Conservative Treatment

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A Practical Approach To Gout
Current management of an 'old' disease

Conservative treatment measures

To treat gout, your doctor will first focus on relieving your pain by controlling the joint inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, naproxen sodium, or indomethacin, are available over-the-counter and are effective in relieving pain and swelling.

If you cannot take these types of drugs because you have a peptic ulcer or kidney disease, your doctor may recommend another anti-inflammatory drug called colchicine.

It has also been very effective in relieving gout, but can cause diarrhea and other side effects while you are taking the drug.

Sometimes, corticosteroids such as prednisone and adrenocorticotropic hormone can be injected directly into the joint to quickly stop the inflammation.

Corticosteroids can also be taken orally, but are never used for more than a few days to avoid side effects.

Aspirin and aspirin-related drugs should be avoided because they only worsen gout.

To prevent future attacks and reduce your risk of permanent joint damage, your doctor will work on lowering your uric acid levels.

Sometimes simply losing weight will reduce these levels.

Doctors recommend that anyone with gout gets plenty of rest, avoids alcoholic beverages, maintains a healthy weight, eats only small amounts of purine-rich foods, and drinks plenty of fluids, such as water.

However, if you have repeated, severe attacks despite these measures, you may need to take drugs such as probenecid and sulfinpyrazone, which increase the excretion of uric acid by the kidneys.

These drugs don't work for everyone and can cause kidney stones. Some people have more success with allopurinol, which actually blocks the production of urate and can dissolve kidney stones. However, it too has potential side effects, including a skin rash and liver damage.

Once you begin to take probenecid, sulfinpyrazone, or allopurinol, you must continue to take them for life to prevent the return of gout.

You can dissolve the urate crystals and relieve pain during an attack by applying hot, then cold compresses.

This is called contrast hydrotherapy, and doctors recommend that you alternate three-minute hot compresses with 30-second cold compresses.

If you have tophi, you will find that they will shrink as your uric acid levels come down, and your range of motion around those joints will improve. However, extremely large tophi may need to be removed surgically.

People with high uric acid levels but no gout symptoms require no treatment at all unless there is a family history of gout or kidney stones.

Self-care tips

While there is no cure for gout, its symptoms can be managed through a combination of drug therapy and lifestyle changes.

Lifestyle changes mean maintaining a healthy weight, getting plenty of rest, exercising, and drinking plenty of water, especially if you are taking diuretics for high blood pressure.

If you must drink alcoholic beverages, drink no more than two ounces in one day. Also avoid foods that are rich in purine, which produces urate.

These include organ meats, such as liver, kidney, and sweetbreads; sardines; anchovies; shrimp; red meat; gravies; dried beans; beer; and wine.

Conservative treatment measures

Patients with gout should be advised to lose weight, moderate their use of alcohol (especially beer), avoid dehydration and repetitive trauma, and control hypertension and hyperlipidemia.

A purine-restricted diet may be unpalatable to many patients and may reduce serum urate levels by only 1 mg/dL.

A more reasonable dietary approach is to reduce consumption of fat, cholesterol, and meat (especially organ meats, which contain high levels of purines).

Patients should also be advised to drink at least eight glasses of liquids daily to prevent dehydration and help reduce uric acid levels.

Use of thiazides and loop diuretics may decrease the clearance of uric acid and reduce plasma volume and therefore should be discontinued or avoided if possible.

Other drugs, such as low-dose aspirin, ethambutol hydrochloride (Myambutol), pyrazinamide, and niacin, decrease uric acid excretion by competing for secretion in renal tubules and also should be avoided.

Agents for acute episodes

Early treatment to reduce inflammation and pain is important in an acute attack of gout. The current pharmacologic options include

  • non-steroidal anti-inflammatory drugs (NSAIDS)

  • colchicine

  • corticosteroids

  • adrenocorticotropic hormone (ACTH)

  • allopurinol

  • probenecid

  • Sulfinpyrazone

NSAIDS, specifically indomethacin, are commonly the first medication prescribed to treat acute gout. Other NSAIDS may be equally effective. NSAIDS are initially prescribed at maximum dosage and reduced as symptoms subside. The medication should be continued until pain and inflammation are non-existent for at least 48 hours. NSAIDS which are COX-2 inhibitors may be useful for patients with gastrointestinal concerns but their use for acute gout has not been specifically reported yet.

