(British Approved Name, US Adopted Name, rINN)
International Nonproprietary Names (INNs) in main languages (French, Latin, Russian, and Spanish):
Description. Allopurinol is a tautomeric mixture of 1H-pyrazolo[3,4-d]pyrimidm-4-ol and l,5-dihydro-4H-pyrazolo[3,4-d]pyrimidin-4-one.
Pharmacopoeias. In China, Europe , International, Japan, and US
European Pharmacopoeia, 6th ed., 2008 and Supplements 6.1 and 6.2 (Allopurinol). A white or almost white powder. Very slightly soluble in water and in alcohol; dissolves in dilute solutions of alkali hydroxides.
The United States Pharmacopeia 31, 2008, and Supplements 1 and 2 (Allopurinol). A fluffy white to off-white powder having only a slight odour. Very slightly soluble in water and in alcohol; practically insoluble in chloroform and in ether; soluble in solutions of potassium and sodium hydroxides.
Allopurinol sodium as a 3 mg/mL solution in 0.9% sodium chloride was visually incompatible with amikacin sulfate, amphotericin B, carmustine, cefotaxime sodium, chlormethine hydrochloride, chlorpromazine hydrochloride, cimetidine hydrochloride, clindamycin phosphate, cytarabine, dacarbazine, daunorubicin hydrochloride, diphenhydramine hydrochloride, doxorubicin hydrochloride, doxycycline hyclate, droperidol, floxuridine, gentamicin sulfate, haloperidol lactate, hydroxyzine hydrochloride, idarubicin hydrochloride, imipenem with cilastatin sodium, methylprednisolone sodium succinate, metoclopramide hydrochloride, minocycline hydrochloride, nalbuphine hydrochloride, netilmicin sulfate, ondansetron hydrochloride, pethidine hydrochloride, prochlorperazine edisilate, promethazine hydrochloride, sodium bicarbonate, streptozocin, tobramycin sulfate, and vinorelbine tartrate.
The most common adverse effect of allopurinol is skin rash. Rashes are generally maculopapular or pruritic, sometimes purpuric, but more serious hyper sensitivity reactions may occur and include exfoliative rashes, the Stevens-Johnson syndrome, and toxic epidermal necrolysis. It is therefore recommended that allopurinol be withdrawn immediately if a rash occurs (see Precautions, below). Further symptoms of hypersensitivity include fever and chills, lymphadenopathy, leucopenia or leucocytosis, eosinophilia, arthralgia, and vasculitis leading to renal and hepatic damage and, very rarely, seizures. These hypersensitivity reactions may be severe, even fatal, and patients with hepatic or renal impairment are at special risk.
Hepatotoxicity and signs of altered liver function may also be found in patients who are not hypersensitive. Haematological effects include thrombocytopenia, aplastic anaemia, agranulocytosis, and haemolytic anaemia.
Many other adverse effects have been noted rarely and include paraesthesia, peripheral neuropathy, alopecia, gynaecomastia, hypertension, taste disturbances, nausea, vomiting, abdominal pain, diarrhoea, headache, malaise, drowsiness, vertigo, and visual disturbances.
Patients with gout may have an increase in acute attacks on beginning treatment with allopurinol, although attacks usually subside after several months.
Incidence of adverse effects
A Boston Collaborative Drug Surveillance Program involving 29 524 hospitalised patients found that, with the exception of skin reactions, 33 of 1835 patients treated with allopurinol (1.8%) had adverse effects. These effects were dose-related and the most frequent were haematological (11 patients, 0.6%), diarrhoea (5 patients, 0.3%), and drug fever (5 patients, 0.3%). Hepatotoxicity was reported in 3 patients (0.2%). Two patients developed possible hypersensitivity reactions to allopurinol.
A further analysis involving 1748 outpatients indicated no instances of acute blood disorders, skin diseases, or hypersensitivity that warranted hospital treatment. Liver disease, although found, was not considered to be associated with allopurinol.
There were only 2 patients in whom renal disease could possibly have been caused by allopurinol.
Effects on the blood
In addition to the haematological abnormalities of leucopenia, thrombocytopenia, haemolytic anaemia, and clotting abnormalities noted in the Boston Collaborative Drug Surveillance Program, aplastic anaemia has also been reported, sometimes in patients with renal impairment. Pure red cell aplasia has also been reported.
