An ultrasonographic study describing the greater presence of thicker digital accessory pulleys in patients with psoriatic arthritis (PsA) than in those with only psoriatic skin disease, rheumatoid arthritis, or no pathology has lent more evidence for a “deep Koebner” response mechanism in the development of joint disease in people with psoriasis.
“The thicker pulleys in RA compared with HCs [healthy controls] might point towards a nonspecific effect of a chronic autoimmune tenosynovitis on the adjacent pulleys,” Ilaria Tinazzi, PhD, of the Sacro Cuore-Don Calabria Hospital, Verona, Italy, and her colleagues wrote in Annals of the Rheumatic Diseases. “However, the greater magnitude of pulley thickening in PsA, especially in the setting of dactylitis, suggests an intrinsic pathology in the pulley contributing to PsA-related tenosynovitis.”
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Dr. Tinazzi and her research team found that the pulleys in patients with PsA were thicker in every digit than they were in patients with RA and healthy controls, but pulley thickness also differed for each group of patients when compared with one another. Patients with RA had thicker pulleys than did healthy controls, particularly in the A1 pulley, but showed no differences in the A2 and A4 pulleys of the second and fourth digit. Even patients with only psoriasis had thicker pulleys than did the healthy controls. Patients with PsA exhibited thicker A1 and A4 pulleys, compared with patients with only psoriasis, while A2 pulleys displayed no statistical difference. Among PsA patients, 165 of 243 (68%) pulleys were thickened, whereas only 41 of 243 (17%) were thickened among RA patients (P less than .001). A multiple-regression analysis revealed that only PsA was associated with the number of thickened pulleys (odds ratio, 4.8; 95% confidence interval, 3.3-6.3; P = .001).