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{{Short description|Medication}}
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===Pharmacogenetics===
===Pharmacogenetics===
The HLA-B*5801 allele is a [[genetic marker]] for allopurinol-induced severe cutaneous adverse reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).<ref name="pharmgkb.org">{{cite web | title = Uric Acid-Lowering Drugs Pathway, Pharmacodynamics | work = PharmGKB | url = http://www.pharmgkb.org/haplotype/PA165956630#tabview=tab3&subtab= | archive-url = https://web.archive.org/web/20140808045855/http://www.pharmgkb.org/haplotype/PA165956630 | archive-date=8 August 2014 }}</ref><ref name="ReferenceA">{{cite web |url=http://www.pharmgkb.org/pathway/PA165980774 |title=PharmGKB |access-date=1 August 2014 |url-status=live |archive-url=https://web.archive.org/web/20140808045844/http://www.pharmgkb.org/pathway/PA165980774 |archive-date=8 August 2014 }}</ref> The frequency of the HLA-B*5801 allele varies between ethnicities: Han Chinese and Thai populations have HLA-B*5801 [[allele frequency|allele frequencies]] of around 8%, as compared to European and Japanese populations, who have allele frequencies of around 1.0% and 0.5%, respectively.<ref>{{cite web | title = Allele Frequency Net Database | url = http://www.allelefrequencies.net | archive-url = https://web.archive.org/web/20090828074156/http://www.allelefrequencies.net/ | archive-date=28 August 2009 }}</ref> The increase in risk for developing allopurinol-induced SJS or TEN in individuals with the HLA-B*5801 allele (as compared to those who do not have this allele) is very high, ranging from a 40-fold to a 580-fold increase in risk, depending on ethnicity.<ref name="pharmgkb.org"/><ref name="ReferenceA"/> As of 2011 the FDA-approved drug label for allopurinol did not contain any information regarding the HLA-B*5801 allele, though FDA scientists did publish a study in 2011 which reported a strong, reproducible and consistent association between the allele and allopurinol-induced SJS and TEN.<ref>{{cite journal | vauthors = Zineh I, Mummaneni P, Lyndly J, Amur S, La Grenade LA, Chang SH, Rogers H, Pacanowski MA | display-authors = 6 | title = Allopurinol pharmacogenetics: assessment of potential clinical usefulness | journal = Pharmacogenomics | volume = 12 | issue = 12 | pages = 1741–9 | date = December 2011 | pmid = 22118056 | doi = 10.2217/pgs.11.131 | url = https://zenodo.org/record/1236437 }}</ref> However, the American College of Rheumatology recommends screening for HLA-B*5801 in high-risk populations (''e.g.'' Koreans with stage 3 or worse chronic kidney disease and those of Han Chinese and Thai descent), and prescribing patients who are positive for the allele an alternative drug.<ref>{{cite journal | vauthors = Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, Pillinger MH, Merill J, Lee S, Prakash S, Kaldas M, Gogia M, Perez-Ruiz F, Taylor W, Lioté F, Choi H, Singh JA, Dalbeth N, Kaplan S, Niyyar V, Jones D, Yarows SA, Roessler B, Kerr G, King C, Levy G, Furst DE, Edwards NL, Mandell B, Schumacher HR, Robbins M, Wenger N, Terkeltaub R | display-authors = 6 | title = 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia | journal = Arthritis Care & Research | volume = 64 | issue = 10 | pages = 1431–46 | date = October 2012 | pmid = 23024028 | pmc = 3683400 | doi = 10.1002/acr.21772 }}</ref> The Clinical Pharmacogenetics Implementation Consortium (CPIC)<ref>{{Cite web |date=2023-11-27 |title=CPIC |url=https://cpicpgx.org/ |access-date=2023-12-10}}</ref> guidelines state that allopurinol is contraindicated in known carriers of the HLA-B*5801 allele.<ref>{{cite web |url=http://www.pharmgkb.org/guideline/PA166105003 |work = PharmGKB | title = Annotation of CPIC Guideline for allopurinol and HLA-B |access-date=1 August 2014 |url-status=live |archive-url= https://web.archive.org/web/20140808045834/http://www.pharmgkb.org/guideline/PA166105003 |archive-date=8 August 2014 }}</ref><ref>{{cite journal | vauthors = Hershfield MS, Callaghan JT, Tassaneeyakul W, Mushiroda T, Thorn CF, Klein TE, Lee MT | title = Clinical Pharmacogenetics Implementation Consortium guidelines for human leukocyte antigen-B genotype and allopurinol dosing | journal = Clinical Pharmacology and Therapeutics | volume = 93 | issue = 2 | pages = 153–8 | date = February 2013 | pmid = 23232549 | pmc = 3564416 | doi = 10.1038/clpt.2012.209 }}</ref>