Colchicine is used to treat acute flares of gouty arthritis and to prevent recurrent acute attacks. Colchicine does not cure gout or take the place of other medicines that lower the amount of uric acid in the body. It prevents or relieves gout attacks by reducing inflammation. Colchicine may be used in 2 ways: some people take small amounts of it regularly for months or years, while others take large amounts of colchicine during a short period of time (several hours).

Corticosteroids or adrenocorticotropic hormone can be used for patients who cannot take NSAIDS or colchicine. Patients with acute gout typically receive daily doses of prednisone (20-40mg) or its equivalent for 3 to 4 days, then it is tapered gradually over one to two weeks. ACTH is administered as an intramuscular injection (an initial dose and subsequent doses over several days as needed).

Allopurinol (brand name - Zyloprim) is prescribed for chronic gout or gouty arthritis and works by affecting the system that manufactures uric acid in the body. It is used to prevent gout attacks, not to treat them once they occur.

Probenecid (brand names - Benemid, Probalan) is prescribed for chronic gout and gouty arthritis. It is used to prevent attacks related to gout, not treat them once they occur. It acts on the kidneys to help the body eliminate uric acid. Probenecid is known as a uricosuric agent.

ColBenemid (other brand names are Col-Probenecid and Proben-C) is a gout medication that contains Probenecid, which is a uricosuric agent, and Colchicine, which has anti-gout properties.

Sulfinpyrazone (brand name - Anturane) is also known as a uricosuric agent and is used to treat gouty arthritis. It works by lowering the amount of uric acid in your blood, preventing gout attacks. The drug helps prevent attacks but is not used to treat an attack once it has started.

Losartan, (brand names - Cozaar and Hyzaar), is not specifically a gout medication but is an angiotensin II receptor antagonist, antihypertensive drug that may help control uric acid levels. Fenofibrate, (brand name - Tricor), is not a specific gout medication but it a lipid-lowering drug that may help uric acid levels.

Analgesic painkillers are also used to relieve the intense pain of gout. All of the aforementioned drugs can be used in combination, to control symptoms, prevent future attacks, and maintain healthy uric acid levels.

Acute Gouty Arthritis

Three treatments currently available for acute gouty arthritis attacks are nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and corticosteroids.

  1. NSAIDs -Indomethacin (Indocin) and Ibuprofen

  2. Colchicine

  3. Corticosteroids - Prednisone, Triamcinolone acetonide and Corticotropin


  • NSAIDs. These rapid-acting drugs are currently the most favored treatment for acute gout attacks.

  • NSAIDs have become first-line therapy for acute episodes because of the many side effects experienced with colchicine and its lack of efficacy if administered beyond 24 hours after onset of an attack.

  • Any NSAID is effective for acute attacks, but agents with a short half-life (eg, indomethacin (Indocin), ibuprofen) are most popular because of their rapid onset of action.

  • Use of NSAIDs should be avoided or monitored carefully in patients with preexisting renal dysfunction or a history of gastrointestinal bleeding. Also, because these agents affect platelet function, they should not be given to patients who have a bleeding propensity or are receiving anticoagulation therapy.

  • All NSAIDs can have serious gastrointestinal side effects, including bleeding and ulceration.

  • These drugs should therefore be used with caution in patients with a history of peptic ulcer disease, congestive heart failure or chronic renal failure.

  • Discretion should be used in giving NSAIDs to patients who are allergic to aspirin or have asthma or nasal polyps.

  • Whether use of the newer cyclooxygenase-2 inhibitors will be beneficial or safer in such patients is yet to be determined. These are a relatively new type of anti-inflammatory drug that are currently under scrutiny. By inhibition of cyclooxygenase-2, the vicious cycle of inflammation and pain caused by gout is impeded. COX-2 expression in monocytes has been suggested to be induced in response to urate crystals.


  • Colchicine. This agent is an effective alternative to NSAIDs in the treatment of acute gouty arthritis.

  • Colchicine is most beneficial when it is given in the first 12 to 36 hours of an attack. It apparently exerts its effect by inhibiting the phagocytosis of uric acid and blocking the release of chemotactic factor.

  • Colchicine has anti-inflammatory activity but no analgesic activity.

  • Colchicine can be given orally or parenterally.

  • Colchicine can be given intravenously, if the oral route is not available or gastrointestinal side effects have to be avoided.

  • Intravenous administration has been associated with an increased risk of toxic side effects, including bone marrow suppression and renal or hepatic cell damage.

  • However, intravenous colchicine therapy is generally unnecessary for an acute flare of gout, and when administered incorrectly, it can cause bone marrow toxicity and irritation of the soft tissues and veins.