Effects on the eyes
Some case reports have suggested an association between allopurinol use and the development of cataracts, but a detailed ophthalmological survey involving 51 patients who had taken allopurinol failed to confirm this. However, a large retrospective case-control study in elderly patients concluded that long-term, or high-dose, allopurinol therapy did increase the risk of cataract extraction.
Effects on the skin
Skin reactions are the most common adverse effects of allopurinol.
One report calculated that of 215 adverse effects noted over a 16-year period 188 (87.4%) were related to the skin or mucous membranes. An analysis by the Boston Collaborative Drug Surveillance Program of data on 15 438 patients hospitalised between 1975 and 1982 detected 6 allergic skin reactions attributed to allopurinol among 784 recipients of the drug. Desensitisation protocols and alternative drugs have been used after cutaneous reactions to allopurinol.
Serious skin reactions to allopurinol may occur as part of a generalised hypersensitivity reaction. A review of the literature between 1970 and the end of 1990 revealed 101 cases of allopurinol hypersensitivity syndrome, 94 of which involved the skin. Skin reactions included erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necro lysis, or a diffuse maculopapular or exfoliative dermatitis; 27 of the 101 patients died. The relative risk of toxic epidermal necro lysis or Stevens-Johnson syndrome occurring with allopurinol was high (calculated to be 5.5) in a case-control study including 13 patients with these cutaneous reactions who had received allopurinol.
This risk was not constant over time, being higher during the first 2 months of treatment. During these 2 months the estimated excess risk was 1.5 cases per million users per week. Another case-control study, involving 379 patients with Stevens-Johnson syndrome or toxic epidermal necro lysis, found that allopurinol was the drug most frequently associated with these reactions. The risk again appeared to be restricted to short-term use (less than 8 weeks) and was greater in patients taking 200 mg or more daily.
Allopurinol should not be used for the treatment of an acute attack of gout; additionally, allopurinol therapy should not be begun for any purpose during an acute attack. However, allopurinol is continued when acute attacks occur in patients already receiving the drug, and the acute attack is treated separately. Treatment should be stopped immediately if any skin reactions or other signs of hypersensitivity develop. A cautious reintroduction at a low dose may be attempted when mild skin reactions have cleared (see Effects on the Skin, above); allopurinol should not be reintro-duced in those patients who have experienced other forms of hypersensitivity reaction.
Dosage should be reduced in renal or hepatic impairment. Care is advised in patients being treated for hypertension or cardiac insufficiency, who may also have renal impairment. To reduce the risk of renal xanthine deposition an adequate fluid intake (2 to 3 litres daily) is required. In addition, a neutral or slightly alkaline urine may be desirable.
Allopurinol and its metabolite, oxipurinol, are distributed into breast milk, and licensed product information recommends that allopurinol should be used with caution in breast-feeding women. Although oxipurinol was detected in the plasma of a breast-fed infant, no adverse effects were noted in the infant during 6 weeks of maternal treatment with allopurinol. The American Academy of Pediatrics noted that there had been no documented problems with allopurinol and considered its use to be usually compatible with breast feeding.
Drugs that can increase uric acid concentrations may decrease the efficacy of allopurinol. Aspirin and the salicylates possess this activity and should generally be avoided in hyperuricaemia and gout. An increase in hypersensitivity reactions, and possibly also other adverse effects, has been reported in patients taking allopurinol with ACE inhibitors orthiazide diuretics, particularly in patients with renal impairment.
The metabolism of azathioprine and mercaptopurine is inhibited by allopurinol and their doses should be markedly reduced when either of them is given with allopurinol to avoid potentially life-threatening toxicity. There have also been reports of allopurinol enhancing the activity of, and possibly increasing the toxicity of, a number of other drugs including some antibacte-rials, some anticoagulants, some other antineoplastics, ciclosporin, some sulfonylurea antidiabetics, theophyl-line, and vidarabine.
An apparent interaction between allopurinol and captopril has been reported in patients with chronic renal failure. In one patient it was suggested that the development of fatal Stevens-Johnson syndrome after the introduction of allopurinol was due to potentiation by captopril. In the second patient hypersensitivity, characterised by fever, arthralgia, and myalgia, occurred and was believed to be due to captopril, or one of its metabolites, potentiated by the addition of allopurinol. Care is advised if allopurinol is used with captopril, especially in patients with chronic renal failure.
