Skip to Content

Sulfinpyrazone (Systemic)

Primary: MS400

Commonly used brand name(s): Anturan; Anturane; Apo-Sulfinpyrazone; Novopyrazone.

Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).


Antigout agent—



Note: Bracketed information in the Indications section refers to uses that are not included in U.S. product labeling.


Gouty arthritis, chronic (treatment) or
Hyperuricemia (treatment)—Sulfinpyrazone is indicated for the long-term management of hyperuricemia associated with chronic gout {01} {02} {03} {04} {05} {06} {07} {08} {09}. It is recommended only for patients whose 24-hour renal excretion of urate is 800 mg (4.8 mmol) or lower (i.e., patients who are hyperuricemic as a result of underexcretion, rather than overproduction, of urate) {03} {05} {06}. The aim of sulfinpyrazone therapy is to reduce the number of acute gout attacks {03} {06} {07}.
—Sulfinpyrazone is not effective in the treatment of acute gout attacks {01} {03} {04} {08} and does not eliminate the need to use colchicine or a nonsteroidal anti-inflammatory drug (NSAID) to relieve an attack {01} {03} {04} {06} {07} {08}. Also, sulfinpyrazone therapy should not be initiated during an attack {03} {04} {06} {07}, because it may induce fluctuations in urate concentration {03} that may result in prolongation of the attack or initiation of a new attack {03} {06}.
—[Sulfinpyrazone is sometimes used in the treatment of hyperuricemia not associated with gout. However, treatment of asymptomatic hyperuricemia is often unnecessary; the need for such therapy should be determined on an individual basis.{03}{06}{07}{24}]1

—Although a few studies have shown that sulfinpyrazone may reduce the risk of reinfarction {10} and/or sudden cardiac death {02} {11} during the first 7 months {02} {11} after an initial myocardial infarction, the results of these studies have been questioned on methodological grounds {12} {13} {14}. Aspirin is the drug of choice for preventing reinfarction, because its efficacy is more clearly established {44}. However, sulfinpyrazone may be a suitable alternative for patients unable to take aspirin for this indication {45}.

Sulfinpyrazone is not recommended in circumstances in which there is an especially high risk of adverse effects associated with crystallization and deposition of urate in renal tissues, such as formation of renal calculi and uric acid nephropathy {03} {05} {06} {07}. It therefore should not be used for treatment of gout in patients whose 24-hour urate excretion exceeds 800 mg (4.8 mmol) {03} {05} or who have extensive tophi {03} {07}, or for treatment of hyperuricemia associated with neoplastic disease or its treatment (chemotherapy with rapidly cytolytic antineoplastic agents or radiation therapy) {03}. Allopurinol, which decreases the quantity of urate that reaches the kidneys in addition to decreasing the concentration of urate in the blood, is recommended in these circumstances {03} {04} {06} {07}.

Sulfinpyrazone has also been used to prevent the occurrence or reoccurrence of venous thrombosis or embolism {02} {16} {17} and thrombotic complications associated with rheumatic mitral stenosis {15}, unstable angina pectoris {18}, and transient cerebral ischemic attacks. {02} {19} Also, sulfinpyrazone has been used to prevent occlusion (by clotted blood) of aortocoronary bypass grafts, {20} {21} arteriovenous shunts, {02} {22} and prosthetic mitral valves. {02} {23} However, sulfinpyrazone's efficacy has not been established and further study has been recommended. {24} Aspirin is the agent of choice for these indications. Dipyridamole is also effective in protecting against thrombotic complications associated with prosthetic valves or other foreign surfaces. {46}

1 Not included in Canadian product labeling.


Physicochemical characteristics:

Chemical group—
    A pyrazole compound chemically related to phenylbutazone {02} {03} {08}
Molecular weight—
    404.48 {01} {02} {25}

    2.8 {04} {08}

Mechanism of action/Effect:

Antigout agent; antihyperuricemic—Sulfinpyrazone is a uricosuric agent {01} {02} {03} {04} {05} {06} {07} {08} {09}. By competitively inhibiting the active reabsorption of urate at the proximal renal tubule {04} {07} {08}, it increases the urinary excretion of uric acid and lowers serum urate concentrations {01} {02} {03} {04} {05} {08}. By lowering serum concentrations of uric acid below its solubility limits {03} {07}, sulfinpyrazone may decrease or prevent urate deposition, tophi formation, and chronic joint changes; promote resolution of existing urate deposits; and, after several months of therapy, reduce the frequency of acute attacks of gout {01} {02} {03} {04} {07} {08}. Sulfinpyrazone does not have clinically useful anti-inflammatory {01} {02} {03} {04} {07} {08} {09} or analgesic {03} {04} {08} activity.

