The extent to which elevated uric acid (UA) levels should merit the medical community’s attention as a cardiovascular risk factor is a long-debated topic. Data accruing from the Framingham Heart Study, founded in 1948, determined that UA is associated with CV disease, but it is important to stress that correlation does not equate to causation. Even in the event that such a causal relationship is found, whether or not modulation of UA can be both safe and effective is unclear.
Rheumatoid arthritis (RA) and psoriasis (with or without psoriatic arthritis) are both typically considered rheumatologic disorders, primarily because of their similar connection to abnormal immunological pathways. General recognition of the increased risk for CVD in psoriasis patients, in fact, followed the widespread identification and appreciation of the amplified risk of CVD conferred by rheumatoid arthritis.
In spite of the acknowledgement that psoriasis and RA correlate with an increase in the risk of cardiovascular problems, the specifics of this risk remains poorly-understood — from this, investigations into the link between hyperuricemia, cardiovascular issues and psoriasis are understandable, if not warranted.
Gisondi et al, in exploring this link, compared serum UA levels in 119 psoriasis patients with 119 controls. The study found that asymptomatic hyperuricemia was nearly three times as common amongst psoriasis patients (19%) as it was amongst the control patients (7%). In addition, Gisondi et al found that the average serum UA levels in psoriasis patients were much higher than the levels of the controls (5.6 md/dL vs 4.9 mg/dL).
As psoriasis is characterized by rapid turnover of skin cells, psoriasis’s symptoms could influence serum UA. Whether the observed spike in CVD rates among psoriasis patients is a product of, or is affected by hyperuricemia and elevated UA levels, however, has yet to be definitively determined.