FROM ANNALS OF THE RHEUMATIC DISEASES
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.”
Dr. Tinazzi and her colleagues designed this study to investigate how PsA could be related to abnormal responses to physical stresses via a Koebner response in the skin and a deep Koebner response in the joints. Researchers enrolled 27 patients with PsA, 27 with RA, 23 with only psoriasis, and 19 healthy controls from two Italian centers. The volar aspects of the second to fourth digits of each patient’s dominant hand were imaged both transversely and longitudinally with ultrasound. Transverse and longitudinal measurements were taken of the A1 pulley at the metacarpophalangeal joint, and a dynamic exam determined the border between the A1 pulley and the flexor tendon. The A2 and A4 pulley thicknesses were analyzed during full extension. In total, 1,732 measurements were taken on 864 pulleys.
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).
The size of the study population and the method for defining pulley thickness limited the study. Measurements were taken only in three digits of the dominant hand of each patient. Among PsA patients, only those with hand involvement participated in the study, which may limit the translation of the results to all PsA patients. Additionally, whether pulley changes trigger PsA tenosynovitis or whether it is a reactive process needs additional investigation.
The results of the study suggest that accessory pulleys are subjected to high physical stress and that they exhibit deep Koebner effects and thicken in response, Dr. Tinazzi and her associates wrote.
“Indeed, these findings suggest that such a mechanism is possible given the frequency of thickening of these structures in PsA” wrote Dr. Tinazzi and her associates. “It will be important to show that such changes are present in early PsA where their presence would support the idea of early biomechanical alterations in tendon function that could contribute to dactylitic tenosynovitis.”
This study received no external funding. Several of the researchers have received grants or honoraria from pharmaceutical companies.
SOURCE: Tinazzi I et al. Ann Rheum Dis. 2018 Mar 6. doi: 10.1136/annrheumdis-2017-212681 .