Antithrombotic; myocardial infarction prophylactic—Sulfinpyrazone restores toward normal the shortened platelet survival time often associated with thromboembolic disorders {02} {08} {17} {19} {23} {27} {28}. It decreases platelet adhesiveness to subendothelial cells {02} {04} {08} and possibly to prosthetic surfaces. {27} Although sulfinpyrazone also inhibits the activity of the enzyme cyclo-oxygenase, resulting in decreased synthesis of thromboxane A 2 (a prostaglandin in platelets that promotes aggregation) {03} {31} and the platelet release reaction (an essential step in platelet aggregation and subsequent thrombus formation), {02} {04} it is a relatively weak inhibitor of platelet aggregation. {27} {29} Whether inhibition of platelet aggregation contributes significantly to the medication's antithrombotic activity has therefore been questioned. {27} {28} Sulfinpyrazone's effects on platelets are due primarily to an active sulfide metabolite. {30} {31} {32} {34}

Other actions/effects:

Although sulfinpyrazone lacks clinically useful anti-inflammatory {01} {02} {03} {04} {07} {08} {09} or analgesic {03} {04} {08} activity, it inhibits prostaglandin synthesis {02} {03} {30} {31} and shares some of the risks associated with phenylbutazone (to which it is chemically related) and other nonsteroidal anti-inflammatory drugs (NSAIDs), including the potential for causing gastrointestinal, renal, or hematologic toxicity. {01} {02}

There is some evidence that sulfinpyrazone induces the activity of hepatic microsomal enzymes {33} {37} and, with chronic use, enhances its own metabolism {37}. Although sulfinpyrazone has been shown to increase antipyrine clearance, {33} the possibility that it may induce the metabolism of other medications has not been fully investigated. However, sulfinpyrazone has been shown to inhibit (rather than increase) metabolism of several medications, including warfarin, {41} tolbutamide, {04} {34} and phenytoin, {34} that are metabolized via the hepatic P-450 microsomal enzyme system.


Rapid and complete. {02} {03} {07} {08}

Protein binding:

Very high (98 {02} {04} {07} {08} {34} {37} to 99% {04} {34} {37}).


Hepatic {33} {37} and intestinal {37} {49}. The sulfide metabolite is formed primarily by intestinal microflora following enterohepatic circulation of sulfinpyrazone {37} {49}. The number and quantity of metabolites formed, {32} {35} especially the quantity of the sulfide metabolite, {35} are subject to considerable interpatient variation.

At least 4 of the known metabolites are active. p–Hydroxy-sulfinpyrazone has about 33 to 50% {34} of the uricosuric activity of the parent compound. {04} {07} {08} {34} The sulfide derivative, but not the sulfone or p-hydroxysulfide derivative, also has slight uricosuric activity. {34} The sulfide, sulfone, and p -hydroxysulfide metabolites are approximately 10, 5, and 2 times as potent, respectively, and the p-hydroxy-sulfinpyrazone metabolite is about half as potent, as sulfinpyrazone itself in altering platelet function {31} {32} {34} {35}. However, only the sulfide metabolite is considered to contribute significantly toward the medication's antithrombotic activity {30} {31} {32} {34} {35}.




Approximately 4 to 6 hours {04} {35} {36} {37}. Single-dose studies have provided some evidence for the existence of an early elimination half-life of approximately 2 to 3 hours and a late elimination half-life (beginning approximately 20 hours after administration) of approximately 6 hours {34}.


200-mg single dose—Approximately 1 hour {34}.

400-mg single dose and

Steady-state, following administration of 400 mg twice a day for 23 days—Approximately 2.6 hours {37}.

Sulfide metabolite—

Single doses—Approximately 11 {35} to 12 {34} hours, although one study reported a mean value of 20.9 hours after a single 400-mg dose {37}.

Steady-state—Approximately 14 hours, following administration of 200 mg 4 times a day for 6 days {36} or 400 mg twice a day for 23 days {37}.

Onset of action:

Antithrombotic effect—Approximately 4 days {28}.

Time to peak concentration:

Sulfinpyrazone—Approximately 1 {03} {07} to 2 {34} {36} hours. Values at steady-state (after administration of 200 mg 4 times a day for 6 days or 400 mg twice a day for 23 days) are not significantly different from those found with single 400-mg oral doses {36} {37}.

p-Hydroxy-sulfinpyrazone—Approximately 2.5 hours, after administration of a single 400-mg dose and at steady-state (following administration of 400 mg twice a day for 23 days) {37}.

Sulfide metabolite—Generally 11 {35} to 12 {36} hours after administration of a single dose, although one study reported a mean value of 19 hours after a single 400-mg dose {37}. Mean values under steady-state conditions (after administration of 200 mg 4 times a day for 6 days or administration of 400 mg twice a day for 23 days) are lower by about 4 to 5 hours than those determined after single doses {36} {37}.

Peak serum concentration


Single 200-mg dose: Approximately 13 mcg per mL (mcg/mL) (32.1 micromoles/L) {35}.

Single 400-mg dose: Approximately 26 {37} to 30 {36} mcg/mL (64.2 to 74.1 micromoles/L).

Chronic administration of 600 to 800 mg a day: Two studies, one in which values were determined in patients who had been treated continuously for 2.5 years and another in which values were determined after administration of 200 mg 4 times a day for 6 days, reported maximum values of approximately 16 {32} to 21 {36} mcg/mL (39.5 to 51.9 micromoles/L). In a third study, maximum concentrations of 13.5 mcg/mL (33.3 micromoles/L) were measured after administration of 400 mg twice a day for 23 days; this value is approximately half of that found in the same study after administration of a single 400-mg dose. {37}


Single 200-mg dose: Less than 0.5 mcg/mL {35}.

Single 400-mg dose: Approximately 0.7 mcg/mL {37}.

Chronic administration of 800 mg a day: Approximately 0.2 mcg/mL {34} {37}.

Sulfide metabolite:

Single 200-mg dose: Approximately 2.6 mcg/mL {35}.

Single 400-mg dose: Approximately 1 mcg/mL in 1 study {37} and 3.5 mcg/mL in another {36}.

