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A narrative review on the impact of β3‐AR polymorphisms on urological disease and its treatment is presented. The overall evidence points to carriers of the 64Arg genotype expressing fewer and/or hypofunctional β3‐ARs and being associated with the presence of OAB but such findings were only detected inconsistently. If this hypofunctionality exists, the consequences may be of insufficient magnitude to allow a robust detection. Only adequately powered studies comparing responses with a β3‐AR agonist in 64Arg carriers versus wild‐type patients can address this.
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