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DESCRIPTION: Silda Tablets are a drug to treat erectile dysfunction (ED, Impotence). Viagra dosage is from 25 to 100 mg taken, as needed, approximately 1 hour before sexual activity, but only once a day.

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But some of them may cause side effects or interact with medications and others haven’t been proven. Here are the facts about 10 popular aphrodisiac herbs and supplements.
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Ginseng is one of the bestselling herbs in the United States. In much of Asia, ginseng is prized as a revitalizer for the whole body, partly due to the human-like shape of the root. For more information about ginseng, read the
Are there male and female natural aphrodisiac products that really work? There is a general suspicion in the modern Western mindset that plants, roots, herbs and other substances purported to enhance sexual passion or interest are barely  — effective. Fortunately, research in this area is beginning to confirm some of the observations made by many shamans and herbal experts who, have used roots, barks, leaves, herbs, various plants and animal parts of all sorts to enhance sexual experience and performance. Some of the observations of these shamans is now being confirmed by double blind, placebo-controlled studies. For instance, a study published in 2009 showed the herb maca was able to reverse SSRI induced sexual dysfunction. SSRI drugs such as Prozac, Zoloft and Paxil reduce sexual pleasure since they increase serotonin levels dampening erectile function and sensation.
Most Westerners would be surprised to find out that there are dozens of natural herbal and natural aphrodisiacs that enhance sexual drive and pleasure in both men and women, along with enhancing erections and providing more satisfying orgasms and climaxes. Some of these herbs are quite powerful. We know because we am familiar with several dozen of them. They not only enhance libido,

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The commercial name of the medication may differ from the brand one. Viagra professional manufactured by RSM Enterprise is available under commercial name Sildigra Prof.

How does Viagra professional work and what pharmaceutical group does it belong to?

Sildenafil citrate is a reversible PDE-5 inhibitor. The preparation works by increasing blood flow to the corpus cavernosum of the penis thus allowing the patient to achieve and maintain a normal erection. Viagra professional contains the same active ingredients as Viagra, however due to unique properties of the pharmaceutical form the effects are longer then in the genuine preparation.

Which conditions are treated with Sildenafil?

The preparation is normally used in treatment of erectile dysfunction in men.

What should a patient know before using Viagra professional?

The Sildenafil should not be used in cases of:

  • Hypersensitivity to any components of the preparation
  • Cardiovascular disorders
  • Liver and renal problems
  • Blood affecting disorders
  • Stomach ulcers
  • Uncontrolled hypertension
  • Retinitis pigmentosa
  • Physical deformation of the penis

Which adverse effects may manifest when using the medication?

The side effects of Viagra professional include:

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  • Nasal congestion
  • Flushing
  • Visual disturbance
  • Gastrointestinal disturbances
  • Sudden vision loss
  • Arrhythmia
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  • Priapism
  • Fainting
  • Chest pain and etc.

It is not necessary that the side effects will manifest in an individual but the possibility still exist. For more information please consult your health care provider.

Which groups of drugs or specific preparations may interact with Sildenafil?

The drug is affected by the following:

  • HIV treatment
  • Antidepressants
  • Nitrates
  • Antibiotics
  • Hypertension treatment
  • NSASID’s

Tell your doctor about all the herbal preparations as well as prescription drugs that you are currently taking even if they are not on the list.

Important information for the patient: Viagra professional is supplied for individual use. Do not use it to treat other conditions not listed in the leaflet. Keep the product out of children reach. Do not reuse any disposable materials if supplied with the preparation.

 

 

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This drug should not be used with nitrates and recreational drugs called «poppers» containing amyl or butyl nitrite; alpha-blocker medications; other medications for impotence; high blood pressure medicines, etc.
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Missed dose
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Storage
Store your medicines at room temperature between 68-77 degrees F (20-25 degrees C) away from light and moisture. Do not store the drugs in the bathroom. Keep all drugs away from reach of children and pets.