Chronic administration of 600 to 800 mg a day: Maximum values of approximately 14 mcg/mL were reported in one study after administration of 200 mg 4 times a day for 6 days {36}. However, lower values (approximately 2.5 to 5 mcg/mL) were reported in other studies in which sulfinpyrazone was administered for a longer time (23 days in 1 study and at least 2.5 years in the other) {32} {37}.

Time to peak effect

Antithrombotic effect—Approximately 1 to 2 weeks after initiation of treatment with 200 mg 4 times a day {34}.

Duration of action:

Single dose—The uricosuric action usually lasts for 4 to 6 hours {08}, but may persist for up to 10 hours in some patients {04} {08}.

    95% renal; 5% fecal. Approximately 25% of a dose is excreted in the urine as free sulfinpyrazone and another 25% as sulfinpyrazone glucuronide. Up to 45% of a dose is excreted in the urine as metabolites, mostly as their glucuronide conjugates. {34}

Precautions to Consider

Cross-sensitivity and/or related problems

Patients sensitive to aspirin, {39} oxyphenbutazone, or phenylbutazone {02} {03} may be sensitive to this medication also. In challenge tests, sulfinpyrazone caused dyspnea, wheezing, and/or a fall in peak expiratory flow rate in 4 of 11 patients with aspirin-induced asthma but no reaction in individuals with documented sensitivity (history of anaphylaxis and positive skin tests) to dipyrone. {39}

The possibility of cross-sensitivity between sulfinpyrazone and other nonsteroidal anti-inflammatory drugs (NSAIDs) should be considered, especially for patients in whom cross-sensitivity between aspirin and other NSAIDs has been reported {61}.


No evidence of carcinogenicity was found in a 2-year study in rats receiving up to 500 mg per kg of body weight per day {02}.


Problems in humans have not been documented.

Studies in animals on the teratogenic potential of sulfinpyrazone have yielded inconclusive results. {01}


It is not known whether sulfinpyrazone is excreted in breast milk {02} {34}.


No published information is available on the relationship of age to the effects of sulfinpyrazone in pediatric patients.


No published information is available on the relationship of age to the effects of sulfinpyrazone in geriatric patients. However, elderly patients are more likely to have age-related renal function impairment, which may decrease the efficacy of uricosuric agents {03} {05} {07} {09} and/or increase the risk of adverse effects in patients receiving sulfinpyrazone. {03}

Drug interactions and/or related problems
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

Note: Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.
In addition to the interactions listed below, the possibility should be considered that additive or multiple effects leading to impaired blood clotting and/or increased risk of bleeding may occur if sulfinpyrazone is administered concurrently with any medication having a significant potential for causing hypoprothrombinemia, thrombocytopenia, or gastrointestinal ulceration or hemorrhage. {40}

Alcohol or
Diazoxide or
Mecamylamine or
Pyrazinamide    (these medications may increase serum uric acid concentrations; dosage adjustment of sulfinpyrazone may be necessary to control hyperuricemia {03} {08})

Aminosalicylate sodium    (sulfinpyrazone may decrease renal tubular secretion of aminosalicylate sodium, resulting in increased and more prolonged serum concentrations and/or toxicity; patient should be monitored and dosage adjusted as necessary {42} {43})

» Anticoagulants, coumarin- or indandione-derivative or
» Heparin or
» Thrombolytic agents, such as:
Alteplase (tissue-type plasminogen activator, recombinant)
Anistreplase (anisoylated plasminogen-streptokinase activator complex, APSAC)
Urokinase    (prolongation of the prothrombin time {34} and severe gastrointestinal or renal bleeding {34} {48} have resulted from concurrent use of sulfinpyrazone with acenocoumarol [nicoumalone] or warfarin {34}; studies have demonstrated that sulfinpyrazone has stereoselective effects on warfarin kinetics, i.e., it displaces from protein-binding sites and increases clearance of the (R)-enantiomer of warfarin, but inhibits metabolism of the substantially more potent (S)-enantiomer by the hepatic P-450 enzyme system, resulting in a net increase in warfarin activity; {50} careful monitoring of the prothrombin time is recommended when sulfinpyrazone therapy is initiated or discontinued so that anticoagulant dosage can be adjusted as needed )

    (although sulfinpyrazone has also been shown to inhibit enzymatic metabolism of phenprocoumon, concurrent use of the 2 medications does not lead to a significant increase in the prothrombin time, possibly because a comparatively small quantity of phenprocoumon is eliminated via this mechanism; {51} however, inhibition of platelet function by sulfinpyrazone, and its potential for causing gastrointestinal ulceration or hemorrhage, may increase the risk of hemorrhage in patients receiving any anticoagulant or thrombolytic agent {40})

Antidiabetic agents, oral    (sulfinpyrazone may decrease the metabolism of an oral antidiabetic agent, leading to prolonged half-life {04} {34} and increased hypoglycemic effect; {04} dosage adjustments may be necessary during and following sulfinpyrazone therapy {44} {45} {46})

Anti-inflammatory drugs, nonsteroidal (NSAIDs) or
» Platelet aggregation–inhibiting medications (See Appendix II )    (concurrent use with sulfinpyrazone may increase the risk of bleeding because of additive inhibition of platelet function and sulfinpyrazone's potential for causing gastrointestinal ulceration or hemorrhage; {40} concurrent use with NSAIDs may also increase the risk of gastrointestinal ulceration or hemorrhage {24})

Antimicrobial agents{49}    (antimicrobial therapy may suppress formation by intestinal microflora of the active sulfide metabolite of sulfinpyrazone, which is responsible for sulfinpyrazone's antithrombotic activity)