  • After intravenous therapy, administration of additional oral colchicine must be avoided for a full week, according to manufacturers' recommendations.

  • Experts are divided about whether to use colchicine or an NSAID to treat inflammation. Colchicine, while highly effective for acute gout, is often not well tolerated.

  • For 50% to 80% of patients, it can cause gastrointestinal side effects before the attack is relieved. Colchicine requires dose adjustment for renally compromised and elderly patients.

  • Even low-dose daily therapy for prophylaxis can be associated with severe adverse effects. Drug interactions must also be considered—concomitant erythromycin, simvastatin, or cyclosporine therapy can alter colchicine's metabolism, predisposing patients to adverse effects.


  • Have anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

  • Oral corticosteroids may be used for patients with gout or pseudo gout who cannot tolerate NSAIDs. Although there have been case reports of adrenal crisis related to multiple interarticular injections of steroids for gout, this has not been clearly proven.

  • Monarthric gout responds well to corticosteroids given by intra-articular injection.

  • Systemic corticosteroids (e.g., prednisone [Deltasone], in a dosage of 20 to 30 mg per day) are used only when NSAIDs and colchicine are not effective or are contraindicated.

  • Long-term therapy is not indicated for a single attack of gout.

  • However, it may be reasonable to identify precipitating factors and to obtain a 24-hour urine collection to determine creatinine clearance and excretion of uric acid.

  • Treatment with allopurinol or a uricosuric drug should be considered in patients who have at least two episodes of gout in 1 year.

  • Asymptomatic hyperuricemia does not usually produce adverse effects before the development of gout and, therefore, does not require treatment. However, it may be advisable to determine the cause of the hyperuricemia.

  • Urate-lowering therapy should not be prescribed without concomitant use of an NSAID or low-dose colchicine. Serum urate levels may fluctuate during the initiation of such therapy and induce a gouty flare or prolong an ongoing attack.

  • Long-term therapy should not be initiated until the patient has returned to baseline in terms of nutrition, activity level, and medication use. Beginning therapy before that time may actually exacerbate a flare or prolong an existing episode.

  • Glucocorticoids

    • Glucocorticoid therapy, either oral or parenteral, is effective in patients who are unable to take or tolerate NSAIDs and colchicine.

    • Side effects of this regimen are rare but may include glucose intolerance, electrolyte shifts, hypertension, and increased susceptibility to infection. A symptom flare may occur after tapering of corticosteroid therapy.

    • Intra-articular steroids are useful in patients with multiple medical problems, involvement of only a few joints, or contraindications to other therapies.

    • A postinjection flare caused by the steroid crystals themselves may occur but is usually short-lived. This approach has been particularly successful in postoperative patients with a single affected joint who are unable to take oral medications.

  • Corticotropin

    • Corticotropin (ACTH) (an exogenously produced corticotropin that stimulates the adrenal cortex to secrete cortisol, corticosterone, and several androgens) is still an option for treating gout.

    • Although this agent has been shown to be as effective as indomethacin, it carries a higher risk of rebound attacks, and multiple injections may be required. Some investigators have reported efficacy in acute attacks, especially in patients with multiple medical conditions.

Prevention of Recurrent Attacks

Hyperuricemic therapy should be initiated in patients with frequent gout attacks, tophi or urate nephropathy.

A low dosage of an NSAID or colchicine is effective in preventing acute gouty attacks.

Hyperuricemic drug therapy should not be started until an acute attack of gouty arthritis has ended, because of the risk of increased mobilization of uric acid stores. A reasonable goal is to reduce the serum uric acid concentration to less than 6 mg per dL (360 µmol per L).

Reduction of serum uric acid levels to normal is the goal of treatment designed to prevent acute attacks of gout.

Antihyperuricemic therapy

When attacks of gout recur despite conservative measures (eg, dietary modifications, reduction in alcohol consumption), treatment with urate-lowering agents is indicated.

The two classes of medications available for reducing serum urate levels are :

  1. uricosuric agents and

  2. xanthine oxidase inhibitors.

In most cases, lifetime treatment with one of these agents is indicated.

Uricosuric Drugs.

These agents decrease the serum uric acid level by increasing renal excretion.

Therapy with uricosuric agents is generally recommended for patients less than 60 years of age who have normal renal function, under-excretion of uric acid (<700 mg/24 hr), and no history of nephrolithiasis .

Although 24-hour uric acid measurement is not required in all patients with gout, it may be useful when uricosuric drug therapy is being considered.