The HLA-B*5801 allele is a [[genetic marker]] for allopurinol-induced severe cutaneous adverse reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).<ref name="pharmgkb.org">{{cite web | title = Uric Acid-Lowering Drugs Pathway, Pharmacodynamics | work = PharmGKB | url = http://www.pharmgkb.org/haplotype/PA165956630#tabview=tab3&subtab= | archive-url = https://web.archive.org/web/20140808045855/http://www.pharmgkb.org/haplotype/PA165956630 | archive-date=8 August 2014 }}</ref><ref name="ReferenceA">{{cite web |url=http://www.pharmgkb.org/pathway/PA165980774 |title=PharmGKB |access-date=1 August 2014 |url-status=live |archive-url=https://web.archive.org/web/20140808045844/http://www.pharmgkb.org/pathway/PA165980774 |archive-date=8 August 2014 }}</ref> The frequency of the HLA-B*5801 allele varies between ethnicities: Han Chinese and Thai populations have HLA-B*5801 [[allele frequency|allele frequencies]] of around 8%, as compared to European and Japanese populations, who have allele frequencies of around 1.0% and 0.5%, respectively.<ref>{{cite web | title = Allele Frequency Net Database | url = http://www.allelefrequencies.net | archive-url = https://web.archive.org/web/20090828074156/http://www.allelefrequencies.net/ | archive-date=28 August 2009 }}</ref> The increase in risk for developing allopurinol-induced SJS or TEN in individuals with the HLA-B*5801 allele (as compared to those who do not have this allele) is very high, ranging from a 40-fold to a 580-fold increase in risk, depending on ethnicity.<ref name="pharmgkb.org"/><ref name="ReferenceA"/> As of 2011 the FDA-approved drug label for allopurinol did not contain any information regarding the HLA-B*5801 allele, though FDA scientists did publish a study in 2011 which reported a strong, reproducible and consistent association between the allele and allopurinol-induced SJS and TEN.<ref>{{cite journal | vauthors = Zineh I, Mummaneni P, Lyndly J, Amur S, La Grenade LA, Chang SH, Rogers H, Pacanowski MA | display-authors = 6 | title = Allopurinol pharmacogenetics: assessment of potential clinical usefulness | journal = Pharmacogenomics | volume = 12 | issue = 12 | pages = 1741–9 | date = December 2011 | pmid = 22118056 | doi = 10.2217/pgs.11.131 | url = https://zenodo.org/record/1236437 }}</ref> However, the American College of Rheumatology recommends screening for HLA-B*5801 in high-risk populations (''e.g.'' Koreans with stage 3 or worse chronic kidney disease and those of Han Chinese and Thai descent), and prescribing patients who are positive for the allele an alternative drug.<ref>{{cite journal | vauthors = Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, Pillinger MH, Merill J, Lee S, Prakash S, Kaldas M, Gogia M, Perez-Ruiz F, Taylor W, Lioté F, Choi H, Singh JA, Dalbeth N, Kaplan S, Niyyar V, Jones D, Yarows SA, Roessler B, Kerr G, King C, Levy G, Furst DE, Edwards NL, Mandell B, Schumacher HR, Robbins M, Wenger N, Terkeltaub R | display-authors = 6 | title = 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia | journal = Arthritis Care & Research | volume = 64 | issue = 10 | pages = 1431–46 | date = October 2012 | pmid = 23024028 | pmc = 3683400 | doi = 10.1002/acr.21772 }}</ref> The Clinical Pharmacogenetics Implementation Consortium (CPIC)<ref>{{Cite web |date=27 November 2023 |title=CPIC |url=https://cpicpgx.org/ |access-date=10 December 2023}}</ref> guidelines state that allopurinol is contraindicated in known carriers of the HLA-B*5801 allele.<ref>{{cite web |url=http://www.pharmgkb.org/guideline/PA166105003 |work = PharmGKB | title = Annotation of CPIC Guideline for allopurinol and HLA-B |access-date=1 August 2014 |url-status=live |archive-url= https://web.archive.org/web/20140808045834/http://www.pharmgkb.org/guideline/PA166105003 |archive-date=8 August 2014 }}</ref><ref>{{cite journal | vauthors = Hershfield MS, Callaghan JT, Tassaneeyakul W, Mushiroda T, Thorn CF, Klein TE, Lee MT | title = Clinical Pharmacogenetics Implementation Consortium guidelines for human leukocyte antigen-B genotype and allopurinol dosing | journal = Clinical Pharmacology and Therapeutics | volume = 93 | issue = 2 | pages = 153–8 | date = February 2013 | pmid = 23232549 | pmc = 3564416 | doi = 10.1038/clpt.2012.209 }}</ref>