» Antineoplastic agents, rapidly cytolytic    (concurrent use with sulfinpyrazone is not recommended because of the risk of uric acid nephropathy; allopurinol is the antihyperuricemic agent of choice for reducing risks [gout and/or urate nephropathy] associated with chemotherapy-induced hyperuricemia; also, rapidly cytolytic antineoplastic agents may increase serum uric acid concentrations and interfere with control of pre-existing hyperuricemia and gout {03} {24})

» Aspirin or other salicylates, including bismuth subsalicylate    (salicylates inhibit sulfinpyrazone's uricosuric action; {01} {02} {03} {04} {08} {09} {34} {41} although occasional use of a salicylate in low to moderate analgesic doses, or chronic administration of 80 mg per day of aspirin as an antithrombotic, is not likely to interfere with sulfinpyrazone's uricosuric effect, {52} chronic use of analgesic or antirheumatic doses of a salicylate together with sulfinpyrazone is not recommended; {41} sulfinpyrazone also inhibits the uricosuria induced by high doses of salicylates; {34} {41} in addition, sulfinpyrazone may decrease excretion of salicylate {34} and/or displace salicylate from its plasma protein-binding sites, possibly leading to increased salicylate concentrations and toxicity)

    (low doses of sulfinpyrazone and aspirin have been used together as an antithrombotic regimen in a few studies; {16} {47} however, whether the combination is more effective than aspirin alone has not been established, {47} and the increased risk of bleeding must be considered {40})

» Cefamandole or
» Cefoperazone or
» Cefotetan or
» Moxalactam or
» Plicamycin or
» Valproic acid    (these medications may cause hypoprothrombinemia; in addition, plicamycin or valproic acid may inhibit platelet aggregation, and moxalactam may also cause irreversible platelet damage; inhibition of platelet function by sulfinpyrazone, as well as its potential for causing gastrointestinal ulceration or hemorrhage, may increase the risk of severe hemorrhage when these medications are used concurrently {40})

» Nitrofurantoin{08}    (sulfinpyrazone may increase serum concentrations of nitrofurantoin by decreasing its renal clearance, possibly increasing the potential for toxic reactions and reducing nitrofurantoin's effectiveness as a urinary tract anti-infective; concurrent use should be avoided)

Phenytoin and possibly other hydantoin anticonvulsants{34}    (sulfinpyrazone may displace these medications from plasma protein-binding sites and decrease their metabolism, possibly leading to increased plasma concentration and elimination half-life; although hydantoin plasma concentration is not consistently increased, it is recommended that patients be monitored for signs of hydantoin toxicity during concurrent use)

Probenecid    (probenecid inhibits the renal tubular secretion of sulfinpyrazone {07} {34} {41} and its active para-hydroxy metabolite; {34} however, the uricosuric effects of the medications are additive, and increased therapeutic benefit has been reported during concurrent use {03} {05} {07})

Laboratory value alterations
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With diagnostic test results
» Aminohippuric acid (PAH) clearance studies and
Phenolsulfonphthalein (PSP) clearance studies    (sulfinpyrazone decreases renal clearance of PAH and PSP, leading to reduced urine concentrations and misleading test results {03} {07})

Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).

Except under special circumstances, this medication should not be used when the following medical conditions exist:
» Any condition in which there is an increased risk of uric acid renal calculus formation or urate nephropathy, such as:
» Cancer chemotherapy with rapidly cytolytic antineoplastic agents
» Radiation therapy for malignancy
» Renal calculi or history of, especially uric acid calculi
» Urate excretion higher than 800 mg (4.8 mmol) in 24 hours
» Urate nephropathy or history of    (sulfinpyrazone is likely to induce, or exacerbate pre-existing, renal calculi and/or urate nephropathy; allopurinol is the antihyperuricemic agent recommended in these circumstances {03} {04} {05} {06} {07} {08} {52})

» Blood dyscrasias    (may be exacerbated {01} {02} {03})

» Peptic ulcer, active    (may be exacerbated {60})

» Renal function impairment, moderate to severe    (may be exacerbated; {56} {57} also, sulfinpyrazone's efficacy as a uricosuric agent decreases with increasing degrees of renal function impairment, {03} {05} {07} {09} and the medication may be completely ineffective when the patient's creatinine clearance is lower than 30 mL per minute [0.5 mL per second] {06} {47})

Risk-benefit should be considered when the following medical problems exist
Bronchospastic reaction to aspirin, history of or{39}
Sensitivity to sulfinpyrazone or to NSAIDs, especially oxyphenbutazone or phenylbutazone, history of{02}{03}    (risk of cross-sensitivity)

Blood dyscrasias, history of    (increased risk of sulfinpyrazone-induced blood dyscrasias)

» Gastrointestinal inflammation or ulceration, active or history of or
» Peptic ulcer, history of    (may be exacerbated or reactivated; if sulfinpyrazone is used for patients with these conditions, concurrent use of an appropriate treatment or prophylactic regimen for gastrointestinal ulceration should be considered)

» Renal function impairment, mild    (may be exacerbated; also, sulfinpyrazone's efficacy as a uricosuric agent begins to decrease when the creatinine clearance is 80 mL per minute [1.33 mL per second] {09})

Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; » = major clinical significance):

Blood counts{01}{02}    (recommended at periodic intervals during therapy)

Renal function determinations{02}{03}    (recommended at periodic intervals during therapy for patients with renal function impairment)

