Advances in the Treatment of Intermediate and Posterior Uveitis

Samantha Fraser-Bell; Carlos Pavesio


Expert Rev Ophthalmol. 2008;3(4):449-456. 

In This Article


Antimetabolites are inhibitors of purine synthesis; they include the prodrug azathioprine, which is converted to its active metabolite 6-mercaptopurine. Thiopurine methyltransferase (TPMT) is the main enzyme for inactivating the toxic products of azathioprine metabolism. Therefore, genetic polymorphisms of TPMT can lead to excessive drug toxicity.[5] Approximately 10% of the population inherits one nonfunctional TPMT allele (heterozygous), conferring intermediate TPMT activity, and 0.3% are homozygous, leading to low or absent TPMT activity. Patients with low or absent TPMT activity are at an increased risk of developing severe, life-threatening myelotoxicity if receiving conventional doses of azathioprine. TPMT genotyping or phenotyping can help identify patients who are at-risk for developing azathioprine toxicity. In this case, azathioprine may be exchanged for another antimetabolite, MMF. Azathioprine has demonstrated efficacy in Behçet's syndrome in treating ocular inflammation, preventing recurrences and in preserving vision in a randomized, controlled trial versus placebo.[6] The literature also shows successful control of corticosteroid-resistant uveitis syndromes, such as serpiginous choroiditis,[7] sympathetic ophthalmia,[8] birdshot retinochoroidopathy[9,10] and Vogt-Koyanagi-Harada syndrome.[11,12,13]


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