these patients even though they have normal testosterone/low testosterone or do you wait?



1. What will you do for a patient with the refractory hypogonadism not responding even to injectable testosterone, from time to time we face something like this cases, and whatever you do testosterone is still low patient is symptomatic even with injectables what will you do?

2. Can Avanafil be used as a salvage therapy as a second generation for patients who failed the first generation?


1. Would you prefer to use a direct testosterone shot or use the aromatase inhibitor to raise the endogenous testosterone?



1. In the slides you mentioned you said that about 8-10 years tolerance may occur to the first generation of PDE5 inhibitors, what are the current criteria of the patient that can tolerate Avanafil?

2. Can we switch between the first and second generation if there are no response to things?


1. Is there any benefit from Avanafil in the cardiac patient who is on nitrate or is it safe?


1. Is it effective in venous leakage?
 
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Giovanni Corona

*ESSENTIALLY TESTOSTERONE IS THE GASOLINE IS THE FUEL OF THE MACHINE WITHOUT TESTOSTERONE THERE IS NO PDE5 AND PDE5 OUTCOMES ARE WORSE

* PROBABLY THE BETTER PDE5 ENZYME SELECTIVITY IS THE MOST IMPORTANT ADVANTAGE OF THIS KIND OF DRUG OF AVANAFIL SO BY BEING MORE SELECTIVE FOR PDE5 IS ABLE TO GIVE A RAPID ONSET OF THE ACTION WITH THE LOWEST INCIDENCE OF SIDE EFFECTS


* 8-10 YEARS TOLERANCE MAY OCCUR TO THE FIRST-GENERATION PDE5 INHIBITORS

*IN MY MIND THE VENOUS LEAK IS MORE RELATED TO ENDOTHELIAL DYSFUNCTION OF THE CORPORA CAVERNOSA MAINLY BECAUSE YOU KNOW THE VAST MAJORITY OF THE SURGICAL OUTCOMES WERE NEGATIVE FOR VENOUS LEAKAGE
 
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