Disclaimer
We provide only general information about medications which does not cover all directions, possible drug integrations, or precautions. Information at the site cannot be used for self-treatment and self-diagnosis. Any specific instructions for a particular patient should be agreed with your health care adviser or doctor in charge of the case. We disclaim reliability of this information and mistakes it could contain. We are not responsible for any direct, indirect, special or other indirect damage as a result of any use of the information on this site and also for consequences of self-treatment.

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Zyloprim

DESCRIPTION

ZYLOPRIM (allopurinol) has the following structural formula:

Structural Formula

ZYLOPRIM is known chemically as 1,5-dihydro-4H-pyrazolo [3,4-d]pyrimidin-4-one. It is a xanthine oxidase inhibitor which is administered orally. Each scored white tablet contains 100 mg allopurinol and the inactive ingredients lactose, magnesium stearate, potato starch, and povidone. Each scored peach tablet contains 300 mg allopurinol and the inactive ingredients corn starch, FD&C Yellow No. 6 Lake, lactose, magnesium stearate, and povidone. Its solubility in water at 37°C is 80.0 mg/dL and is greater in an alkaline solution.

CLINICAL PHARMACOLOGY

ZYLOPRIM acts on purine catabolism, without disrupting the biosynthesis of purines. It reduces the production of uric acid by inhibiting the biochemical reactions immediately preceding its formation.

ZYLOPRIM is a structural analogue of the natural purine base, hypoxanthine. It is an inhiboitor of xanthine oxidase, the enzyme responsible for the conversion of hypoxanthine to xanthine and of xanthine to uric acid, the end product of purine metabolism in man. ZYLOPRIM is metabolized to the corresponding xanthine analogue, oxipurinol (alloxanthine), which also is an inhibitor of xanthine oxidase.

Generic Zyloprim is used in the treatment of many symptoms of gout, including acute attacks, tophi (collection of uric acid crystals in the tissues, especially around joints), joint destruction, and uric acid stones. Allopurinol works by reducing uric acid production in the body, thus preventing crystals from forming.

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It has been shown that reutilization of both hypoxanthine and xanthine for nucleotide and nucleic acid synthesis is markedly enhanced when their oxidations are inhibited by ZYLOPRIM and oxipurinol. This reutilization does not disrupt normal nucleic acid anabolism, however, because feedback inhibition is an integral part of purine biosynthesis. As a result of xanthine oxidase inhibition, the serum concentration of hypoxanthine plus xanthine in patients receiving ZYLOPRIM for treatment of hyperuricemia is usually in the range of 0.3 to 0.4 mg/dL compared to a normal level of approximately 0.15 mg/dL. A maximum of 0.9 mg/dL of these oxypurines has been reported when the serum urate was lowered to less than 2 mg/dL by high doses of ZYLOPRIM. These values are far below the saturation levels at which point their precipitation would be expected to occur (above 7 mg/dL).

The renal clearance of hypoxanthine and xanthine is at least 10 times greater than that of uric acid. The increased xanthine and hypoxanthine in the urine have not been accompanied by problems of nephrolithiasis. Xanthine crystalluria has been reported in only three patients. Two of the patients had Lesch-Nyhan syndrome, which is characterized by excessive uric acid production combined with a deficiency of the enzyme, hypoxanthineguanine phosphoribosyltransferase (HGPRTase). This enzyme is required for the conversion of hypoxanthine, xanthine, and guanine to their respective nucleotides. The third patient had lymphosarcoma and produced an extremely large amount of uric acid because of rapid cell lysis during chemotherapy.

ZYLOPRIM is approximately 90% absorbed from the gastrointestinal tract. Peak plasma levels generally occur at 1.5 hours and 4.5 hours for ZYLOPRIM and oxipurinol respectively, and after a single oral dose of 300 mg ZYLOPRIM, maximum plasma levels of about 3 mcg/mL of ZYLOPRIM and 6.5 mcg/mL of oxipurinol are produced.