» Uric acid determinations{59}    (monitoring of uric acid concentrations may be required for proper dosing in uricosuric therapy; the effect of sulfinpyrazone may be measured by a reduction of serum uric acid concentration [the upper limit of normal is about 7 mg per 100 mL (420 micromoles/L) for men and postmenopausal women and about 6 mg per 100 mL (360 micromoles/L) for premenopausal women but may vary, depending on the patient and laboratory methodology] or, more directly, by a significant increase in 24-hour urinary uric acid excretion)

Side/Adverse Effects
The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:

Those indicating need for medical attention
Incidence more frequent
Renal calculi, urate{01}{03}{09} (lower back and/or side pain, painful urination, with or without blood in urine)—may occur in up to 10% of patients early in sulfinpyrazone treatment{09}

Incidence less frequent
Dermatitis, allergic{01}{02}{03} (skin rash)

Incidence rare
Agranulocytosis{01}{03} (fever with or without chills; sores, ulcers, or white spots on lips or in mouth; sore throat)
anemia{01}{02}{03} (unusual tiredness or weakness)
aplastic anemia
[pancytopenia]{01} (shortness of breath, troubled breathing, tightness in chest, and/or wheezing; sores, ulcers, or white spots on lips or in mouth; swollen and/or painful glands; unusual bleeding or bruising; unusual tiredness or weakness)
fever, allergic
{08} gastrointestinal bleeding{02} (bloody or black, tarry stools; vomiting of blood or material that looks like coffee grounds)
leukopenia{01}{02}{03} (fever with or without chills; sore throat; unusual tiredness or weakness)
renal failure,{01}{02}{53}{54}{55}{56}{57}{58} possibly associated with urate nephropathy{03}{04}{05}{06}{07}{08} (increased blood pressure; shortness of breath, troubled breathing, tightness in chest, and/or wheezing; sudden decrease in amount of urine; swelling of face, fingers, feet, and/or lower legs; unusual tiredness or weakness; weight gain)
thrombocytopenia{01}{02}{03} (rarely, unusual bleeding or bruising; black, tarry stools; blood in urine or stools; pinpoint red spots on skin)—usually asymptomatic

Note: Renal failure not associated with urate nephropathy {01} {02} {53} {54} {57} has been reported, rarely, during sulfinpyrazone therapy, but a direct causal relationship has not always been clearly established. {01} {02} Sulfinpyrazone has caused acute interstitial nephritis {54} {55} (including cases documented as being hypersensitivity-mediated) {55} and acute renal tubular necrosis {53} in a few patients. Also, transient renal function impairment (which improved despite continued administration) has occurred in postmyocardial infarction patients {56} {57} and postaortocoronary bypass patients {58} receiving sulfinpyrazone. It has been proposed that sulfinpyrazone may cause transient renal ischemia by temporarily inhibiting the synthesis of renal vasodilator prostaglandins {57} and/or kinins, {57} {58} and that the presence of congestive heart failure may be a predisposing factor in the development of sulfinpyrazone-induced renal complications. {55}

Those indicating need for medical attention only if they continue or are bothersome
Incidence more frequent
Gouty arthritis, acute attack{01}{03}{04}{05}{06}{07} (joint pain; redness; swelling)
nausea or vomiting
stomach pain
Note: An increase in the frequency of acute attacks of gout during the first few months of therapy may be anticipated, unless adequate prophylaxis with colchicine (or, if the patient is unable to take colchicine, a nonsteroidal anti-inflammatory drug [NSAID]) is given concurrently with the sulfinpyrazone {03} {04} {05} {06} {07}. Up to 20% of patients started on treatment with a uricosuric agent alone may experience acute attacks within the first few days of treatment {07}.

For specific information on the agents used in the management of sulfinpyrazone overdose, see:
   • Acetazolamide in Carbonic Anhydrase Inhibitors (Systemic) monograph;
   • Allopurinol (Systemic) monograph; and/or
   • Potassium citrate in Citrates (Systemic) monograph.
For more information on the management of overdose or unintentional ingestion, contact a Poison Control Center (see Poison Control Center Listing ).

Clinical effects of overdose
The following effects have been selected on the basis of their clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:
Acute and chronic
Clumsiness or unsteadiness
nausea or vomiting, severe or continuing
stomach pain, severe or continuing
difficulty in breathing{01}{02}

Treatment of overdose
To decrease absorption—Emptying the stomach by induction of emesis or performing gastric lavage {01} {02}.

Specific treatment—If severe renal function impairment occurs, hemodialysis may be needed {02}.

For uric acid calculi or urate nephropathy:

Recommended measures include administration of large quantities of fluids and of allopurinol to increase urine flow and reduce uric acid formation, respectively {09}. A urinary pH of 6 to 6.5 should be achieved and maintained by administration of alkali {09} {60} such as potassium citrate {09} {60}. If necessary to maintain the desired urinary pH through the night, acetazolamide may also be given at bedtime {09}. Other interventions designed to facilitate removal of renal calculi may also be needed. {09}

Supportive care—Monitoring the patient and instituting supportive treatment as needed {01} {02}. Patients in whom intentional overdose is known or suspected should be referred for psychiatric consultation.

Patient Consultation
As an aid to patient consultation, refer to Advice for the Patient, Sulfinpyrazone (Systemic).

