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BY-DR. MADHUMITA DIXIT
JR-3
PHARMACOLOGY DEPARTMENT
MLN MEDICAL COLLEGE
PRAYAGRAJ, UP
Allopurinol
Introduction-
 Allopurinol, an Anti-gout
drug is used as Uric acid
synthesis inhibitor.
 It is on the World Health
Organization's List of
Essential Medicines.
Allopurinol (Anti-gout drug).pptx
Mechanism of action-
Hypoxanthine
Xanthine urate
Xanthine oxidase
Allopurinol
Oxypurinol
-
Allopurinol acts on purine catabolism, and thus reduces
production of urate without disrupting the biosynthesis
of vital purines.
• Allopurinol also is a substrate of Xanthine
oxidase
• It is a competitive inhibitor of Xanthine
oxidase at low concentrations and non-
Competitive inhibitor of Xanthine oxidase at
higher concentrations.
• Oxypurinol is Non-competitive inhibitor of
Xanthine Oxidase.
Uses-
 Gout treatment (chronic urate-lowering therapy)also facilitates
dissolution of Tophi and inhibits development or progression
of Chronic Gouty Arthritis.
 Nephrolithiasis (prevention of recurrent calcium or uric acid stones)
 Tumor lysis syndrome prevention (To prevent hyperuricemia in
patients with hematological malignancies about to undergo
chemotherapy)
 Inflammatory Bowel Disease
IN CHILDREN-
 Lesch-Nyhan syndrome (Hyperuricemia associated
with errors of purine metabolism)
 Glycogen storage diseases(recurrent calcium oxalate renal stones)
Pharmacokinetics-
 Bioavailability- 78 ±20%
 Plasma Protein Binding-Negligible
 Metabolism-Liver (80% oxipurinol,10% allopurinol
ribosides)
 Elimination half life -2 hours (Oxypurinol 18-30 hours)
 Elimination-Feces-20%
urine-10-30%
Colchicine + Allopurinol
 The incidence of acute attacks of gouty arthritis
may increase during the early months of
allopurinol therapy as a consequence of
mobilization of tissue stores of uric acid.
 Coadministration of colchicine helps suppress
such acute attacks. After reduction of excess
tissue stores of uric acid, the incidence of acute
attacks decreases and colchicine can be
discontinued.
Adverse effects-
 The most common adverse effects are
hypersensitivity reactions(pruritic,
erythematous, or maculopapular eruption)
Rarely, Toxic Epidermal Necrolysis or Stevens-
Johnson syndrome occurs, which can be fatal.
 1-10%-Nausea, vomiting, acute gout, Renal
insufficiency
 Pregnancy-Category ‘C’
 Lactation-Excreted in breastmilk, caution must be
exercised when administering Allopurinol to
breastfeeding women.
Routes of administration-
 Oral (tablet)
 intravenous
Pregnancy and Lactation-
Drug interactions-
 Allopurinol +Probenecid-
Allopurinol increases the t1/2 of probenecid and
enhances its uricosuric effect, while probenecid
increases the clearance of Oxypurinol, thereby
increasing dose requirements of allopurinol.
 Allopurinol + Mercaptopurine/Azathioprine-
Allopurinol inhibits enzymatic inactivation of
mercaptopurine and azathioprine by xanthine
oxidase. Thus, when used together dosage of the
antineoplastic agent must be reduced by 25–33%
This is of importance when treating gout in the
transplant recipient.
 Allopurinol + Cyto-toxic agents
The risk of bone marrow suppression also is
increased when allopurinol is administered with
cytotoxic agents that are not metabolized by
xanthine oxidase, particularly cyclophosphamide.
 Allopurinol + Warfarin-
It interferes with the hepatic inactivation of
Warfarin .Increased monitoring of prothrombin
activity is recommended in patients receiving
both medications.
Summary-
 Allopurinol a uric acid synthesis inhibitor works
by inhibition of Xanthine Oxidase.
 It is used for Chronic Gout treatment
 It has a primary metabolite-Oxypurinol
 Most common adverse effects are
hypersensitivity reactions.