Approximately 20% of the ingested ZYLOPRIM is excreted in the feces. Because of its rapid oxidation to oxipurinol and a renal clearance rate approximately that of glomerular filtration rate, ZYLOPRIM has a plasma half-life of about 1 to 2 hours. Oxipurinol, however, has a longer plasma half-life (approximately 15 hours) and therefore effective xanthine oxidase inhibition is maintained over a 24-hour period with single daily doses of ZYLOPRIM. Whereas ZYLOPRIM is cleared essentially by glomerular filtration, oxipurinol is reabsorbed in the kidney tubules in a manner similar to the reabsorption of uric acid.

The clearance of oxipurinol is increased by uricosuric drugs, and as a consequence, the addition of a uricosuric agent reduces to some degree the inhibition of xanthine oxidase by oxipurinol and increases to some degree the urinary excretion of uric acid. In practice, the net effect of such combined therapy may be useful in some patients in achieving minimum serum uric acid levels provided the total urinary uric acid load does not exceed the competence of the patient’s renal function.

Hyperuricemia may be primary, as in gout, or secondary to diseases such as acute and chronic leukemia, polycythemia vera, multiple myeloma, and psoriasis. It may occur with the use of diuretic agents, during renal dialysis, in the presence of renal damage, during starvation or reducing diets, and in the treatment of neoplastic disease where rapid resolution of tissue masses may occur. Asymptomatic hyperuricemia is not an indication for treatment with ZYLOPRIM (see INDICATIONS AND USAGE).

Gout is a metabolic disorder which is characterized by hyperuricemia and resultant deposition of monosodium urate in the tissues, particularly the joints and kidneys. The etiology of this hyperuricemia is the overproduction of uric acid in relation to the patient’s ability to excrete it. If progressive deposition of urates is to be arrested or reversed, it is necessary to reduce the serum uric acid level below the saturation point to suppress urate precipitation.

Administration of ZYLOPRIM generally results in a fall in both serum and urinary uric acid within 2 to 3 days. The degree of this decrease can be manipulated almost at will since it is dose-dependent. A week or more of treatment with ZYLOPRIM may be required before its full effects are manifested; likewise, uric acid may return to pretreatment levels slowly (usually after a period of 7 to 10 days following cessation of therapy). This reflects primarily the accumulation and slow clearance of oxipurinol. In some patients a dramatic fall in urinary uric acid excretion may not occur, particularly in those with severe tophaceous gout. It has been postulated that this may be due to the mobilization of urate from tissue deposits as the serum uric acid level begins to fall.

The action of ZYLOPRIM differs from that of uricosuric agents, which lower the serum uric acid level by increasing urinary excretion of uric acid. ZYLOPRIM reduces both the serum and urinary uric acid levels by inhibiting the formation of uric acid. The use of ZYLOPRIM to block the formation of urates avoids the hazard of increased renal excretion of uric acid posed by uricosuric drugs.

ZYLOPRIM can substantially reduce serum and urinary uric acid levels in previously refractory patients even in the presence of renal damage serious enough to render uricosuric drugs virtually ineffective. Salicylates may be given conjointly for their antirheumatic effect without compromising the action of ZYLOPRIM. This is in contrast to the nullifying effect of salicylates on uricosuric drugs.

ZYLOPRIM also inhibits the enzymatic oxidation of mercaptopurine, the sulfur-containing analogue of hypoxanthine, to 6-thiouric acid. This oxidation, which is catalyzed by xanthine oxidase, inactivates mercaptopurine. Hence, the inhibition of such oxidation by ZYLOPRIM may result in as much as a 75% reduction in the therapeutic dose requirement of mercaptopurine when the two compounds are given together.