Two common uricosuric agents are :

  1. probenecid (Benemid, Benuryl) and

  2. sulfinpyrazone (Anturane).

Sulfinpyrazone has an antiplatelet effect that may be beneficial for patients with a cardiac condition who are unable to take low-dose aspirin.

The major side effects of these drugs--hypersensitivity reactions and an increased risk of uric acid nephro-lithiasis - may be avoided by alkalization of the urine. However, this process involves use of additional medications, which may decrease patient compliance.

Sulfinpyrazone is a uricosuric agent that is related to phenylbutazone.

Because it can act as an antiplatelet drug, it should be used cautiously in patients who are anticoagulated or have bleeding problems.

Sulfinpyrazone can also cause gastrointestinal problems. Thus, caution should also be exercised in giving this drug to patients with peptic ulcer disease.

Probenecid (Benemid) and sulfinpyrazone (Anturane) are used in patients who are considered underexcretors of uric acid. Uricosuric drugs should not be given to patients with a urine output of less than 1 mL per minute, a creatinine clearance of less than 50 mL per minute (0.84 mL per second) or a history of renal calculi. The physiologic decline in renal function that occurs with aging frequently limits the use of uricosuric agents.

Probenecid, it is important to note that the drug also blocks the tubular secretion of other organic acids. This may result in increased plasma concentrations of penicillins, cephalosporins, sulfonamides and indomethacin.

Xanthine oxidase inhibitors

Allopurinol (Purinol, Zyloprim) decreases uric acid production by inhibiting the enzyme xanthine oxidase.

Dosage adjustments are necessary in patients with impaired creatinine clearance.

The increased risk of precipitating an acute attack during drug initiation can be decreased by starting with a dosage of 50 to 100 mg/day.

In addition, medications such as azathioprine (Imuran) and mercaptopurine (Purinethol) are inactivated by xanthine oxidase.

Allopurinol is indicated in patients with a history of nephrolithiasis, renal impairment, and an inadequate response to uricosuric drug therapy. Most patients with tophaceous gout need allopurinol therapy.

It is also indicated in patients with myeloproliferative disease who are undergoing chemotherapy and in those with hyperuricemia due to HGPRT deficiency or PRPP synthetase overactivity.

Patients with cancer and gout are at risk for drug interactions because allopurinol can affect the metabolism of some cancer therapies. In addition, cancer patients may be taking drugs that will elevate uric acid levels, potentially precipitating gout.

Allopurinol. As a xanthine oxidase inhibitor, allopurinol (Zyloprim) impairs the conversion of hypoxanthine to xanthine and the conversion of xanthine to uric acid. The effect of the drug depends on the dosage.

Allopurinol in a dosage of 300 mg per day has been reported to reduce serum urate concentrations to less than 7 mg per dL (420 µmol per L)

Allopurinol is the drug of choice in patients with severe tophaceous deposits and in patients with a history of impaired renal function (creatinine clearance of less than 50 mL per minute [0.84 mL per second]), uric acid nephropathy or nephrolithiasis.

The drug is also preferred as a pretreatment agent to protect against uric acid nephropathy in patients with lymphoproliferative or myeloproliferative disorders.

The side effects of allopurinol include skin rash (e.g., Stevens-Johnson syndrome and toxic epidermal necrolysis), leukopenia and gastrointestinal disturbances. The initiation of allopurinol therapy can also precipitate an acute gout attack. The dosage of allopurinol should be adjusted in patients with renal impairment.

Prophylactic drugs

Because flares may occur during a fall in serum urate levels, low doses of either colchicine or an NSAID may be effective in preventing acute attacks of gout. Such treatment should be started before the initiation of urate-lowering therapy. Colchicine can reduce recurrence of gouty flares regardless of the serum uric acid level.


Gouty arthritis is the culmination of a number of physiologic mechanisms that ultimately result in deposition of uric acid within joints and soft tissues.

Decreased uric acid clearance through the kidney is the most common cause of gout. Tophaceous gout occurs in less than 10% of patients.

Acute episodes are treated with NSAIDs or colchicine.

Low-dose therapy with these agents can also prevent recurrent attacks. Most patients with gout need long-term treatment with either uricosuric agents or xanthine oxidase inhibitors.

General treatment recommendations <.....More>

The above opinionated views and information serves to educated and informed consumer .  The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. .It should not replaced professional advise and consultation.  A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions 

Epidemiologic Factor
Clinical Presentation
Conservative Treatment
General Treatment
Diet for Gout

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