In providing consultation, consider emphasizing the following selected information (» = major clinical significance):

Before using this medication
»   Conditions affecting use, especially:
Sensitivity to sulfinpyrazone or NSAIDs, especially aspirin, oxyphenbutazone, or phenylbutazone, history of
Other medications, especially anticoagulants, rapidly cytolytic antineoplastic agents, aspirin or other salicylates, hypoprothrombinemia-inducing cephalosporins, moxalactam, nitrofurantoin, platelet aggregation inhibitors, plicamycin, and valproic acid
Other medical problems, especially cancer treated with rapidly cytolytic antineoplastic agents or radiation therapy, renal calculi or history of (especially uric acid calculi), renal function impairment, blood dyscrasias, gastrointestinal inflammation or ulceration, and active peptic ulcer

Proper use of this medication
» Taking with food or an antacid to minimize gastrointestinal irritation

» Compliance with therapy

Importance of high fluid intake and compliance with therapy for alkalinization of urine, if prescribed, to minimize kidney stone formation

» Proper dosing
Missed dose: Taking as soon as possible; not taking if almost time for next dose; not doubling doses

» Proper storage

For use as antigout agent
Several months of continuous therapy may be required for maximum effectiveness

» Medication does not relieve acute gout attacks but rather helps to prevent them; need to continue taking sulfinpyrazone with medication prescribed for gout attacks

Precautions while using this medication
Regular visits to physician to check progress during therapy

Caution if any laboratory tests required; possible interference with test results

For use as antihyperuricemic (including gout therapy)
» Aspirin or other salicylates may decrease the uricosuric effects of sulfinpyrazone; checking with physician regarding concurrent use, since effect is dependent on salicylate dose and duration of use

» Possibility that alcohol taken in large amounts may increase blood uric acid concentration and reduce effectiveness of medication

Side/adverse effects
Signs and symptoms of potential side effects, especially renal calculi, dermatitis, blood dyscrasias, fever, gastrointestinal bleeding, and renal failure

General Dosing Information
Sulfinpyrazone therapy for gouty arthritis should not be initiated until 2 to 3 weeks after an acute attack has subsided. {08} However, if an acute attack occurs in a patient already receiving sulfinpyrazone, the medication should be continued at the same dose while therapeutic doses of colchicine or a nonsteroidal anti-inflammatory drug (NSAID) are given to relieve the attack. {01} {02} {08}

Sulfinpyrazone may be administered with food or an antacid to reduce gastrointestinal irritation {01}.

Because sulfinpyrazone may increase the frequency of acute attacks of gout during the early months of therapy, prophylactic doses of colchicine (or, if the patient is unable to take colchicine, an NSAID) should be administered concurrently during the first 3 to 6 months of sulfinpyrazone therapy. {03} {06} {08} However, even with prophylactic therapy, acute attacks of gout requiring treatment with full therapeutic doses of colchicine or an NSAID may occur.

To reduce the risk of urate stone formation, especially in patients with hyperuricemia, it is recommended that sulfinpyrazone therapy be initiated with a low dose, followed by a gradual increase in dosage. {01} {02} {03} Also, a high fluid intake {01} {02} {03} {07} (no less than 2.5 to 3 liters daily) and maintenance of an alkaline urine {01} {02} {03} {07} {09} by administration of sodium bicarbonate (3 to 7.5 grams daily), {09} potassium citrate (7.5 grams daily), {52} or acetazolamide (250 mg daily) {09} are recommended. The risk of urate stone formation is highest during the first few weeks of therapy, when urate excretion is high; after hyperuricemia has been controlled and urinary excretion of uric acid decreases, the need for these measures is reduced. {52}

Sulfinpyrazone may be given concurrently with allopurinol for treatment of gout; the antihyperuricemic effects of the 2 medications are additive {03} {06} {07}.

Determination of serum or urine (24-hour) uric acid concentrations may be necessary for proper dosing in uricosuric therapy {01} {02} {59}.

Oral Dosage Forms

Note: Bracketed uses in the Dosage Forms section refer to categories of use and/or indications that are not included in U.S. product labeling.


Usual adult dose
Antigout agent

Oral, 100 {01} {02} to 200 {01} mg two times a day, the dose being increased by 200 mg a day at two-day intervals, if necessary, {02} up to a maximum of 800 mg per day {01} {02}.

Note: Some clinicians recommend initiating treatment with a lower dose of 50 mg two times a day and increasing the dose more gradually (e.g., at three- to four-day intervals) {06} {07} {09}.
Patients who were previously controlled with other uricosuric therapy may be transferred to sulfinpyrazone at full maintenance dosage {01} {02}.

Oral, dosage to be adjusted to the lowest dose that maintains the serum uric acid concentration at the desired level, usually 200 to 400 mg per day. However, some patients may require maintenance doses of up to 800 mg a day. {01} {02}

Note: The initial dose recommended for treatment of gout is also appropriate if sulfinpyrazone is used as an antithrombotic. However, it is recommended that myocardial reinfarction prophylaxis with sulfinpyrazone not be initiated until at least fourteen days after the acute event. {02} Delaying treatment may decrease the risk of renal function impairment in patients receiving sulfinpyrazone for this purpose. {57}
For preventing myocardial reinfarction, the usual maintenance dose is 800 mg per day, in four divided doses {02}. For other antithrombotic indications, the usual maintenance dose is 600 to 800 mg per day, in three or four divided doses {02}.

Usual pediatric dose
Dosage has not been established.

Strength(s) usually available

200 mg (Rx) [Anturane][Generic]

Not commercially available.

Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Store in a well-closed container.


Usual adult dose
See Sulfinpyrazone Capsules USP.