== History ==
== History ==

Revision as of 05:33, 18 January 2024

Allopurinol
Clinical data
Trade namesZyloprim, Caplenal, Zyloric, others
AHFS/Drugs.comMonograph
MedlinePlusa682673
License data
Pregnancy
category
Routes of
administration		Oral, intravenous
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability78±20%
Protein bindingNegligible
Metabolismliver (80% oxipurinol, 10% allopurinol ribosides)
Elimination half-life2 h (oxipurinol 18–30 h)
Identifiers
  • 1H-Pyrazolo[3,4-d]pyrimidin-4(2H)-one
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.005.684 Edit this at Wikidata
Chemical and physical data
FormulaC5H4N4O
Molar mass136.114 g·mol−1
3D model (JSmol)
  • C1=NNC2=C1C(=O)NC=N2
  • InChI=1S/C5H4N4O/c10-5-3-1-8-9-4(3)6-2-7-5/h1-2H,(H2,6,7,8,9,10) checkY
  • Key:OFCNXPDARWKPPY-UHFFFAOYSA-N checkY
  (verify)

Allopurinol is a medication used to decrease high blood uric acid levels.[4] It is specifically used to prevent gout, prevent specific types of kidney stones and for the high uric acid levels that can occur with chemotherapy.[5][6] It is taken orally (by mouth) or intravenously (injected into a vein).[6]

Common side effects when used orally include itchiness and rash.[6] Common side effects when used by injection include vomiting and kidney problems.[6] While not recommended historically, starting allopurinol during an attack of gout appears to be safe.[7][8] In those already on the medication, it should be continued even during an acute gout attack.[7][5] While use during pregnancy does not appear to result in harm, this use has not been well studied.[1] Allopurinol is in the xanthine oxidase inhibitor family of medications.[6]

Allopurinol was approved for medical use in the United States in 1966.[6] It is on the World Health Organization's List of Essential Medicines.[9][10] Allopurinol is available as a generic medication.[6] In 2021, it was the 40th most commonly prescribed medication in the United States, with more than 15 million prescriptions.[11][12]

Medical uses

Gout

Allopurinol is used to reduce urate formation in conditions where urate deposition has already occurred or is predictable. The specific diseases and conditions where it is used include gouty arthritis, skin tophi, kidney stones, idiopathic gout; uric acid lithiasis; acute uric acid nephropathy; neoplastic disease and myeloproliferative disease with high cell turnover rates, in which high urate levels occur either spontaneously, or after cytotoxic therapy; certain enzyme disorders which lead to overproduction of urate, for example: hypoxanthine-guanine phosphoribosyltransferase, including Lesch–Nyhan syndrome; glucose 6-phosphatase including glycogen storage disease; phosphoribosyl pyrophosphate synthetase, phosphoribosyl pyrophosphate amidotransferase; adenine phosphoribosyltransferase.

