Increased urotensin-II activity in patients with Raynaud's phenomenon and systemic lupus erythematosus

Raynaud's phenomenon (RP) commonly co-exists with systemic lupus erythematosus (SLE). The obvious pathophysiological mechanism in RP is vasoconstriction. Although the roles of certain vasoconstrictor substances, like endothelin-1, have been identified in RP, underlying mechanisms remain unclear.

In this pilot study, we researched a relatively recently identified, very potent vasoconstrictor peptide, urotensin-II (U-II), in SLE patients versus those without RP. In addition to its vasoconstrictor effect, U-II has been implicated in cardiovascular events and atherosclerosis. Increased frequencies of atherosclerosis and cardiovascular events comprise another issue in SLE patients. To address these effects, we included 15 Raynaud's (+) and 15 Raynaud's (-) SLE patients and compared both cohorts against age and sex-matched controls.

We found significantly elevated U-II activity in both RP (+) and RP (-) SLE patients, relative to controls (P < 0.0001); however, the difference among RP (+) SLE patients was more prominent. U-II was significantly elevated in RP (+) SLE patients when compared to RP (-) SLE patients (P < 0.001).

The results of our study suggest that, either as a cause or by-product, U-II may have some role in Raynaud's-related vasoconstriction. It also might contribute to atherosclerosis and cardiovascular diseases in SLE patients. Further studies clearly are warranted.