Allopurinol failed to reduce blood-uric-acid concentrations when given at the same time as aluminium hydroxide in 3 patients on chronic haemodialysis. However, if allopurinol was given 3 hours before aluminium hydroxide the expected decrease in uric acid concentration did occur.
Although an increased incidence of skin rashes has been noted when allopurinol has been used with ampicillin or amoxicillin, data currently available are insufficient to confirm whether this is due to allopurinol or not. For further details, see Ampicillin.
For the effect of allopurinol on dicoumarol, phenprocoumon, or warfarin, see Warfarin.
For a report of allopurinol possibly inhibiting the metabolism of phenytoin, see under Antigout Drugs.
Uricosuric drugs are likely to increase the renal elimination of oxipurinol (the major active metabolite of allopurinol). For example, benzbromarone lowered plasma concentrations of oxipurinol by about 40% when used with allopurinol, although plasma concentrations of allopurinol itself were not affected. The interaction was not of concern, since the combination was more effective than allopurinol alone in lowering serum concentrations ofuric acid.
Licensed product information recommends reassessing the dosage of allopurinol on an individual basis when a uricosuric drug is added. Probenecid has been reported to decrease the clearance of oral allopurinol riboside. In a pharmacokinetic study in healthy subjects, giving allopurinol and probenecid together significantly reduced oxipurinol concentrations; however, this combination had a greater hypouricaemic effect than either drug given alone.
Allopurinol inhibits the metabolism of mercaptopurine and marked dosage reduction of this drug to one-quarter to one-third of the usual dose is required if it is used with allopurinol. There are also reports of interactions between allopurinol and other antineoplastics. Mild chronic allopurinol-induced hepatotoxicity has been reported in a male patient to have been exacerbated by tamoxifen. Hypersensitivity vasculitis resulting in the death of a patient receiving allopurinol and pentostatin has been described. Although it could not be ascertained whether this effect was due to one of the drugs alone or to an interaction it was believed that this combination should not be used.
For a report of an increased incidence of bone-marrow toxicity in patients given allopurinol with cyclophosphamide.
For the effect of allopurinol on didanosine.
Allopurinol inhibits the metabolism of mercaptopurine, the metabolite of azathioprine, and marked dosage reduction of azathioprine to one-quarter to one-third of the usual dose is required if it is used with allopurinol. Similar caution is also required with mercaptopurine itself (see Antineoplastics, above). The effects of allopurinol on ciclosporin concentrations (a marked increase) are reported.
For the effect of allopurinol on the pharmacokinetics of caffeine and theophylline.
Up to 90% of an oral dose of allopurinol is rapidly absorbed from the gastrointestinal tract; its plasma half-life is about 1 to 2 hours. Allopurinol’s major metabolite is oxipurinol (alloxanthine), which is also an inhibitor of xanthine oxidase with a plasma half-life of about 15 or more hours in patients with normal renal function, although this is greatly prolonged by renal impairment. Both allopurinol and oxipurinol are conjugated to form their respective ribonucleosides.
Allopurinol and oxipurinol are not bound to plasma proteins. Excretion is mainly through the kidney, but it is slow since oxipurinol undergoes tubular reabsorption. About 70% of a daily dose may be excreted in the urine as oxipurinol and up to 10% as allopurinol; prolonged use may alter these proportions, as allopurinol inhibits its own metabolism. The remainder of the dose is excreted in the faeces. Allopurinol and oxipurinol have also been detected in breast milk.
Uses and Administration
Allopurinol is used to treat hyperuricaemia associated with chronic gout, acute uric acid nephropa-thy, recurrent uric acid stone formation, certain enzyme disorders, or cancer and its treatment (see Tumour Lysis Syndrome). It is notused for asymptomatic hyperuricaemia. Allopurinol is also used in the management of renal calculi caused by the deposition of calcium oxalate (in the presence of hyperuricosuria) and of 2,8-dihydroxyadenine (see Renal Calculi, below). It may have the potential to reduce oxidative stress by blocking the production of free radicals and is an ingredient of kidney preservation solutions. In addition allopurinol has antiprotozoal activity and has been used in leishmaniasis and American trypanosomiasis.
