Independent integrative reanalysis · manuscript in preparation
Does asymptomatic hyperuricemia sit on a simple molecular path to gout?
Higher and longer urate exposure raises future gout risk, but clinical conversion remains incomplete. I therefore tested a stronger molecular-continuum hypothesis rather than assuming it: if asymptomatic hyperuricemia were a simple intermediate stage, inflammatory proteins should rise monotonically from normouricemia to asymptomatic hyperuricemia and then gout. The current data reject that simple pattern and instead support a two-axis model—continuous urate-related risk alongside state-specific and heterogeneous immune programmes.








