Hyperuricemia and the accompanying deposition of aggregated monosodium urate (MSU) crystals in articular and extra-articular regions create the most prevalent inflammatory arthritis known as gout. Hyperuricemia, gout, and the development of cardiovascular disease all have strong connections to one another. Deposition of MSU in the vasculature of gout patients has been detected using CT (DECT), and there is an association between the volume of the tophus and the risk of cardiovascular disease. Arterial artery wall inflammation can be measured with high accuracy using vascular Positron Emission Tomography (PET/CT). Researchers hypothesized that local vascular inflammation might be brought on by uric acid accumulation in the blood vessels. This mechanism may contribute to the development of atherosclerosis and speed up the onset of cardiovascular complications. About 10 people with tophaceous gout were enlisted, all of whom had failed or shown intolerance to urate-lowering medication. To avoid the development of anti-pegloticase antibodies, patients were pretreated with a low-dosage immunomodulator (Azathioprine or Methotrexate) before receiving pegloticase infusions every 2 weeks for 6 months. Standard uptake value, SUV mean to assess systemic uptake across a vessel segment, SUV max to identify hotspots; Target-to-blood pool ratio, TBR means, and TBR max calculated by dividing the vascular wall SUV with the venous blood pool SUV means to correct for blood uptake) DECT and PET/CT were measured before and 6 months after pegloticase treatment, respectively, to detect vascular MSU deposition (MSU volume) and vessel wall inflammation. The information was summarized by means and standard deviations. Investigators used mixed effect models to compare each variable’s pre- and post-treatment values. After pegloticase treatment, they saw a reduction in SUV mean (P=0.0003) and SUV max (P=0.0090) in all analyzed arteries. The maximum and average TBR values showed a non-significant downward trend. They discovered a non-significant tendency toward a smaller MSU volume following pegloticase treatment regarding MSU accumulation. When pegloticase was administered to individuals with tophaceous gout, they saw a reduction in vessel wall inflammation (SUV mean and SUV max) and a trend toward a reduction in MSU deposition (MSU volume). Despite the limited sample size, their findings showed that aggressively decreasing uric acid reduced artery wall inflammation and MSU deposition. These results indicate that MSU functions in vascular inflammation and show that vessel inflammation decreases in tandem with lowered serum urate levels. Whether or not this predicts better cardiovascular outcomes is yet to be determined.