Allopurinol is used in gout and hyperuricaemia to inhibit the enzyme xanthine oxidase, thus preventing the oxidation of hypoxanthine to xanthine and xanthine to uric acid. The urinary purine load, normally almost entirely uric acid, is thereby divided between hypoxanthine, xanthine, and uric acid, each with its independent solubility. This results in the reduction of urate and uric acid concentrations in plasma and urine, ideally to such an extent that deposits of monosodium urate monohydrate or uric acid are dissolved or prevented from forming. At low concentrations allopurinol acts as a competitive inhibitor of xanthine oxidase and at higher concentrations as a non-competitive inhibitor. However, most of its activity is due to the metabolite oxipurinol which is a non-competitive inhibitor of xanthine oxidase.
Allopurinol is used in chronic gout to correct hyperuricaemia, reduce the likelihood of acute attacks, and prevent the sequelae of chronic gout. Initially, it may increase plasma-concentrations of urate and uric acid by dissolving deposits. This can trigger or exacerbate acute attacks, hence allopurinol should not be started until an acute attack has completely subsided, and treatment should be started with a low dose increased gradually; an NSAID (but not aspirin or salicylates) or colchicine should also be given for at least 1 month after hyperuricaemia is corrected, usually 3 months. It may take several months to deplete the uric acid level sufficiently to control acute attacks.
A suggested oral starting dose of allopurinol is 100 mg daily, gradually increased by 100 mg for example at weekly intervals until the concentration of urate in plasma is reduced to 0.36 mmol/litre (6 mg per 100 mL) or less. A daily dose range of 100 to 300 mg may be adequate for those with mild gout and up to 600 mg for those with moderately severe tophaceous gout. The maximum recommended daily dose is 800 mg in the USA and 900 mg in the UK. Up to 300 mg may be taken as a single daily dose; larger amounts should be taken in divided doses to reduce the risk of gastric irritation. Taking allopurinol after food will also minimise gastric irritation. Patients should maintain an adequate fluid intake to prevent renal xanthine deposition.
Doses of allopurinol should be reduced in patients with renal impairment (see below)
When used for the prevention of uric acid nephropathy associated with cancer therapy 600 to 800 mg may be given daily, generally for 2 or 3 days before starting the cancer treatment. A high fluid intake is essential. In hyperuricaemia secondary to cancer or cancer chemotherapy, maintenance doses of allopurinol are similar to those used in gout and are given according to the response.
The main use of allopurinol in children is for hyperuricaemia associated with cancer or cancer chemotherapy or with enzyme disorders. The dosage used may vary: in the UK a dose of 10 to 20 mg/kg daily up to a maximum of 400 mg daily is recommended for children under 15 years of age, while in the USA the dose is 150 mg daily for children under 6 years of age and 300 mg daily for those aged 6 to 10 years, adjusted if necessary after 48 hours.
Allopurinol sodium has been given by intravenous infusion in sodium chloride 0.9% or glucose 5% to patients (usually cancer patients) unable to take allopurinol orally. The recommended dose in adults is the equivalent of allopurinol 200 to 400 mg/m daily up to a maximum of 600 mg daily. Allopurinol sodium 116.2 mg is equivalent to 100 mg of allopurinol.
Administration in renal impairment
Excretion of allopurinol and its active metabolite oxipurinol is primarily via the kidneys and therefore the dosage should be reduced in renal impairment according to creatinine clearance (CC).
In the USA the following doses are suggested for oral and intravenous use:
- CC 10 to 20 mL/mmute: 200 mg daily
- CC less than 10 mL/minute: no more than 100 mg daily
- CC less than 3 mL/minute: consider also a longer dosage interval
In the UK a maximum initial oral daily dosage of 100 mg is recommended for those with renal impairment, increased only if the response is inadequate. Doses less than 100 mg daily or 100 mg at intervals longer than 1 day are recommended for those with severe renal insufficiency. Because of the imprecision of low creatinine clearancevalues, it is suggested that, if facilities are available for monitoring, the allopurinol dose should be adjusted to maintain plasma-oxipurinol concentrations below 100 micromoles/litre (15.2 micrograms/mL). A suggested alternative dose for patients requiring dialysis two or three times weekly is 300 to 400 mg allopurinol immediately after dialysis only.
