Viagra (Sildenafil Citrate) Reviews and Drug Information

A drug like Viagra belongs to the most sought after product over the net. To stay ahead in the competition that involves many online Viagra vendors, various tools like keywords optimization, back links etc can be found incorporated.

Viagra Australia is main. It is plain logic that everyone who likes to buy Viagra would use the word ‘Viagra’ in his search for the erectile dysfunction drug on-line. Rarely would a person key in a word that is not related to Viagra if he’s planning to buy Viagra. Would you? So, what does a Viagra vendor do, keeping in mind this kind of particular psychological aspect of the buyers? He would try to inculcate in the content of his site, words like Viagra, buy Viagra, buy Viagra online, cheap Viagra, Viagra on the internet, discounted Viagra and a plethora of such keywords that millions of buyers use, while going through google search or yahoo search. And well, they are just one of the few ways to oil google and the search engines to achieve up your site ranking.

Well, what does it all mean? Simply put, an illegal Viagra hawker, who provides you nothing the drug mechanisms, benefits, area effects, dosages, storage information along with vital information that are a ‘must-know’ for a Viagra user can occupy the top rank in Viagra search for google, yahoo or msn, by employing the search engine optimization techniques.

Just check for yourself and you will be surprised at the damage that has been currently done, using the tool for wrong ends. Go through ‘Viagra’ as well as ‘buy Viagra’ search in google and you will find that more than half of the sites that come in the first page have Buy Viagra, Buy Cheap Viagra, Discounted Viagra, Viagra On the internet, Best Price, Best Place to obtain Viagra etc. written all over the page, and yes, they don’t forget to give a link to the pharmacies where you can buy only the best and cheap Viagra.

But, never do they mention the indications, contraindications, drug interactions, area effects, safe drug usage et al. Well, a word of advice, don’t trust them. Have I inserted you in a dilemma? You’ll as well ask me, who to trust and where to obtain Viagra from?

Most people who order Viagra online use it for some special reason or maybe the other; either they don’t have the guts to walk up the counter with a prescription to buy Viagra or you can find no regular pharmacies nearby. Let’s keep aside the case in the illegal Viagra buyers, who buy Viagra without prescriptions for reasons best known to be able to them; I have absolutely no worries about them. As far as my experience goes, it’s not the sites with the buy Viagra, inexpensive Viagra, best Viagra Australia online and the likes plastered all through them that give you the information on the right Viagra dosage, together with an expert follow high. They are no lower than the touts peddling illegal fakes in the roadside; avoid them as you do a plague or an epidemic. Always try sites with authentic Viagra information.

There are many sites that provide instructive and educational information on the use of Viagra. With their latest news, researches, critical and analytical articles, many of these sites keep themselves abreast in the recent happenings in the erectile dysfunction drug market. It is safe to buy Viagra online from the best well-informed vendors, because they know what they are selling, and the effects it contains on your sexual well being.

1. “How does Viagra work?”

Viagra works by increasing the flow of blood into internal areas of the penis. Viagra adds to the effects of a normal body chemical released when the male is sexually aroused. The result is that the flow of blood is also increased into a specific internal area of the penis which temporarily cures erectile dysfunction.

2. “When will a generic be available for Viagra?”

There are some generic erectile dysfunction drugs sold online now. Some ED generic drugs sold are Kamagra, Caverta, Silagra, Zenegra and Edegra.

3. “How do I use Viagra?”

Viagra is used one hour before sexual activity is to be commenced. Viagra is drug sold in tablet form that is taken orally and can only be used once in a twenty four hour time frame.

4. “How to buy a generic for Viagra?”

Online sites that sell drugs have generic Viagra under ed drugs. You don’t need a prescription to buy generic Viagra as you would if you wanted to buy Pfizer’s brand name Viagra.

5. “How can I buy Viagra online?”

Viagra can be bought at many online websites that sell drugs

6. “How to save money on Indian Viagra?”

You can save money on Viagra by buying in quantity. The more you buy, the cheaper it costs.

7. “Does Viagra help with Erectile Dysfunction?”

Viagra was formulated to help men with problems like erectile dysfunction.

8. “Is Viagra the same as Sildenafil?”

Sildenafil is the generic name for Viagra.

9. “Where can I get information on how to use Viagra?”

For complete information on how to use Viagra, your health care provider is the best source.

10. “How many people are taking Indian Viagra?”

No figures are kept on men taking Viagra. In England, 6.5 million tablets of Viagra.