Usual pediatric dose
Dosage has not been established.

Strength(s) usually available

100 mg (Rx) [Anturane][Generic]


100 mg (Rx) [Anturan] [Apo-Sulfinpyrazone] [Novopyrazone]

200 mg (Rx) [Anturan] [Apo-Sulfinpyrazone] [Novopyrazone]

Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Store in a well-closed container.

Revised: 01/19/1993

  1. Prescribing information, Anturane, Ciba, U.S., in: Physician's desk reference, 46th ed. Montvale: Medical Economics Data, 1992: 853-4.
  1. Product monograph Anturan, Geigy, Canada, revised 5/17/88.
  1. AMA drug evaluations annual. Chicago: American Medical Association, 1992: 1831-3, 1838-9.
  1. Gilman AG, Rall TW, Nies AS, Taylor P, eds. Goodman and Gilman's The pharmacological basis of therapeutics. 8th ed. New York: Pergamon Press, 1990: 679, 746-7.
  1. Speight TM, ed. Avery's drug treatment. Principles and practice of clinical pharmacology and therapeutics. 3rd ed. Baltimore: Williams & Wilkins, 1987: 944-7.
  1. Rakel RE, ed. Conn's current therapy. Philadelphia: W.B. Saunders, 1991: 501-4.
  1. Kelley WN, Harris ED Jr, Ruddy S, Sledge CB, eds. Textbook of rheumatology. 2nd ed. Philadelphia: W.B. Saunders, 1985: 857-8, 861.
  1. McEvoy GK, ed. AHFS drug information. Bethesda: American Society of Hospital Pharmacists, 1992: 1581-3.
  1. Wilson JD, Braunwald E, Isselbacher KJ, Petersdorf RG, Martin JB, Fauci AS, Root R, eds. Harrison's principles of internal medicine, 12th ed. New York: McGraw-Hill, 1991: 1834-41.
  1. Anturan Reinfarction Italian Study Group. Sulphinpyrazone in post-myocardial infarction. The Lancet 1982; 319: 237-42.
  1. The Anturane Reinfarction Trial Research Group. Sulfinpyrazone in the prevention of sudden death after myocardial infarction. N Engl J Med 1980; 302: 250-6.
  1. Temple R, Pledger GW. The FDA's critique of the anturane reinfarction trial. N Engl J Med 1980; 303: 1488-92.
  1. Loeliger EA. Does sulphinpyrazone prevent recurrence of myocardial infarction? The Lancet 1982; 319: 735 (letters).
  1. Malhotra SL. Does sulphinpyrazone prevent recurrence of myocardial infarction? The Lancet 1982; 319: 735 (letters).
  1. Steele P, Rainwater J. Favorable effect of sulfinpyrazone on thromboembolism in patients with rheumatic heart disease. Circulation 1980; 62: 462-5.
  1. Sautter RD, Koch EL, Myers WO, et al. Aspirin-sulfinpyrazone in prophylaxis of deep venous thrombosis in total hip replacement. JAMA 1983; 250: 2649-54.
  1. Steele PP, Weily HS, Genton E. Platelet survival and adhesiveness in recurrent venous thrombosis. N Engl J Med 1973; 288: 1148-52.
  1. Cairns JA. Aspirin, sulfinpyrazone, or both in unstable angina. Results of a Canadian multicenter trial. N Engl J Med 1985; 313: 1369-75.
  1. Steele P, Carroll J, Overfield D, Genton E. Effect of sulfinpyrazone on platelet survival time in patients with transient ischemic attacks. Stroke 1977; 8: 396-8.
  1. Baur HR, VanTassel RA, Pierach CA, Gobel FL. Effects of sulfinpyrazone on early graft closure after myocardial revascularization. Am J Cardiol 1982; 49: 420-4.
  1. Gitler B, Gitler ES. Efficacy of antiplatelet drugs in the maintenance of aortocoronary vein bypass graft patency. Am Heart J 1983; 106: 563-70.
  1. Kaegi MB, Pineo GF, Shimizu A, Trivedi HJ, Hirsh J, Gent M. Arterio-venous shunt thrombosis. N Engl J Med 1974; 209: 304-6.
  1. Weily HS, Genton E. Altered platelet function in patients with prosthetic mitral valves: effects of sulfinpyrazone therapy. Circulation 1970; 42: 967-72.
  1. Panel consensus, Sulfinpyrazone monograph, draft for USP DI 1985.
  1. Fleeger CA, ed. USAN and the USP dictionary of drug names. Rockville, MD: The U.S. Pharmacopeial Convention, Inc., 1992: 604.
  1. Ali M, McDonald JWD. Effects of sulfinpyrazone on platelet prostaglandin synthesis and platelet release of serotonin. J Lab Clin Med 1977; 89: 868-75.
  1. Nunn B, James FJ. Effect of sulphinpyrazone on human platelet aggregation, 5-hydroxy-tryptamine release and adhesion ex vivo: comparison with naproxen. Br J Clin Pharmacol 1980; 9: 239-45.
  1. de Gaetano G, Cerletti C, Bertele V. Pharmacology of antiplatelet drugs and clinical trials on thrombosis prevention: a difficult link. The Lancet 1982; 320: 974-7.
  1. Latour J-G, Theroux P, Bourassa MG. Sulfinpyrazone decreases epinephrine-induced platelet aggregation after myocardial infarction. Am J Cardiol 1982; 50: 938-44.
