HCP Live
Contagion LiveCGT LiveNeurology LiveHCP LiveOncology LiveContemporary PediatricsContemporary OBGYNEndocrinology NetworkPractical CardiologyRheumatology Netowrk

New Clue in Diagnosing Rheumatic Diseases

Type X collagen, which is expressed by hypertrophic chondrocytes, is suppressed by tumor necrosis factor alpha inhibitors (TNFi) treatments, arthritis researchers report.The finding could lead to a molecular marker for early diagnosis of psoriatic arthritis and axial spondyloarthritis.

A recent study examined the biochemical cartilage marker profiles in people with psoriatic arthritis (PsA), axial spondyloarthritis (axSpA), and healthy controls, and found that type X collagen, which is expressed by hypertrophic chondrocytes, is suppressed by tumor necrosis factor alpha inhibitors (TNFi) treatments.

The study, conducted by Natasja Gudmann of Nordic Bioscience Biomarkers and Research, and colleagues, was published in the journal Arthritis Research and Therapy on June 16, 2016.

Early diagnosis appears to improve outcomes for patients with diseases such as PsA and axSpA, which are chronic inflammatory rheumatic diseases.

However, both diseases progress differently among individual patients, and few diagnostic tests exist, making early intervention difficult.

The objective of this study was to investigate whether or not molecular markers in cartilage collagen metabolism could be of use from a diagnostic perspective.

Patients were recruited from three treatment centers in Denmark from November 2011 through February 2014. There were 110 patients with axSpA and 101 with PsA compared with 118 healthy controls in this study. The researchers measured two cartilage biochemical markers, C-Col10 and Pro-C2 in order “to study chondrocyte differentiation and mature cartilage collagen IIB formation in axSpA and PsA,” they said.

They found that Pro-C2 levels were significantly higher in both the axSpA and PsA groups compared to the controls. “The current increased Pro-C2 level may reflect an anabolic chondrocyte response to counterbalance increased collagen type II degradation in active disease,” report the researchers.

The fact that type X collagen of hypertrophic chondrocytes was suppressed by TNFi treatments, but other types of collagen production were unaffected led the researchers to conclude “the SpA-related type II collagen response of normal chondrocytes is preserved, while the collagen type X expression of cartilaginous and enthesopathic lesions is modified by TNFi.”

However, more studies are necessary in order to validate that conclusion.