High uric acid is what produces gout, and obesity raises it, so a drug that removes a fifth of someone's body weight ought to lower it. A post hoc analysis of SURMOUNT-1 confirmed that and then asked the more interesting question of why [1]. The comparison between drug classes on gout itself is in what a comparator can and cannot tell you.
Across 72 weeks, serum uric acid fell by 0.69, 0.92 and 0.95 mg/dL on the 5, 10 and 15 mg doses, against 0.18 mg/dL on placebo. Weight fell by up to 20.9% over the same period, broadly in line with the pooled figures in the weight-loss averages.
The mediation analysis attributed 72.7% of the uric acid reduction to weight loss. That leaves roughly a quarter attributed to something else about the drug, which is the part worth following up — though as with every mediation analysis, the split is the output of a model resting on assumptions that cannot be tested against the data, the same caution set out in the liver mediation analysis.
Two nulls in this paper are easy to skim past and shouldn’t be. The reduction did not differ by baseline uric acid quartile (P = .610), so people who started with the highest levels did not drop further than those who started lower. Nor did it differ by baseline BMI (P = .362). That is unusual: most outcomes in this literature show bigger changes in people with more room to move, as the sleep apnea subgroups illustrate, and the absence of that pattern here suggests a fairly uniform effect.
The practical translation is narrow. If you have gout and are taking one of these drugs for other reasons, your urate is likely to fall, which is the direction gout treatment aims for. If you are considering one specifically for gout, nothing here supports that yet — the trial that would, counting flares rather than measuring blood, has not been done.