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Published on: February 8, 2019
Plasma proteome differences between giant cell arteritis and polymyalgia rheumatica: a pilot study
S Seidlberger1, S Castañeda2,3, G Wietzorrek1
1Institute of Pharmacology, Medical University of Innsbruck, Innsbruck, Austria.
Insights
This study identified unique plasma proteomic signatures for polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) patients. These findings may aid in classifying these vasculitis diseases and monitoring disease activity.
Area of Science:
- Proteomics
- Immunology
- Rheumatology
Background:
- Giant cell arteritis (GCA) is a prevalent vasculitis in the elderly, with visual loss as a severe complication.
- Current diagnostic methods include imaging and temporal artery biopsy (TAB), but new laboratory tests are needed for disease assessment.
- Polymyalgia rheumatica (PMR) is a related inflammatory condition.
Purpose of the Study:
- To characterize distinct proteomic signatures for classifying PMR and GCA.
- To identify specific markers for disease activity in PMR and GCA.
- To find markers that differentiate between PMR and GCA.
Main Methods:
- Plasma samples from 15 PMR and 13 GCA patients were analyzed using mass spectrometry.
- An UltiMate 3000 nano-HPLC system coupled to an Orbitrap Eclipse mass spectrometer was employed.
- Immunofluorescence analyses of TABs confirmed elevated S100A12 expression.
Main Results:
- 50 protein signatures were characteristic of active GCA, and 83 were altered only in active PMR.
- Only 13 proteins showed altered expression in both groups, indicating distinct signatures.
- GCA signatures involved mitochondrial activity and clotting cascade; PMR signatures involved erythrocyte integrity, muscle contraction, and glucocorticoid resistance. S100A12 was elevated in plasma and TABs for both.
Conclusions:
- Active PMR and GCA share a small plasma proteome signature related to immune activation.
- Active PMR is characterized by distinct erythrocyte and muscle contraction proteome changes.
- Active GCA is driven by mitochondrial and clotting cascade alterations, suggesting distinct pathophysiological pathways.
Background:
Giant cell arteritis (GCA) is the most prevalent vasculitis in the elderly of Caucasian ancestry, with the risk of visual loss as the most serious complication if the glucocorticoid therapy does not succeed. While imaging and temporal artery biopsy (TAB) remain diagnostic gold standards, new laboratory tests are needed to assess disease activity and follow-up monitoring.
Objective:
We aimed to characterize distinct proteomic signatures for the classification of polymyalgia rheumatica (PMR) and GCA (independent of concurrent therapy) and to identify specific markers of disease activity and markers that differentiate the two diseases.
Methods:
The plasma of 15 PMR and 13 GCA patients was analysed via mass spectrometry with the UltiMate 3000 nano-HPLC system coupled to an Orbitrap Eclipse mass spectrometer. Immunofluorescence analyses in TABs were performed to confirm the elevated plasma expression of S100A12.
Results:
We identified 50 protein signatures characteristic of active GCA patients, and 83 signatures altered only in active PMR samples. Strikingly, both groups shared only 13 proteins with altered protein expression levels. The newly identified proteins point to activation of biological pathways not yet linked to the diseases: mitochondrial membrane activity (ACACA, SLC25A31) and clotting cascade (VWF, TUBB) in active GCA; erythrocyte integrity (SLC4A1, SPTA1), muscle contraction (MYLK, MYL6B/12B), and glucocorticoid resistance (PTGES3) in active PMR. Importantly, S100A12 was increased not only in plasma (~ 1.6-fold), but also in PMR and GCA TABs.
Conclusion:
Active PMR and active GCA patients share an unexpectedly small plasma proteome signature related to immune activation (8.9%: 13 proteins). Instead, active PMR is characterized by distinct erythrocyte and muscle contraction proteome changes, whereas active GCA appears driven by mitochondrial and clotting cascade alterations. Prospective, longitudinal validation studies of the described proteomic signatures might support the clinical classification of both diseases.