It is also used to treat kidney stones caused by deficient activity of adenine phosphoribosyltransferase.

Tumor lysis syndrome

Allopurinol was also commonly used to treat tumor lysis syndrome in chemotherapeutic treatments, as these regimens can rapidly produce severe acute hyperuricemia;[13] however, it has gradually been replaced by urate oxidase therapy.[14] Intravenous formulations are used in this indication when people are unable to swallow medication.[3]

Inflammatory bowel disease

Allopurinol cotherapy is used to improve outcomes for people with inflammatory bowel disease and Crohn's disease who do not respond to thiopurine monotherapy.[15][16] Cotherapy has also been shown to greatly improve hepatoxicity side effects in treatment of IBD.[17] Cotherapy invariably requires dose reduction of the thiopurine, usually to one-third of the standard dose depending upon the patient's genetic status for thiopurine methyltransferase.[18]

Psychiatric disorders

Allopurinol has been tested as an augmentation strategy for the treatment of mania in bipolar disorder. Meta-analytic evidence showed that adjunctive allopurinol was superior to placebo for acute mania (both with and without mixed features).[19] Its efficacy was not influenced by dosage, follow-up duration, or concurrent standard treatment.[19]

Cardiovascular disease

There is a correlation between uric acid levels and cardiovascular disease and mortality, and so allopurinol has been explored as a potential treatment to reduce risk of cardiac disease.[20] However, the data is inconsistent and conflicting, and the use of allopurinol for use in cardiovascular disease is controversial. Independently of its effects on uric acid, it may also have effects on oxidative stress and inflammation.[21]

Side effects

Because allopurinol is not a uricosuric, it can be used in people with poor kidney function. However, for people with impaired kidney function, allopurinol has two disadvantages. First, its dosing is complex.[22] Second, some people are hypersensitive to the drug; therefore, its use requires careful monitoring.[23][24]

Allopurinol has rare but potentially fatal adverse effects involving the skin. The most serious adverse effect is a hypersensitivity syndrome consisting of fever, skin rash, eosinophilia, hepatitis, and worsened renal function, collectively referred to as DRESS syndrome.[23] Allopurinol is one of the drugs commonly known to cause Stevens–Johnson syndrome and toxic epidermal necrolysis, two life-threatening dermatological conditions.[23] More common is a less-serious rash that leads to discontinuing this drug.[23]

More rarely, allopurinol can also result in the depression of bone marrow elements, leading to cytopenias, as well as aplastic anemia. Moreover, allopurinol can also cause peripheral neuritis in some patients, although this is a rare side effect. Another side effect of allopurinol is interstitial nephritis.[25]

Drug interactions

Drug interactions are extensive, and are as follows:[13]

  • Azathioprine and 6-mercaptopurine: Azathioprine is metabolised to 6-mercaptopurine which in turn is inactivated by the action of xanthine oxidase - the target of allopurinol. Giving allopurinol with either of these drugs at their normal dose will lead to overdose of either drug; only one-quarter of the usual dose of 6-mercaptopurine or azathioprine should be given;
  • Didanosine: plasma didanosine Cmax and AUC values were approximately doubled with concomitant allopurinol treatment; it should not be co-administered with allopurinol and if it must be, the dose of should be reduced and the person should be closely monitored.

