The use of monoclonal antibody ustekinumab (Stelara) might help prevent progression to psoriatic arthritis (PsA) by suppressing subclinical enthesopathy, according to a new study published in the journal Arthritis & Rheumatology.
Ustekinumab is an inhibitor of interleukin (IL)-12/23, and preclinical studies have demonstrated that overexpression of IL-23 results in an enthesis-centered spondyloarthropathy. It is approved for the treatment of active PsA in adults.
Psoriatic arthritis (PsA) can quickly lead to irreversible joint damage, functional limitation and quality-of-life impairment. So, it is essential that the disease is diagnosed and treated earlier. Nearly that 70% of patients who develop PsA have antecedent psoriasis, dermatologists are required to identify joint abnormalities as early as possible.
It is estimated that 2% of patients with psoriasis each year develop PsA, and the prevalence of undiagnosed PsA among patients seen in dermatology clinics has been reported to be as high as 29%. Enthesitis is hypothesized to be the primary abnormality in PsA. Enthesitis, or inflammation of the entheses — sites, where tendons and ligaments insert into bone, is thought to be the primary site of musculoskeletal inflammation in PsA.
Laura Savage and his associated performed a cohort study to investigate whether sonographically determined subclinical enthesopathy in patients with moderate-to-severe psoriasis regressed under therapy with ustekinumab, initiated for skin disease.
Seventy-three systemic therapy-naive patients with moderate-to-severe psoriasis and without symptoms of PsA and 23 healthy volunteers were screened using ultrasound for subclinical enthesitis.
According to the authors,49.3% of screened patients with psoriasis had at least one inflammatory entheseal abnormality on ultrasound. Mean inflammation scores were higher in psoriasis patients compared with healthy volunteers: 9.9 vs. 1.0.
The investigators found that by week 24 of treatment with ustekinumab, mean entheseal inflammation scores decreased by 42.2%, with a reduction of −4.2 points, and by 47.5% by week 52, with a decline of −4.7.
The study concluded that IL-12/23 inhibition for psoriasis appears to suppress subclinical enthesopathy within 12 weeks of treatment, maintained to week 52.
For full information log on to