Abstract
In recent years, the benefits of early aggressive treatment paradigms for inflammatory bowel disease have emerged. Symptomatic improvement is no longer considered adequate; instead, the aim of treatment has become mucosal healing and altered natural history. Nonetheless, we still fail to achieve these end points in a large number of our patients. There are many reasons why patients fail to respond or develop toxicity when exposed to drugs used for inflammatory bowel disease, but genetic variation is likely to account for a significant proportion of this. Some examples, notably thiopurine methyltransferase polymorphism in thiopurine treatment, are already established in clinical practice. We present a review of the expanding literature in this field, highlighting many interesting developments in pharmacogenomics applied to inflammatory bowel disease and, where possible, providing guidance on the translation of these developments into clinical practice.
| Original language | English |
|---|---|
| Pages (from-to) | 421-437 |
| Number of pages | 17 |
| Journal | PHARMACOGENOMICS |
| Volume | 11 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Mar 2010 |
Keywords
- 5-aminosalicylate
- 6-mercaptopurine
- azathioprine
- drug metabolism
- inflammatory bowel disease
- infliximab
- methotrexate
- pharmacogenetics
- pharmacogenomics
- steroid
- sulphasalazine
- THIOPURINE S-METHYLTRANSFERASE
- INOSINE TRIPHOSPHATE PYROPHOSPHATASE
- GLUCOCORTICOID-RECEPTOR BETA
- ACUTE LYMPHOBLASTIC-LEUKEMIA
- ADVERSE DRUG-REACTIONS
- NECROSIS-FACTOR-ALPHA
- RESISTANT BRONCHIAL-ASTHMA
- ALDEHYDE OXIDASE ACTIVITY
- BLOOD MONONUCLEAR-CELLS
- BONE-MARROW TOXICITY