INDICATIONS AND USAGE

THIS IS NOT AN INNOCUOUS DRUG. IT IS NOT RECOMMENDED FOR THE TREATMENT OF ASYMPTOMATIC HYPERURICEMIA.

ZYLOPRIM reduces serum and urinary uric acid concentrations. Its use should be individualized for each patient and requires an understanding of its mode of action and pharmacokinetics (see CLINICAL PHARMACOLOGY, CONTRAINDICATIONS, WARNINGS, and PRECAUTIONS).

ZYLOPRIM is indicated in:

  1. the management of patients with signs and symptoms of primary or secondary gout (acute attacks, tophi, joint destruction, uric acid lithiasis, and/or nephropathy).
  2. the management of patients with leukemia, lymphoma and malignancies who are receiving cancer therapy which causes elevations of serum and urinary uric acid levels. Treatment with ZYLOPRIM should be discontinued when the potential for overproduction of uric acid is no longer present.
  3. the management of patients with recurrent calcium oxalate calculi whose daily uric acid excretion exceeds 800 mg/day in male patients and 750 mg/day in female patients. Therapy in such patients should be carefully assessed initially and reassessed periodically to determine in each case that treatment is beneficial and that the benefits outweigh the risks.

CONTRAINDICATIONS

Patients who have developed a severe reaction to ZYLOPRIM should not be restarted on the drug.

WARNINGS

ZYLOPRIM SHOULD BE DISCONTINUED AT THE FIRST APPEARANCE OF SKIN RASH OR OTHER SIGNS WHICH MAY INDICATE AN ALLERGIC REACTION. In some instances a skin rash may be followed by more severe hypersensitivity reactions such as exfoliative, urticarial, and purpuric lesions, as well as Stevens-Johnson syndrome (erythema multiforme exudativum), and/or generalized vasculitis, irreversible hepatotoxicity, and, on rare occasions, death.

In patients receiving PURINETHOL® (mercaptopurine) or IMURAN® (azathioprine), the concomitant administration of 300 to 600 mg of ZYLOPRIM per day will require a reduction in dose to approximately one-third to one-fourth of the usual dose of mercaptopurine or azathioprine. Subsequent adjustment of doses of mercaptopurine or azathioprine should be made on the basis of therapeutic response and the appearance of toxic effects (see CLINICAL PHARMACOLOGY).

A few cases of reversible clinical hepatotoxicity have been noted in patients taking ZYLOPRIM, and in some patients, asymptomatic rises in serum alkaline phosphatase or serum transaminase have been observed. If anorexia, weight loss, or pruritus develop in patients on ZYLOPRIM, evaluation of liver function should be part of their diagnostic workup. In patients with pre-existing liver disease, periodic liver function tests are recommended during the early stages of therapy.

Due to the occasional occurrence of drowsiness, patients should be alerted to the need for due precaution when engaging in activities where alertness is mandatory.

The occurrence of hypersensitivity reactions to ZYLOPRIM may be increased in patients with decreased renal function receiving thiazides and ZYLOPRIM concurrently. For this reason, in this clinical setting, such combinations should be administered with caution and patients should be observed closely.

PRECAUTIONS

General: An increase in acute attacks of gout has been reported during the early stages of administration of ZYLOPRIM , even when normal or subnormal serum uric acid levels have been attained. Accordingly, maintenance doses of colchicine generally should be given prophylactically when ZYLOPRIM is begun. In addition, it is recommended that the patient start with a low dose of ZYLOPRIM (100 mg daily) and increase at weekly intervals by 100 mg until a serum uric acid level of 6 mg/dL or less is attained but without exceeding the maximum recommended dose (800 mg per day). The use of colchicine or anti-inflammatory agents may be required to suppress gouty attacks in some cases. The attacks usually become shorter and less severe after several months of therapy. The mobilization of urates from tissue deposits which cause fluctuations in the serum uric acid levels may be a possible explanation for these episodes. Even with adequate therapy with ZYLOPRIM, it may require several months to deplete the uric acid pool sufficiently to achieve control of the acute attacks.