Selective Serotonin Reuptake Inhibitors Selective serotonin reuptake inhibitors (SSRIs) have gained notoriety as a common cause of several manifestations of sexual dysfunction. SSRI-induced ED rather than sexual dysfunction, though, is rarely reported in the literature and is limited mostly to case reports.

Antihypertensive Agents Several antihypertensive agents have been implicated in ED, yet the evidence is limited. Older thiazide diuretic treatments have been associated with mild effects on erectile function.

Many of these studies have limited clinical implications as they were conducted with chlorthalidone, a thiazide-like diuretic. A recent study suggested that beta-blocker-induced ED is likely psychogenic rather than organic. Clonidine is reported to cause ED in both human and animal studies through agonism of central alpha-2 adrenoreceptors.

Statins Statins are HMG-CoA reductase inhibitors that are a commonly used medication for the treatment of hyperlipidemia. Do et al. conducted a study to investigate the association between exposure to statins and the occurrence of ED. The study was limited to males age 18–30. They found a statistically significant association for statins with induction and worsening of ED. Further studies are needed to distinguish the severity of the effect on ED between the many different statin drugs that are currently in use.

In cases of ED and hypogonadism, recent randomized controlled trials suggest that patients who are initially refractory to type V phosphodiesterase (PDE5) inhibitors (sildenafil, vardenafil, and tadalafil) can be rescued by the concurrent administration of testosterone with PDE5 inhibitors. The administration of testosterone alone, without PDE5 inhibitors, has also been shown to improve erectile function in hypogonadal men. Androgen deficiency has been shown to result in penile tissue atrophy, increased adipose tissue within the subtunical region, and severe venous leak resulting in ED. All of these effects can potentially be reversed by the administration of testosterone. A number of distinct pathways of the endocrine system lead to ED when functioning abnormally. Several studies show that hypogonadism of any cause is an uncommon cause of ED.

The role of testosterone and other androgens in the achievement and maintenance of penile erection is controversial due to the lack of standardization in defining low testosterone. A recent study found that the prevalence of “low testosterone” in men with ED was largely dependent on the accepted definition of this disease state. Reported prevalence increased from 7% to 47% for definitions of testosterone level less than 200 ng/dL versus less than 400 ng/dL, respectively.

The role of androgens in erectile physiology as demonstrated in the animal model is to potentiate the effects of neurologic and vascular/ endothelial mechanisms of erection. Although tumescence is possible with decreased testosterone, the quality of the erection may be diminished. Importantly, the efficacy of PDE5 inhibitors is greatly diminished in the absence of androgens. Furthermore, in rats, dihydrotestosterone is the primary androgen responsible for erectile physiology at the level of the endothelial cell. Mexican Viagra Online

This decline in serum testosterone level can be age-related or the result of hypogonadism of any cause. A recently published study evaluated the prevalence of both hypogonadism and depression in men presenting to an ED clinic. They also tested the correlation of hypogonadism and the presence of depressive symptoms. They indeed found hypogonadal men to be more likely to have overt depression scores compared to eugonadal controls. The authors derived the conclusion that depression symptoms are strongly associated with hypogonadism and that physicians should consider the evaluation of testosterone levels in men with overt symptoms of depression.

Testicular Failure In recent years, there has been increasing interest in the study of aging males. Testicular failure increases with age as serum testosterone levels gradually decline. This process is not universal. When it does occur, there is significant variability in the age at the onset and the degree of the androgen decline associated with age.

Androgen Deficiency The estimated prevalence of androgen deficiency among men 40–70 years of age ranges from 12% to 45%. Approximately 481,000 new cases of androgen deficiency are diagnosed yearly in the USA.

Physiologic levels of testosterone support several critical processes involved in penile erectile response, including the maintenance of libido and energy levels, in addition to the cascade of events mediated by nitric oxide leading to arteriolar dilatation and relaxation. Screening for hypogonadism in men initially presenting with ED can help identify these men. Drug-Induced ED Erectile dysfunction is a common adverse effect of a number of drugs, and it often has a great effect on patient compliance.

This subject as a risk factor is lightly discussed here and further discussed in more detail later in the textbook. It is important to recognize that many of the drugs associated with ED are used to treat conditions that are themselves risk factors for ED, thus the interpretation of ED in the setting of pharmacological therapy is often difficult in the clinical setting.