Allopurinol may also increase the activity or half-life of the following drugs, in order of seriousness and certainty of the interaction:[13]

Co-administration of the following drugs may make allopurinol less active or decrease its half-life:[13]

Co-administration of the following drugs may cause hypersensitivity or skin rash:[13]

Pharmacology

A common misconception is that allopurinol is metabolized by its target, xanthine oxidase, but this action is principally carried out by aldehyde oxidase.[26] The active metabolite of allopurinol is oxipurinol, which is also an inhibitor of xanthine oxidase. Allopurinol is almost completely metabolized to oxipurinol within two hours of oral administration, whereas oxipurinol is slowly excreted by the kidneys over 18–30 hours. For this reason, oxipurinol is believed responsible for the majority of allopurinol's effect.[27]

Mechanism of action

Allopurinol is a purine analog; it is a structural isomer of hypoxanthine (a naturally occurring purine in the body) and is an inhibitor of the enzyme xanthine oxidase.[4] Xanthine oxidase is responsible for the successive oxidation of hypoxanthine to xanthine and subsequently uric acid, the product of human purine metabolism.[4] In addition to blocking uric acid production, inhibition of xanthine oxidase causes an increase in hypoxanthine and xanthine. While xanthine cannot be converted to purine ribonucleotides, hypoxanthine can be salvaged to the purine ribonucleotides adenosine and guanosine monophosphates. Increased levels of these ribonucleotides may cause feedback inhibition of amidophosphoribosyl transferase, the first and rate-limiting enzyme of purine biosynthesis. Allopurinol, therefore, decreases uric acid formation and may also inhibit purine synthesis.[28]

Pharmacogenetics

The HLA-B*5801 allele is a genetic marker for allopurinol-induced severe cutaneous adverse reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).[29][30] The frequency of the HLA-B*5801 allele varies between ethnicities: Han Chinese and Thai populations have HLA-B*5801 allele frequencies of around 8%, as compared to European and Japanese populations, who have allele frequencies of around 1.0% and 0.5%, respectively.[31] The increase in risk for developing allopurinol-induced SJS or TEN in individuals with the HLA-B*5801 allele (as compared to those who do not have this allele) is very high, ranging from a 40-fold to a 580-fold increase in risk, depending on ethnicity.[29][30] As of 2011 the FDA-approved drug label for allopurinol did not contain any information regarding the HLA-B*5801 allele, though FDA scientists did publish a study in 2011 which reported a strong, reproducible and consistent association between the allele and allopurinol-induced SJS and TEN.[32] However, the American College of Rheumatology recommends screening for HLA-B*5801 in high-risk populations (e.g. Koreans with stage 3 or worse chronic kidney disease and those of Han Chinese and Thai descent), and prescribing patients who are positive for the allele an alternative drug.[33] The Clinical Pharmacogenetics Implementation Consortium (CPIC)[34] guidelines state that allopurinol is contraindicated in known carriers of the HLA-B*5801 allele.[35][36]

History

Allopurinol was first synthesized and reported in 1956 by Roland K. Robins (1926-1992), in a search for antineoplastic agents.[4][37] Because allopurinol inhibits the breakdown (catabolism) of the thiopurine drug mercaptopurine, and it was later tested by Wayne Rundles, in collaboration with Gertrude Elion's lab at Wellcome Research Laboratories to see if it could improve treatment of acute lymphoblastic leukemia by enhancing the action of mercaptopurine.[4][38] However, no improvement in leukemia response was noted with mercaptopurine-allopurinol co-therapy, so that work turned to other compounds and the team then started testing allopurinol as a potential therapeutic for gout.[39] Allopurinol was first marketed as a treatment for gout in 1966.[38]

Society and culture

Pure allopurinol is a white powder.

Formulations

Allopurinol is sold as an injection for intravenous use[3] and as a tablet.[13]

Brands

Allopurinol has been marketed in the United States since 19 August 1966, when it was first approved by FDA under the trade name Zyloprim.[40] Allopurinol was marketed at the time by Burroughs Wellcome. Allopurinol is a generic drug sold under a variety of brand names, including Allohexal, Allosig, Milurit, Alloril, Progout, Ürikoliz, Zyloprim, Zyloric, Zyrik, and Aluron.[41]