  1. Wallis RB. Mechanisms of action of sulphinpyrazone. Thromb Res 1983; suppl IV: 31-8.
  1. Kirstein Pedersen A, FitzGerald GA. Cyclooxygenase inhibition, platelet function, and metabolite formation during chronic sulfinpyrazone dosing. Clin Pharmacol Ther 1985; 37: 36-42.
  1. Kirstein Pedersen A, Jakobsen P. Sulphinpyrazone metabolism during long-term therapy. Br J Clin Pharmaol 1981; 11: 597-603.
  1. Walter E, Staiger Ch., de Vries J, Zimmermann R, Weber E. Induction of drug metabolizing enzymes by sulfinpyrazone. Eur J Clin Pharmacol 1981; 19: 353-8.
  1. Kirstein Pedersen A, Jakobsen P, Kampmann JP, Molholm Hansen J. Clinical pharmacokinetics and potentially important drug interactions of sulphinpyrazone. Clin Pharmacokinet 1982; 7: 42-56.
  1. Mahony C, Wolfram KM, Nash PV, Bjornsson TD. Kinetics and metabolism of sulfinpyrazone. Clin Pharmacol Ther 1983; 33: 491-7.
  1. Rosenkranz B, Fischer C, Jakobsen P, Kirstein Pedersen A, Frohlich JC. Plasma levels of sulfinpyrazone and two of its metabolites after a single dose and during the steady state. Eur J Clin Pharmacol 1983; 24: 231-5.
  1. Schlicht F, Staiger Ch., de Vries J, et al. Pharmacokinetics of sulphinpyrazone and its major metabolites after a single dose and during chronic treatment. Eur J Clin Pharmacol 1985; 28: 97-103.
  1. Kaegi A, Pineo GF, Shimizu A, Trivedi H, Hirsh J. The role of sulfinpyrazone in the prevention of arterio-venous shunt thrombosis. Circulation 1975; 62: 497-9.
  1. Szczeklik A, Czerniawska-Mysik G, Nizankowska E. Sulfinpyrazone and aspirin-induced asthma. N Engl J Med 1980; 303: 702-3 (letters).
  1. Panel consensus, Ballot 3/85.
  1. Hansten PD, Horn JR. Drug interactions. 6th ed. Philadelphia: Lea & Febiger, 1989: 105, 416, 362.
  1. Reed MD, Blumer JL. Clinical pharmacology of antitubercular drugs. Pediatr Clin N Am 1983; 30: 177-87.
  1. Gilman AG, Goodman LS, Rall TW, Murad F, eds. Goodman and Gilman's The pharmacological basis of therapeutics 7th ed. New York: Macmillan, 1985: 1208-9.
  1. Resnekov L, Chediak J, Hirsh J, Lewis HD Jr. Antithrombotic Agents in Coronary Artery Disease. Report of the second American College of Chest Physicians conference on antithrombotic therapy. Chest 1989; 95(suppl): 52S-72S.
  1. Panelist comment, draft 8/92.
  1. Panelist comment, draft 8/92.
  1. Canadian Cooperative Study Group. A randomized trial of aspirin and sulfinpyrazone in threatened stroke. N Engl J Med 1978; 299: 53-9.
  1. Thompson PL, Serjeant C. Potentially serious interaction of warfarin with sulphinpyrazone. Med J Aust 1981; 1: 41 (letters).
  1. Strong HA, Angus R, Oates J, et al. Effects of ischaemic heart disease, Crohn's disease and antimicrobial therapy on the pharmacokinetics of sulphinpyrazone. Clin Pharmacokinet 1986; 11: 402-10.
  1. Toon S, Low LK, Gibaldi M, et al. The warfarin-sulfinpyrazone interaction: stereochemical considerations. Clin Pharmacol Ther 1986; 39: 15-24.
  1. Heimark LD, Toon S, Gibaldi M, Trager WF, O'Reilly RA, Goulart DA. The effect of sulfinpyrazone on the disposition of pseudoracemic phenprocoumon in humans. Clin Pharmacol Ther 1987; 42: 312-9.
  1. Panel consensus, Probenecid monograph, draft 3/92.
  1. Durham DS, Ibels LS. Sulphinpyrazone-induced acute renal failure. Br Med J 1981; 282: 609.
  1. Butler AL. Renal dysfunction due to anturane. N Engl J Med 1981; 306: 106 (letters).
  1. Howard T, Hoy RH, Warren S, Georgiev M, Selinger H. Acute renal dysfunction due to sulfinpyrazone therapy in post-myocardial infarction cardiomegaly: reversible hypersensitive interstitial nephritis. Am Heart J 1981; 102: 294-5.
  1. Boelaert J, van Eeghem P, Daneels R, et al. Renal dysfunction due to anturane. N Engl J Med 1981; 306: 1154 (letters).
  1. Lijnen P, Boelaert J, van Eeghem P, et al. Decrease in renal function due to sulphinpyrazone treatment early after myocardial infarction. Clin Nephrol 1983; 19: 143-6.
  1. Boelaert J, Lijnen P, Robbens E, et al. Impairment of renal function due to sulphinpyrazone after coronary artery bypass surgery: a prospective double-blind study. J Cardiovasc Pharmacol 1986; 8: 386-91.
  1. Panelist comment, approved by consensus, 1987 revision, Probenecid monograph.
  1. Wyngaarden JB, Smith LH, eds. Cecil textbook of medicine, 18th ed. Philadelphia: WB Saunders, 1988: 643.
  1. Panel consensus, draft 8/92.