
Systemic sclerosis (SSc) is an autoimmune disorder where the immune system attacks the body. When dealing with SSc, systemic sclerosis-associated pulmonary arterial hypertension (SSc-PAH) is one of the leading causes of death in SSc. In a study published in Arthritis Research & Therapy, researchers aim to assess if identification and validation of novel proteins could potentially facilitate the identification of SSc-PAH, as well as point to important protein mediators in pathogenesis.
Study of 13 Rx naive systemic sclerosis patients shows that the proteomic biomarkers Midkine and Follistatin-like 3 (FSTL3), were highly associated with the presence of pulmonary arterial hypertension. https://t.co/sOzH7UwgOe
— Dr. John Cush (@RheumNow) August 28, 2018
In this study, 13 treatment-naïve SSc-PAH patients had serum collected at time of diagnosis. These patients were used as the discovery cohort for the protein-expression biomarker. Using enzyme-linked immunosorbent assays, the two proteins, Midkine and Follistatin-like 3 (FSTL3), were validated.
#NIAMSResearch @UPittTweet: “Serum biomarker for diagnostic evaluation of pulmonary arterial hypertension in systemic #sclerosis.” https://t.co/yxBaK3dtdD. Open Access paper @ArthritisRes. #scleroderma.
— NIAMS (@NIH_NIAMS) August 29, 2018
Congrats to my colleagues and hap farber on this cool and important paper @ATSBlueEditor @accpchest Serum biomarker for diagnostic evaluation of pulmonary arterial hypertension in systemic sclerosis https://t.co/pJiRezmvc8 #
— Matthew Moll, MD, MPH (@MattMollpulmccm) August 27, 2018
According to the results, 82 proteins were found to be differentially regulated in SSc-PAH sera, with Midkine and FSTL3 shown to be elevated in publicly available data. Findings showed that there is a clear delineation between overall protein expression in sera from SSc patients and those with SSc-PAH. “The combination of Midkine and FSTL3 can serve as an SSc-PAH biomarker and are potential drug targets for this rare disease population,” the researchers concluded.
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SOURCE: Arthritis Research & Therapy