 Pregnancy- Category ‘C’
THANK-YOU

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Allopurinol (Anti-gout drug).pptx

  • 1. BY-DR. MADHUMITA DIXIT JR-3 PHARMACOLOGY DEPARTMENT MLN MEDICAL COLLEGE PRAYAGRAJ, UP Allopurinol
  • 2. Introduction-  Allopurinol, an Anti-gout drug is used as Uric acid synthesis inhibitor.  It is on the World Health Organization's List of Essential Medicines.
  • 4. Mechanism of action- Hypoxanthine Xanthine urate Xanthine oxidase Allopurinol Oxypurinol - Allopurinol acts on purine catabolism, and thus reduces production of urate without disrupting the biosynthesis of vital purines.
  • 5. • Allopurinol also is a substrate of Xanthine oxidase • It is a competitive inhibitor of Xanthine oxidase at low concentrations and non- Competitive inhibitor of Xanthine oxidase at higher concentrations. • Oxypurinol is Non-competitive inhibitor of Xanthine Oxidase.
  • 6. Uses-  Gout treatment (chronic urate-lowering therapy)also facilitates dissolution of Tophi and inhibits development or progression of Chronic Gouty Arthritis.  Nephrolithiasis (prevention of recurrent calcium or uric acid stones)  Tumor lysis syndrome prevention (To prevent hyperuricemia in patients with hematological malignancies about to undergo chemotherapy)  Inflammatory Bowel Disease IN CHILDREN-  Lesch-Nyhan syndrome (Hyperuricemia associated with errors of purine metabolism)  Glycogen storage diseases(recurrent calcium oxalate renal stones)
  • 7. Pharmacokinetics-  Bioavailability- 78 ±20%  Plasma Protein Binding-Negligible  Metabolism-Liver (80% oxipurinol,10% allopurinol ribosides)  Elimination half life -2 hours (Oxypurinol 18-30 hours)  Elimination-Feces-20% urine-10-30%
  • 8. Colchicine + Allopurinol  The incidence of acute attacks of gouty arthritis may increase during the early months of allopurinol therapy as a consequence of mobilization of tissue stores of uric acid.  Coadministration of colchicine helps suppress such acute attacks. After reduction of excess tissue stores of uric acid, the incidence of acute attacks decreases and colchicine can be discontinued.
  • 9. Adverse effects-  The most common adverse effects are hypersensitivity reactions(pruritic, erythematous, or maculopapular eruption) Rarely, Toxic Epidermal Necrolysis or Stevens- Johnson syndrome occurs, which can be fatal.  1-10%-Nausea, vomiting, acute gout, Renal insufficiency
  • 10.  Pregnancy-Category ‘C’  Lactation-Excreted in breastmilk, caution must be exercised when administering Allopurinol to breastfeeding women. Routes of administration-  Oral (tablet)  intravenous Pregnancy and Lactation-
  • 11. Drug interactions-  Allopurinol +Probenecid- Allopurinol increases the t1/2 of probenecid and enhances its uricosuric effect, while probenecid increases the clearance of Oxypurinol, thereby increasing dose requirements of allopurinol.  Allopurinol + Mercaptopurine/Azathioprine- Allopurinol inhibits enzymatic inactivation of mercaptopurine and azathioprine by xanthine oxidase. Thus, when used together dosage of the antineoplastic agent must be reduced by 25–33% This is of importance when treating gout in the transplant recipient.
  • 12.  Allopurinol + Cyto-toxic agents The risk of bone marrow suppression also is increased when allopurinol is administered with cytotoxic agents that are not metabolized by xanthine oxidase, particularly cyclophosphamide.  Allopurinol + Warfarin- It interferes with the hepatic inactivation of Warfarin .Increased monitoring of prothrombin activity is recommended in patients receiving both medications.
  • 13. Summary-  Allopurinol a uric acid synthesis inhibitor works by inhibition of Xanthine Oxidase.  It is used for Chronic Gout treatment  It has a primary metabolite-Oxypurinol  Most common adverse effects are hypersensitivity reactions.  Pregnancy- Category ‘C’