This will most likely enhance their outcomes, while ensuring we do not develop an overly heavy

“top-down” approach, exposing many patients who have an otherwise good prognosis to potentially hazardous immunosuppression. This is a particular problem in many areas of Asia, where there is a high prevalence of infections, such as tuberculosis. Yoon et al.1 report an inverse, statistically-significant relationship between the Mayo score at baseline and the likelihood of a good response to steroid therapy, such that those with a higher baseline score are more likely to do poorly. However, when one examines the data in greater detail (figure 2 in their manuscript), one can appreciate that the separation of Mayo scores between those with good versus poor TSA HDAC supplier outcomes is not great, and in their tables 2 and 3, one sees considerable overlap in actual scores for Ponatinib concentration individual patients. From this, we can deduce that worse disease at baseline is a poor prognostic factor, but that it is a relatively blunt tool for individual prediction. Of note, this Korean cohort appears overall to have relatively mild disease as assessed by C-reactive protein, erythrocyte sedimentation rate, hemoglobin and albumin measures, and the fact that only 62% of their patients were admitted to hospital during their course of steroids. The concept that more severe disease is a poor prognostic

factor is more precisely documented at the most severe end of the UC spectrum, when patients are admitted with acute severe colitis.3 Yet even here, we do not have the precision we seek in terms of prediction. There is some hope that genetics might be able to offer some assistance in the future in terms of assigning selleck products an early warning for patients who are at higher risk of severe disease. This approach is appealing, as genes have the potential to be assessed at diagnosis, before waiting for treatment outcomes. To date, one study has recently published an single nucleotide polymorphism (SNP)-based risk profile for identifying refractory UC.4 Haritunians et al. used a gene-wide association study approach in a North

American cohort of 861 UC patients to develop a 46-SNP scoring system for colectomy risk. They reported a sensitivity of 79% and a specificity of 86%. There is hope that greater knowledge here will eventually allow a personalized, pharmacogenetic approach, with patients being first started on the therapy most likely to benefit them. Unfortunately, this is not yet available, although many potentially interesting loci are under current investigation. What we can predict from the current data, however, is that we do not need to wait longer than 1 month in non-responders having a first course of corticosteroids. In the study by Yoon et al., none of these 19 patients demonstrated a prolonged response at 1 year.