The difficulties of maintaining an appropriate dose in such patients were illustrated by a study in New Zealand involving 227 allopurinol-treated patients. The guidelines used suggested maintenance doses based on CC as follows:
- less than 10 mL/minute: 100 mg every 3 days
- 10 mL/minute: 100 mg every 2 days
- 20 mL/minute: 100 mg daily
- 40 mL/minute: 150 mg daily
- 60 mL/minute: 200 mg daily
The recommended dose or less was used in the majority of cases (183 of 227). However, of 214 patients for whom serum-uric acid concentrations were available, only 48 achieved values of 0.36 mmol/litre or less. The proportion of patients achieving acceptable serum-uric acid concentrations was higher (38%) in patients given higher than recommended doses than in those on doses recommended by the guidelines (19%). Although guidelines might be useful for initial dosing, longer term use could lead to inadequate control of hyperuricaemia.
Diagnosis and testing
Deficiency of the enzyme ornithine carbamoyltransferase can result in severe CNS dysfunction or even in death, and identification of women at risk of being carriers of this genetic enzyme deficiency has been described. The enzyme deficiency causes carbamoyl phosphate to accumulate, which stimulates the synthesis of orotidine. The test relies on giving a single dose of allopurinol, which will, in carriers, greatly increase the urinary excretion of orotidine. However, mutation analysis is now more usually used to establish the diagnosis.
Duchenne muscular dystrophy
Controlled studies of the use of allopurinol in an attempt to increase muscle ATP in Duchenne muscular dystrophy failed to show any benefit from treatment.
Reduction in the frequency of seizures has been described in some patients with severe or intractable epilepsy when allopurinol was added to their existing antiepileptic therapy. Although the mode of action was not known it was noted that the patients were not hyperuricaemic and that allopurinol did not affect plasma concentrations of existing antiepileptics. However, others have seen no benefit.
Organ and tissue transplantation
Allopurinol 25 mg on alternate days has been added to the immunosuppressive treatment for renal transplantation, and is reported to reduce the frequency of acute rejection. One possible explanation for this effect is allopurinors ability to suppress the production of free radicals (see Oxidative Stress, below). Organ and tissue transplantation, and the more usual drugs used in immunosuppressive regimens are discussed. It should be noted that allopurinol interacts with azathioprine (see Immunosuppressants, under Interactions, above) and ciclosporin.
Allopurinol, through its inhibition of xanthine oxidase, can block the development of superoxide free radicals during reperfusion after an ischaemic episode. Consequently, the ability of allopurinol to reduce oxidative stress has been investigated in a number of clinical situations. In a small study of patients with idiopathic dilated cardiomyopathy, short-term intracoronary allopurinol improved myocardial efficiency by decreasing the oxygen demand of left ventricular contraction.
In patients undergoing coronary artery bypass graft surgery, perioperative allopurinol reduced hospital mortality, the incidence of arrhythmias, the number of ischaemic events, and the need for inotropic support, although the findings were not consistent in all studies.
Improved endothehal dysfunction has been found in patients with chronic heart failure given allopurinol. A large study in neonates undergoing cardiac surgery found that allopurinol caused a reduction in seizures and cardiac events in those with hypoplastic left heart syndrome. No benefit was found in neonates with less severe forms of congenital heart disease, considered to be at lower risk of adverse surgical outcome or reperfusion injury.
Allopurinol also failed to reduce the incidence of periventricular leucomalacia (thought to represent ischaemic infarction of the developing brain) in preterm infants compared with placebo in a large study. Similarly, allopurinol did not reduce the incidence of infarct extension in patients with acute myocardial infarction.
The possibility that allopurinol limits the production of free radicals has also led to allopurinol sodium being included as an ingredient of the University of Wisconsin solution [UW Solution; Belzer UW Solution (commercially available as Viaspan)] which is used for the preservation of organs for transplantation. A pilot study using allopurinol showed a beneficial effect on free radical formation, cerebral blood volume, and electrical brain activity in severely asphyxiated newborns. However, a systematic review of this and 2 other studies in such infants was unable to determine whether allopurinol produced clinically important benefits.
Although allopurinol has been reported to be of benefit in a small study in patients with chronic prostatitis, a systematic review found no other satisfactory evidence of benefit, and considered that the clinical relevance of the original study results was unclear.
Allopurinol has been widely used as an adjunct to pentavalent antimonials in the treatment of Old World visceral leishmaniasis, particularly where resistance to antimony alone is likely, although the degree of benefit has been called into question. It has also been used with other drugs such as pentamidine or azole antifungals, including in transplant patients or those with AIDS, or in whom antimonials were otherwise poorly tolerated. Allopurinol has also been tried alone or with other drugs in both Old World and New World cutaneous or mucocutaneous leishmaniasis; results, particularly in the latter, have been variable.