See also

References

  1. ^ a b "Allopurinol Use During Pregnancy". Drugs.com. Archived from the original on 20 August 2016. Retrieved 20 December 2016.
  2. ^ "Allopurinol tablet". DailyMed. 13 December 2023. Retrieved 16 January 2024.
  3. ^ a b c "Label for injectable Allopurinol". DailyMed. June 2014. Archived from the original on 13 September 2016.
  4. ^ a b c d e Pacher P, Nivorozhkin A, Szabó C (March 2006). "Therapeutic effects of xanthine oxidase inhibitors: renaissance half a century after the discovery of allopurinol". Pharmacological Reviews. 58 (1): 87–114. doi:10.1124/pr.58.1.6. PMC 2233605. PMID 16507884.
  5. ^ a b World Health Organization (2009). Stuart MC, Kouimtzi M, Hill SR (eds.). WHO Model Formulary 2008. World Health Organization. p. 39. hdl:10665/44053. ISBN 9789241547659.
  6. ^ a b c d e f g "Allopurinol". The American Society of Health-System Pharmacists. Archived from the original on 29 April 2016. Retrieved 8 December 2016.
  7. ^ a b Robinson PC, Stamp LK (May 2016). "The management of gout: Much has changed". Australian Family Physician. 45 (5): 299–302. PMID 27166465.
  8. ^ Satpanich P, Pongsittisak W, Manavathongchai S (January 2022). "Early versus Late Allopurinol Initiation in Acute Gout Flare (ELAG): a randomized controlled trial". Clinical Rheumatology. 41 (1): 213–221. doi:10.1007/s10067-021-05872-8. PMID 34406530. S2CID 237156638.
  9. ^ World Health Organization (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. hdl:10665/325771. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
  10. ^ World Health Organization (2021). World Health Organization model list of essential medicines: 22nd list (2021). Geneva: World Health Organization. hdl:10665/345533. WHO/MHP/HPS/EML/2021.02.
  11. ^ "The Top 300 of 2021". ClinCalc. Archived from the original on 15 January 2024. Retrieved 14 January 2024.
  12. ^ "Allopurinol - Drug Usage Statistics". ClinCalc. Retrieved 14 January 2024.
  13. ^ a b c d e f "300 mg Allopurinol tables". UK Electronic Medicines Compendium. 7 April 2016. Archived from the original on 11 September 2016.
  14. ^ Jeha S (October 2001). "Tumor lysis syndrome". Seminars in Hematology. 38 (4 Suppl 10): 4–8. doi:10.1016/S0037-1963(01)90037-X. PMID 11694945.
  15. ^ Bradford K, Shih DQ (October 2011). "Optimizing 6-mercaptopurine and azathioprine therapy in the management of inflammatory bowel disease". World Journal of Gastroenterology. 17 (37): 4166–73. doi:10.3748/wjg.v17.i37.4166. PMC 3208360. PMID 22072847.
  16. ^ Sparrow MP, Hande SA, Friedman S, Cao D, Hanauer SB (February 2007). "Effect of allopurinol on clinical outcomes in inflammatory bowel disease nonresponders to azathioprine or 6-mercaptopurine". Clinical Gastroenterology and Hepatology. 5 (2): 209–14. doi:10.1016/j.cgh.2006.11.020. PMID 17296529.
  17. ^ Ansari A, Patel N, Sanderson J, O'Donohue J, Duley JA, Florin TH (March 2010). "Low-dose azathioprine or mercaptopurine in combination with allopurinol can bypass many adverse drug reactions in patients with inflammatory bowel disease". Alimentary Pharmacology & Therapeutics. 31 (6): 640–7. doi:10.1111/j.1365-2036.2009.04221.x. PMID 20015102. S2CID 6000856.
  18. ^ Ansari AR, Duley JA (March 2012). "Azathioprine co-therapy with allopurinol for inflammatory bowel disease: trials and tribulations" (PDF). Rev Assoc Med Bras. 58 (Suppl.1): S28–33.