A fluid intake sufficient to yield a daily urinary output of at least 2 liters and the maintenance of a neutral or, preferably, slightly alkaline urine are desirable to (1) avoid the theoretical possibility of formation of xanthine calculi under the influence of therapy with ZYLOPRIM and (2) help prevent renal precipitation of urates in patients receiving concomitant uricosuric agents.

Some patients with pre-existing renal disease or poor urate clearance have shown a rise in BUN during administration of ZYLOPRIM. Although the mechanism responsible for this has not been established, patients with impaired renal function should be carefully observed during the early stages of administration of ZYLOPRIM and the dosage decreased or the drug withdrawn if increased abnormalities in renal function appear and persist.

Renal failure in association with administration of ZYLOPRIM has been observed among patients with hyperuricemia secondary to neoplastic diseases. Concurrent conditions such as multiple myeloma and congestive myocardial disease were present among those patients whose renal dysfunction increased after ZYLOPRIM was begun. Renal failure is also frequently associated with gouty nephropathy and rarely with hypersensitivity reactions associated with ZYLOPRIM. Albuminuria has been observed among patients who developed clinical gout following chronic glomerulonephritis and chronic pyelonephritis.

Patients with decreased renal function require lower doses of ZYLOPRIM than those with normal renal function. Lower than recommended doses should be used to initiate therapy in any patients with decreased renal function and they should be observed closely during the early stages of administration of ZYLOPRIM . In patients with severely impaired renal function or decreased urate clearance, the half-life of oxipurinol in the plasma is greatly prolonged. Therefore, a dose of 100 mg per day or 300 mg twice a week, or perhaps less, may be sufficient to maintain adequate xanthine oxidase inhibition to reduce serum urate levels.

Bone marrow depression has been reported in patients receiving ZYLOPRIM, most of whom received concomitant drugs with the potential for causing this reaction. This has occurred as early as 6 weeks to as long as 6 years after the initiation of therapy of ZYLOPRIM . Rarely, a patient may develop varying degrees of bone marrow depression, affecting one or more cell lines, while receiving ZYLOPRIM alone.

Information for Patients: Patients should be informed of the following:

(1) They should be cautioned to discontinue ZYLOPRIM and to consult their physician immediately at the first sign of a skin rash, painful urination, blood in the urine, irritation of the eyes, or swelling of the lips or mouth. (2) They should be reminded to continue drug therapy prescribed for gouty attacks since optimal benefit of ZYLOPRIM may be delayed for 2 to 6 weeks. (3) They should be encouraged to increase fluid intake during therapy to prevent renal stones. (4) If a single dose of ZYLOPRIM is occasionally forgotten, there is no need to double the dose at the next scheduled time. (5) There may be certain risks associated with the concomitant use of ZYLOPRIM and dicumarol, sulfinpyrazone, mercaptopurine, azathioprine, ampicillin, amoxicillin, and thiazide diuretics, and they should follow the instructions of their physician. (6) Due to the occasional occurrence of drowsiness, patients should take precautions when engaging in activities where alertness is mandatory. (7) Patients may wish to take ZYLOPRIM after meals to minimize gastric irritation.

Laboratory Tests: The correct dosage and schedule for maintaining the serum uric acid within the normal range is best determined by using the serum uric acid as an index.

In patients with pre-existing liver disease, periodic liver function tests are recommended during the early stages of therapy (see WARNINGS).

ZYLOPRIM and its primary active metabolite, oxipurinol, are eliminated by the kidneys; therefore, changes in renal function have a profound effect on dosage. In patients with decreased renal function or who have concurrent illnesses which can affect renal function such as hypertension and diabetes mellitus, periodic laboratory parameters of renal function, particularly BUN and serum creatinine or creatinine clearance, should be performed and the patient’s dosage of ZYLOPRIM reassessed.

