Abstract
To assess the effect of methotrexate on the development of distal interphalangeal joint extensor tendon enthesopathy in psoriasis, thirty-two people aged 34 to 57 years with nail psoriasis and distal interphalangeal joint extensor tendon enthesopathy (19 patients with Ps (psoriasis) and 13 with PsA (psoriatic arthritis) were started on methotrexate at 15 to 25 mg/week and the treatment was continued for 6 months). A total of 319 nails were examined. After six months of treatment, the thicknesses of the nail plate, nail bed and nail matrix were found to decrease in both groups of patients. Methotrexate treatment resulted in a decrease in the joint extensor tendon thickness only in patients with Ps (0.94 ± 0.05 vs. 0.96 ± 0.04, p < 0.001), where the tendon thickness after treatment correlated with the matrix thickness (r = 0.337, p = 0.018) and with the bed thickness (r = 0.299, p = 0.039). Methotrexate treatment resulted in a decrease in the extensor tendon thickness only in patients with Ps but not in PsA. The findings of this study may suggest the effectiveness of systemic treatment of nail psoriasis in patients without arthritis and the use of US nail examinations in Ps and PsA patients in morphological change assessment and response to treatment.
Highlights
Nail psoriasis is one of the risk factors for psoriatic arthritis (PsA) [1], with distal interphalangeal (DIP) joints being especially affected [2]
In the development of arthritis associated with nail psoriasis and extensor tendon enthesitis, among others, locally released inflammatory mediators [4] and an abnormal pattern of vascularity observed in the synovium in PsA can participate [5]
Because of the aim of the study, enthesopathies of DIP joint tendons in at least one digit were observed in a US examination
Summary
Nail psoriasis is one of the risk factors for psoriatic arthritis (PsA) [1], with distal interphalangeal (DIP) joints being especially affected [2]. Nail changes in psoriasis have been observed in 10–55% of patients without arthritis and in up to 80% in PsA patients [3,4]. The anatomical conditions of the nail apparatus facilitate the spread of nail psoriasis-related inflammation to adjacent structures, including DIP joints and digital extensor tendons [4]. It seems that synovitis in the course of PsA is a secondary process to ongoing inflammation in adjacent entheses. In the development of arthritis associated with nail psoriasis and extensor tendon enthesitis, among others, locally released inflammatory mediators [4] and an abnormal pattern of vascularity observed in the synovium in PsA can participate [5]
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