From the Journals

Palindromic rheumatism has a distinct imaging phenotype



Palindromic rheumatism, while often challenging to distinguish from persistent arthritis, has a distinct imaging pattern characterized by extracapsular inflammation, often with no synovitis, results of a recent prospective study show.

Finding the phenotype on ultrasound evaluation may help to separate cases of inflammatory arthritis, which may need early disease-modifying treatment, from palindromic rheumatism, which can be managed conservatively, the study authors reported in Annals of the Rheumatic Diseases.

“These findings may refine diagnosis and improve management of this important condition,” wrote Kulveer Mankia, MD, of the Leeds (England) Institute of Rheumatic and Musculoskeletal Medicine, and his coauthors.

High-resolution imaging studies in palindromic rheumatism have been sparse, in part because of the sporadic nature of flares in these patients, according to Dr. Mankia and his colleagues.

Their report included 79 patients with palindromic rheumatism recruited from two U.K. rheumatology clinics and a national primary care program and compared them with other populations.

The patients underwent ultrasound evaluation by experienced rheumatologists and sonographers, as well as MRI on the most symptomatic region during flares. Those results were compared with clinical and ultrasound assessments in a cohort of patients with new-onset RA, and a second cohort of anticyclic citrullinated peptide (CCP)–positive at-risk individuals.

The investigators were able to assess 31 of the palindromic rheumatism patients during a flare episode. Extracapsular inflammation was frequently found during these episodes, with one or more instances of periarticular inflammation, peritendinous edema, or subcutaneous edema occurring in 19 (61%) of 31 patients.

However, tenosynovitis was detected in just seven of those patients (23%), while peritendinous edema was seen in three (10%).

By contrast, ultrasound abnormalities were infrequent in 27 nonflare evaluations taken in those 31 patients. For example, just four scans (15%) showed extracapsular inflammation.

Overall, extracapsular inflammation was found in 65% of palindromic rheumatism patients, compared with just 29% of new-onset RA cases (P less than .023).

Of particular note, extracapsular inflammation without synovitis was specific for palindromic rheumatism, occurring in 42%, compared with only 4% of RA cases (P = .003) and 6% of anti–CCP-positive at-risk patients (P = .0012).

A total of 13 of the 79 palindromic rheumatism patients (16%) went on to develop persistent inflammatory arthritis over a median follow-up of 42-49 days. Of the 31 patients evaluated during flare, 7 (23%) developed persistent inflammatory arthritis over the follow-up period. Those seven patients all met American College of Rheumatology/European League Against Rheumatism (EULAR) 2010 classification criteria for RA.

The MRI studies concurred with the ultrasound findings and identified some additional abnormalities, the investigators reported.

Altogether, these imaging findings are important to note because of the “variable” progression seen in palindromic rheumatism, Dr. Mankia and his colleagues wrote.

While anti-CCP antibody positivity confers high risk of progression in palindromic rheumatism, presence of this marker does not always mean the patient will develop persistent arthritis on follow-up, they added. In fact, this study showed that, among 47 anti–CCP-positive palindromic rheumatism patients, 35 (74%) did not develop persistent inflammatory arthritis in follow-up.

“In clinical practice, these patients may be inappropriately treated [e.g., with methotrexate] as they often meet ACR/EULAR criteria for rheumatoid arthritis,” the investigators wrote in their report.

Funding for the study came from the National Institute for Health Research Leeds Clinical Research Facility with additional support from an Arthritis Research U.K. grant. The authors reported no competing interests related to their study.

SOURCE: Mankia K et al. Ann Rheum Dis. 2018 Oct 8. doi: 10.1136/annrheumdis-2018-214175.

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