Some beneficial results have been noted in indeterminate and chronic Chagas’ disease (American trypanosomiasis), although it may be less effective than itraconazole. The selective antiparasitic action of allopurinol is believed to be due to its incorporation into the protozoal, but not the mammalian, purine salvage pathway. This leads to the formation of 4-aminopyrazolopyrimidine ribonucleotide triphosphate, a highly toxic analogue of adenosine triphosphate, that is incorporated into ribonucleic acid. This action of allopurinol is shared by allopurinol riboside, one of the minor metabolites in man, but not by oxipurinol, the major human metabolite. Thus, some studies have been conducted with allopurinol riboside, rather than allopurinol, in an attempt to enhance activity by avoiding host-mediated inactivation.
In conjunction with a reduced dietary purine intake, high fluid intake, and potassium citrate, allopurinol may be used to prevent the recurrence of calcium oxalate renal calculi in patients with hyperuricosuria. The recommended oral dose of allopurinol is 200 to 300 mg daily adjusted on the basis of subsequent 24-hour urinary urate excretion. Allopurinol is also advocated for the management of 2,8-dihydroxyadenine (2,8-DHA) renal stones associated with deficient activity of the enzyme adenine phosphoribosyltransferase.
Although corticosteroids remain the mainstay of drug therapy for sarcoidosis, and other drugs are very much second line, there are reports of benefit in cutaneous disease from the use of allopurinol.
Involvement of purinergic neurotransmission has been hypothesised to play some role in schizophrenia, and allopurinol has been investigated as a possible adjunctive treatment, with some evidence of benefit, especially in patients with refractory positive symptoms.
Reactive perforating collagenosis (RPC) is a condition in which altered collagen is eliminated through the epidermis; it may be inherited or acquired. In 3 of 4 patients with RPC refractory to antibacterials and oral and topical corticosteroids, significant improvement was seen with allopurinol, in terms of reduction of new lesions, improvement of existing lesions, and reduction of pruritus. The fourth patient died from unrelated causes before review.
British Pharmacopoeia 2008; Allopurinol Tablets;
The United States Pharmacopeia 31, 2008, and Supplements 1 and 2: Allopurinol Oral Suspension; Allopurinol Tablets.
The symbol ¤ denotes a preparation which is discontinued or no longer actively marketed.
Argentina: Alfadiman; Alloboxal¤; Gotir¤; Puritenk;
Australia: Allohexal; Alloremed¤; Allorin¤; Allosig; Capurate; Progout; Zygout¤; Zyloprim;
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Netherlands: Apurin; Zyloric;
Norway: Allopur; Arturic; Zyloric;
New Zealand: Allohexal; Allorin; Progout; Z 300¤; Zyloprim¤;
Portugal: Alosfar; Uriprim; Zurim; Zyloric; Russia: Purinol (Пуринол);
South Africa: Abburic¤; Be-Uric¤; Ethipurinol¤; Lo-Uric¤; Lonol; Puricos; Pyrazol¤; Ranpuric¤; Redurate; Urinol; Urozyl-SR¤; Zyloprim; Singapore: Allorin¤; Erloric¤; Progout; Valeric¤; Zyloric;
Spain: Allopurin¤; Allural¤; Zyloric;
Sweden: Zyloric; Switzerland: Allo-300-Tablinen¤; allo-basan; Allopur; Cellidrine; Foligan¤; Lysuron¤; Mephanol; Sigapurol N; Uredimin¤; Uriconorme; Zyloric;
Thailand: Alinol; Allopin; Allorin¤; Apnol; Apurol; Loporic¤; Medoric; Mephanol¤; Puricin; Puride; Sigapurol¤; Uricad; Valeric; Xanol; Zyloric;
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Argentina: Artrex; Colpuril;
Austria: Allobenz; Duovitan¤; Gichtex plus; Uroplus¤;
Belgium: Comburic; France: Anurate¤; Desatura¤;
Germany: Acifugan¤; Allo.comp.; Allomaron¤; Harpagin; Uricovac comp¤;
Italy: Uricodue; Urifugan¤; Portugal: Acifugan¤;
South Africa: Allomaron;
Spain: Acifugan¤; Biuricowas¤; Facilit¤; Uricina¤;