KQ 1. The clinical utility of routine blood tests—testosterone, prolactin, LH, FSH – in identifying and affecting therapeutic outcomes for treatable causes of ED was examined using reports of measurements of serum testosterone, FSH, LH, prolactin, and/or other hormone levels, (but not gonadotrophin-releasing hormone [GnRH], Inhibin, Activin, or Follistim). It was also examined in reports of the prevalence of reversible hormonal disorders in males with erectile dysfunction. The study selection criteria included the following:

• Source: Primary study report published in English
• Study design: Any (prevalence studies)
• Population: Adults (age ≥ 18 years) diagnosed with ED with or without concurrent endocrinopathy (i.e., hypogonadism, hyperprolactinemia, abnormal levels of LH/FSH)
• Intervention (experimental): Hormonal blood tests (i.e., testosterone/prolactin/LH/FSH)
• Outcomes: Prevalence of endocrinopathies (i.e., hypogonadism, hyperprolactinemia, abnormal levels of LH/FSH)

KQ 2. Benefits of pharmaceutical treatments (e.g. oral, injections, hormonal, topical, intra-urethral suppositories) in males with ED. To address how patient specific characteristics (e.g. specific symptoms/origin, duration, severity of ED/comorbid conditions) affect prognosis/treatment success for ED patients. Evidence on the following treatment modalities was excluded from this review: Natural health products (e.g. herbals), yohimbine, vacuum constriction devices, and sex or surgical therapies (e.g. penile prosthesis implantation, penile arterial reconstructive surgery). Study selection criteria included the following:

• Source: Primary study report published in English
• Study design: RCTs (comparative efficacy and harms studies)
• Population: Adults (age => 18 years) diagnosed with ED (with or without comorbidities)
• Interventions (experimental/control): Oral (PDE–5 inhibitors, sublingual) injections (IC, cream)
• Outcomes: Clinically relevant efficacy measures (i.e., scores for the IIEF “EF” domain, IIEF–Q3/Q4, SEP-Q2/Q3, GAQ-Q1, EDITS)

KQ 3. Harms of pharmaceutical treatments (e.g. oral, injections, hormonal, topical, intra-urethral suppositories) in males with ED. Evidence on the following treatment modalities was excluded from this review: Natural health products (e.g. herbals), yohimbine, vacuum constriction devices, and sex or surgical therapies (e.g. penile prosthesis implantation, penile arterial reconstructive surgery). Study selection criteria included the following:

• Source: Primary study report published in English
• Study design: RCTs (comparative efficacy and harms studies)
• Population: Adults (age ≥ 18 years) diagnosed with ED (with or without comorbidities)

Antipsychotics Antipsychotic medications are also implicated in ED. These drugs exert their effects primarily by antagonism of dopamine receptors but have effects on several other receptors.

In addition, dopamine antagonism causes hyperprolactinemia which contributes to the sexual dysfunction associated with these drugs. Antiandrogens Antiandrogens are a well-known cause of sexual dysfunction and ED. In recent studies, finasteride has been shown to cause minimal ED at higher doses (5 mg) for prostate cancer prevention, and almost no effect on erectile function at low doses (1 mg) for the treatment of alopecia Illicit Substances and Nicotine Several illicit substances cause ED. In addition, men on methadone maintenance therapy for heroin dependence have been reported to have significant impairment of erectile function.

The use of tobacco products, and specifically nicotine, is associated with ED in both chronic and acute exposure. Nicotine produces vasoconstriction through its actions on endothelial cells through a likely underproduction and degradation of nitric oxide.

A recent study of healthy men between the ages of 18 and 27 reported that the use of nicotine gum immediately decreased erectile response to visual stimuli despite unchanged subjective measurements of sexual arousal. This study may imply an immediate neurogenic and hemodynamic response of the penile tissue to nicotine. Furthermore, chronic cigarette smoking is also associated with an independently increased risk of ED and clinically significant damage to penile vasculature

Ethanol
The role of ethanol, while classically thought to impede erectile function, has been less clear in the literature. Despite the association of alcohol consumption and sexual activity, very little objective evidence exists on the effect of acute ethanol intoxication on erectile function. The data on chronic ethanol exposure is also mixed. Ethanol exposure in an animal model showed histologic evidence of both endothelial damage and metabolicdysfunction.

Impairment of smooth muscle relaxation due to endothelial dysfunction was pronounced while neurogenic smooth muscle relaxation remained intact. Age and Chronic Illness There is no consensus as to whether ED is a nonpathologic, natural aspect of aging in healthy males, though older males do have higher rates of ED. The association between naturally declining testosterone level in older males, socalled andropause, and ED, is complex, but no clear association is found to date.