The prothrombin time should be reassessed periodically in the patients receiving dicumarol who are given ZYLOPRIM.

Drug Interactions: In patients receiving PURINETHOL (mercaptopurine) or IMURAN (azathioprine), the concomitant administration of 300 to 600 mg of ZYLOPRIM per day will require a reduction in dose to approximately one third to one fourth of the usual dose of mercaptopurine or azathioprine. Subsequent adjustment of doses of mercaptopurine or azathioprine should be made on the basis of therapeutic response and the appearance of toxic effects (see CLINICAL PHARMACOLOGY).

It has been reported that ZYLOPRIM prolongs the half-life of the anticoagulant, dicumarol. The clinical basis of this drug interaction has not been established but should be noted when ZYLOPRIM is given to patients already on dicumarol therapy.

Since the excretion of oxipurinol is similar to that of urate, uricosuric agents, which increase the excretion of urate, are also likely to increase the excretion of oxipurinol and thus lower the degree of inhibition of xanthine oxidase. The concomitant administration of uricosuric agents and ZYLOPRIM has been associated with a decrease in the excretion of oxypurines (hypoxanthine and xanthine) and an increase in urinary uric acid excretion compared with that observed with ZYLOPRIM alone. Although clinical evidence to date has not demonstrated renal precipitation of oxypurines in patients either on ZYLOPRIM alone or in combination with uricosuric agents, the possibility should be kept in mind.

The reports that the concomitant use of ZYLOPRIM and thiazide diuretics may contribute to the enhancement of allopurinol toxicity in some patients have been reviewed in an attempt to establish a cause-and-effect relationship and a mechanism of causation. Review of these case reports indicates that the patients were mainly receiving thiazide diuretics for hypertension and that tests to rule out decreased renal function secondary to hypertensive nephropathy were not often performed. In those patients in whom renal insufficiency was documented, however, the recommendation to lower the dose of ZYLOPRIM was not followed. Although a causal mechanism and a cause-and-effect relationship have not been established, current evidence suggests that renal function should be monitored in patients on thiazide diuretics and ZYLOPRIM even in the absence of renal failure, and dosage levels should be even more conservatively adjusted in those patients on such combined therapy if diminished renal function is detected.

An increase in the frequency of skin rash has been reported among patients receiving ampicillin or amoxicillin concurrently with ZYLOPRIM compared to patients who are not receiving both drugs. The cause of the reported association has not been established.

Enhanced bone marrow suppression by cyclophosphamide and other cytotoxic agents has been reported among patients with neoplastic disease, except leukemia, in the presence of ZYLOPRIM. However, in a well-controlled study of patients with lymphoma on combination therapy, ZYLOPRIM did not increase the marrow toxicity of patients treated with cyclophosphamide, doxorubicin, bleomycin, procarbazine, and/or mechlorethamine.

Tolbutamide’s conversion to inactive metabolites has been shown to be catalyzed by xanthine oxidase from rat liver. The clinical significance, if any, of these observations is unknown.

Chlorpropamide’s plasma half-life may be prolonged by ZYLOPRIM, since ZYLOPRIM and chlorpropamide may compete for excretion in the renal tubule. The risk of hypoglycemia secondary to this mechanism may be increased if ZYLOPRIM and chlorpropamide are given concomitantly in the presence of renal insufficiency.

Rare reports indicate that cyclosporine levels may be increased during concomitant treatment with ZYLOPRIM. Monitoring of cyclosporine levels and possible adjustment of cyclosporine dosage should be considered when these drugs are co-administered.

Drug/Laboratory Test Interactions: ZYLOPRIM is not known to alter the accuracy of laboratory tests.

