Life threatening myelotoxicity secondary to azathioprine in a patient with atopic eczema and normal thiopurine methyltransferase activityBMJ 2011; 342 doi: http://dx.doi.org/10.1136/bmj.d1417 (Published 25 March 2011) Cite this as: BMJ 2011;342:d1417
- Jamie S Wee, specialist trainee year 1 in dermatology1,
- Anthony Marinaki, principal biochemist1,
- Catherine H Smith, consultant in dermatology1
- 1St Thomas’ Hospital, London SE1 7EH
- Correspondence to: J S Wee
- Accepted 2 November 2010
Azathioprine is an immunosuppressive agent belonging to a class of drugs known as thiopurines. Azathioprine was originally used to prevent rejection of transplant organs and is now widely used as a steroid sparing agent in the treatment of autoimmune and chronic inflammatory diseases. Use in atopic eczema has been supported by randomised controlled trials, with a reported improvement in disease activity of 37% after 12 weeks.1 Treatment can be limited by adverse effects, leading to withdrawal in 10-28% of patients,2 with the most serious complication, myelosuppression, occurring in 7% of cases.3 Thiopurine methyltransferase (TPMT) is a key enzyme in the metabolism of azathioprine, methylating azathioprine metabolites at the expense of formation of cytotoxic thioguanine nucleotides. TPMT deficiency is a well documented cause of azathioprine induced myelosuppression,4 and routine TPMT testing is established best practice for identifying patients at risk.5
We report a patient with normal TPMT activity who was prescribed azathioprine for severe atopic eczema and subsequently developed profound, life threatening myelotoxicity, which could potentially have been identified earlier.
A 24 year old Filipino man presented to the dermatology department with a lifelong history of generalised atopic eczema that was uncontrolled with superpotent topical corticosteroids. Infective exacerbations were frequent, with an overall adverse effect on his quality of life. He had a history of asthma, and his only medication was a salbutamol …
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