186 Chapter 8 being taken, so is likely to be subject to ascertainment bias and under-ascertainment of these outcomes. Finally, although receipt of adjunctive rifampicin was randomised in the ARREST trial, reducing the risk of confounding, the numbers within each sub-phenotype were relatively small so these results must be interpreted as strictly hypothesis-generating. Overall, it remains possible the sub-phenotypes will not be replicable in other patient cohorts, or that additional sub-phenotypes may exist (e.g. associated with MRSA infection), or that outcomes/treatment responses could differ. We are conducting further replication studies to address these questions. In summary, our findings support the hypothesis that clinically-relevant subphenotypes do exist within SAB, and suggest that patient stratification within SAB clinical trials is required to identify strategies to improve outcomes for patients. This could inform a personalised medicine approach to SAB.
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