Interestingly, penile vibrotactile sensation of the penis decreases significantly with age, but this has not been directly linked with ED.

Approximately 82% of men with chronic renal failure (CRF) on hemodialysis have some degree of erectile function, with 45% having severe ED. Additionally, regardless of treatment, patient with CRF have significantly decreased mean nocturnal penile tumescence when compared to both normal and chronically ill controls. The pathophysiology of ED in patients with CRF is complex. A majority of men with CRF have hyperprolactinemia. Uremia also interferes with the HPA such that oligospermia, azoospermia, and impaired steriodogenesis with elevations in LH are common in uremic men.

Zinc deficiency has also been postulated as a potential cause of ED in uremic men and has been targeted for possible therapeutic interventions.

While hyperprolactinemia is often clinically associated with the existence of ED and hypoactive sexual desire, the prevalence and pathophysiology of this association are debated in the literature. The prevalence of hyperprolactinemia in men with ED or sexual dysfunction ranges from 1.5% to 10% in recent literature.

While several studies support the classic hypothesis that hyperprolactinemia causes ED through the suppression of GnRH, there is no consensus as of yet.
While severe hyperprolactinemia is a risk factor for sexual dysfunction, the role of moderate hyperprolactinemia in the pathophysiology of ED is unclear.

Thus, as with androgens, it is unclear if pathophysiologic findings from clinical studies and animal models are applicable to the clinical evaluation of ED. There is also evidence that prolactin may have a dichotomous role in erectile physiology. A recent study found that men with prolactin levels below 5 ng/mL had increased prevalence of arteriogenic ED, while men with hyperprolactinemia only had an increased prevalence of hypoactive sexual desire.

Thyroid Disease Both hypothyroid and hyperthyroid states are associated with ED, though the specific pathophysiology remains elusive. A recent study compared men with thyroid dysfunction to controls and reported that men with both hypothyroidism and hyperthyroidism had significantly increased the prevalence of and more severe ED. Overall, 79% of men with thyroid dysfunction had ED compared to 34% of controls. Both hyperthyroid and hypothyroid men had a prevalence of ED that exceeded the prevalence of ED in the control group. Additionally, both groups had significant response to treatment.

While extrapolation of specific physiologic mechanisms from clinical treatment is limited, these findings suggest that thyroid dysfunction acts at multiple sites to cause ED. There is some evidence that hypothyroidism causes a decline in both testosterone and steroid hormone binding globulin (SHBG).

Interventions (experimental/control): Oral (PDE–5 inhibitors, sublingual) injections (IC, SC), hormonal (e.g. testosterone), intra-urethral suppositories, CPAP, and/or topical (e.g. patch, cream)

Outcomes: Any adverse events, serious adverse events, withdrawals due to adverse events, and specific adverse events.

KQ 3a. The incidence of specific harms such as Nonarteritic Anterior Ischemic Optic Neuropathy (NAION) and penile fibrosis associated with use of PDE–5 inhibitor and injection therapies, respectively. The review included reports of non-RCTs or observational studies. For identification of data on fibrosis related to use of injection therapies, only studies with at least 6 months of followup were included.

Study selection criteria included the following:

Source: Primary study report published in English

Study design: Non-RCTs (experimental or observational case-control and cohort studies, case reports and case-series)

Population: Adults (age ≥ 18 years) diagnosed with ED (with or without comorbidities) Interventions (experimental/control): Oral (PDE–5 inhibitors), injections (IC, SC)

Outcomes: NAION, penile fibrosis Systematic and narrative reviews, case reports, editorials, commentaries or letters to the editor were excluded for all questions except Q3–a (specific harms). Studies evaluating interventions such as penile implant devices or natural health products used for the treatment of ED were also excluded.

The results of the literature search were uploaded to the software program TrialStat SRS version 4.0 along with screening questions developed by the review team and any supplemental instructions. A calibration exercise was undertaken to pilot and refine the screening process. One reviewer screened bibliographic records (i.e., title, authors, key words, abstract) using broad screening criteria (Appendix B). All potentially relevant records and those records that did not contain enough information to determine eligibility (e.g. no abstract was available) were retained. The reasons for exclusion are noted in the QUOROM flow diagram. Two reviewers independently performed full-text relevance screening. Disagreements were resolved by consensus.

Relevant studies were then evaluated to determine study design and were categorized accordingly for inclusion by question. The level of eligible evidence on efficacy was limited to RCTs, since systematic bias is minimized in RCTs compared with all other study designs (e.g. cross-sectional, retrospective cohort).