  19. ^ a b Bartoli F, Cavaleri D, Bachi B, Moretti F, Riboldi I, Crocamo C, Carrà G (September 2021). "Repurposed drugs as adjunctive treatments for mania and bipolar depression: A meta-review and critical appraisal of meta-analyses of randomized placebo-controlled trials". Journal of Psychiatric Research. 143: 230–238. doi:10.1016/j.jpsychires.2021.09.018. PMID 34509090. S2CID 237485915.
  20. ^ Kelkar A, Kuo A, Frishman WH (November 2011). "Allopurinol as a cardiovascular drug". Cardiology in Review. 19 (6): 265–271. doi:10.1097/CRD.0b013e318229a908. PMID 21983313. S2CID 7385203.
  21. ^ Connor M (January 2009). "Allopurinol for pain relief: more than just crystal clearance?". British Journal of Pharmacology. 156 (1): 4–6. doi:10.1111/j.1476-5381.2008.00065.x. PMC 2697767. PMID 19133987.
  22. ^ Dalbeth N, Stamp L (2007). "Allopurinol dosing in renal impairment: walking the tightrope between adequate urate lowering and adverse events". Seminars in Dialysis. 20 (5): 391–5. doi:10.1111/j.1525-139X.2007.00270.x. PMID 17897242. S2CID 1150852.
  23. ^ a b c d Chung WH, Wang CW, Dao RL (July 2016). "Severe cutaneous adverse drug reactions". The Journal of Dermatology. 43 (7): 758–66. doi:10.1111/1346-8138.13430. PMID 27154258. S2CID 45524211.
  24. ^ Tsai TF, Yeh TY (2010). "Allopurinol in dermatology". American Journal of Clinical Dermatology. 11 (4): 225–32. doi:10.2165/11533190-000000000-00000. PMID 20509717. S2CID 36847530.
  25. ^ De Broe ME, Bennett WM, Porter GA (2003). Clinical Nephrotoxins: Renal Injury from Drugs and Chemicals. Springer Science+Business Media. ISBN 9781402012778. Acute interstitial nephritis has also been reported associated with by the administration of allopurinol.
  26. ^ Reiter S, Simmonds HA, Zöllner N, Braun SL, Knedel M (March 1990). "Demonstration of a combined deficiency of xanthine oxidase and aldehyde oxidase in xanthinuric patients not forming oxipurinol". Clinica Chimica Acta; International Journal of Clinical Chemistry. 187 (3): 221–34. doi:10.1016/0009-8981(90)90107-4. PMID 2323062.
  27. ^ Day RO, Graham GG, Hicks M, McLachlan AJ, Stocker SL, Williams KM (2007). "Clinical pharmacokinetics and pharmacodynamics of allopurinol and oxypurinol". Clinical Pharmacokinetics. 46 (8): 623–44. doi:10.2165/00003088-200746080-00001. PMID 17655371. S2CID 20369375.
  28. ^ Cameron JS, Moro F, Simmonds HA (February 1993). "Gout, uric acid and purine metabolism in paediatric nephrology". Pediatric Nephrology. 7 (1): 105–18. doi:10.1007/BF00861588. PMID 8439471. S2CID 34815040.
  29. ^ a b "Uric Acid-Lowering Drugs Pathway, Pharmacodynamics". PharmGKB. Archived from the original on 8 August 2014.
  30. ^ a b "PharmGKB". Archived from the original on 8 August 2014. Retrieved 1 August 2014.
  31. ^ "Allele Frequency Net Database". Archived from the original on 28 August 2009.
  32. ^ Zineh I, Mummaneni P, Lyndly J, Amur S, La Grenade LA, Chang SH, et al. (December 2011). "Allopurinol pharmacogenetics: assessment of potential clinical usefulness". Pharmacogenomics. 12 (12): 1741–9. doi:10.2217/pgs.11.131. PMID 22118056.
  33. ^ Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, et al. (October 2012). "2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia". Arthritis Care & Research. 64 (10): 1431–46. doi:10.1002/acr.21772. PMC 3683400. PMID 23024028.
  34. ^ "CPIC". 27 November 2023. Retrieved 10 December 2023.
  35. ^ "Annotation of CPIC Guideline for allopurinol and HLA-B". PharmGKB. Archived from the original on 8 August 2014. Retrieved 1 August 2014.
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Further reading

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