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Teratogenic Effects: Pregnancy Category C. Reproductive studies have been performed in rats and rabbits at doses up to twenty times the usual human dose (5 mg/kg per day), and it was concluded that there was no impaired fertility or harm to the fetus due to allopurinol. There is a published report of a study in pregnant mice given 50 or 100 mg/kg allopurinol intraperitoneally on gestation days 10 or 13. There were increased numbers of dead fetuses in dams given 100 mg/kg allopurinol but not in those given 50 mg/kg. There were increased numbers of external malformations in fetuses at both doses of allopurinol on gestation day 10 and increased numbers of skeletal malformations in fetuses at both doses on gestation day 13. It cannot be determined whether this represented a fetal effect or an effect secondary to maternal toxicity. There are, however, no adequate or well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.

Experience with ZYLOPRIM during human pregnancy has been limited partly because women of reproductive age rarely require treatment with ZYLOPRIM. There are two unpublished reports and one published paper of women giving birth to normal offspring after receiving ZYLOPRIM during pregnancy.

Nursing Mothers: Allopurinol and oxipurinol have been found in the milk of a mother who was receiving ZYLOPRIM. Since the effect of allopurinol on the nursing infant is unknown, caution should be exercised when ZYLOPRIM is administered to a nursing woman.

Pediatric Use: ZYLOPRIM is rarely indicated for use in children with the exception of those with hyperuricemia secondary to malignancy or to certain rare inborn errors of purine metabolism (see INDICATIONS AND USAGE and DOSAGE AND ADMINISTRATION).

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The Latin term impotentia coeundi describes simple inability to insert the penis into the vagina. It is now mostly replaced by more precise terms.[vague] The study of erectile dysfunction within medicine is covered by andrology, a sub-field within urology.

 

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* if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement
* if you have allergies to medicines, foods, or other substances
* if you have a deformed penis (eg, cavernosal fibrosis, Peyronie disease), blood problems (eg, leukemia, multiple myeloma, sickle cell anemia), or any other condition that may increase the risk of a prolonged erection (eg, priapism)
* if you have a history of certain eye problems (eg, macular degeneration, optic neuropathy, retinitis pigmentosa, sudden vision loss)
* if you have a history of liver or kidney problems, high or low blood pressure, ulcers, bleeding problems, heart problems (eg, angina, aortic stenosis, heart failure, irregular heartbeat), or blood vessel problems
* if you have a history of heart attack, stroke, or life-threatening irregular heartbeat, especially within the past 6 months
* if you are using any other medical treatments that cause erections (eg, medicines injected or inserted into the penis, implants or vacuum pumps)

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* Alpha-blockers (eg, doxazosin), amlodipine, medicines for high blood pressure, nitrates (eg, isosorbide, nitroglycerin), or nitroprusside because severe low blood pressure with dizziness, lightheadedness, and fainting may occur
* Azole antifungals (eg, itraconazole, ketoconazole), fluvoxamine, H2 antagonists (eg, cimetidine, famotidine), HIV protease inhibitors (eg, ritonavir, saquinavir), macrolide antibiotics (eg, erythromycin), narcotic analgesics (eg, dihydrocodeine), or telithromycin because they may increase the risk of Viagra ‘s side effects
* Bosentan or rifampin because they may decrease Viagra ‘s effectiveness

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Use Viagra as directed by your doctor. Check the label on the medicine for exact dosing instructions.

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Seek medical attention right away if any of these SEVERE side effects occur:

Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); chest pain; fainting; fast or irregular heartbeat; memory loss; painful or prolonged erection; ringing in the ears; seizure; severe or persistent dizziness; severe or persistent vision changes; sudden decrease or loss of vision in one or both eyes; sudden hearing loss.

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The National Association of Boards of Pharmacy (NABP) was established in 1904 to assist state licensing boards in developing, implementing, and enforcing uniform standards to protect the Public Health. NABP’s member boards of pharmacy are grouped into eight districts that include all 50 United States, the District of Columbia, Guam, Puerto Rico, the Virgin Islands, eight Canadian provinces, and New Zealand.

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