Nonalcoholic fatty liver disease (
NAFLD), the most common chronic
liver disease in Western countries with potential progression to
nonalcoholic steatohepatitis (NASH) and
cirrhosis, is associated with
cardiovascular disease (CVD) mortality. Several studies have reported a relationship between
uric acid and
NAFLD/NASH and it seems that serum
uric acid (SUA) is a significant independent factor for the development of
NAFLD. Potential mediating mechanisms include
insulin resistance, endothelial dysfunction, and activation of
inflammasome, especially NLRP3. Moreover, emerging evidence indicates a strong association between elevated SUA,
metabolic syndrome (MetS),
NAFLD, and CVD. The emphasis of the present review is whether common
therapy of elevated SUA levels and
NAFLD can improve compliance. There are several drugs with "off target" properties that show some separate benefit on SUA reduction (e.g.
losartan) or
NAFLD/NASH (
pioglitazone); however, there is no randomized controlled trial (RCT) of a single drug with beneficial outcome for both diseases.
Allopurinol reduces SUA levels and ameliorates
NAFLD/NASH; however, no RCTs have been performed up to now to explore potential survival benefits.
Atorvastatin, which has proven safe in
NAFLD/NASH, reduces SUA levels, ameliorates
NAFLD/NASH, prevents
liver fibrosis, and above all substantially reduces CVD morbidity and mortality in comparison with those on
statins but without
NAFLD/NASH. This drug could be a
solution to improve compliance in both diseases, which are prevalent and becoming even more common with the
obesity, MetS, and
type 2 diabetes mellitus epidemic.