Interleukin-17 and interleukin-23: importance in the pathogenesis of lung impairment in patients with systemic sclerosis (SSc). The changes in concentrations of IL-17, IL-21 and IL-23 support the hypothesis that these cytokines may play a role in the pathogenesis of SSc. PubMed, Int J Rheum Dis, 2014 Jan 28. (Also see Causes of Scleroderma: Cytokines)
Faecal levels of calprotectin (FC) in systemic sclerosis (SSc) are stable over time and are higher compared to primary Sjogren's syndrome and rheumatoid arthritis. FC could be a useful marker when novel, more specific drugs targeting the GI tract in SSc will be introduced. PubMed, Arthritis Res Ther, 2014 Feb 6. (Also see Systemic Scleroderma Prognosis and Mortality: Biomarkers)
Relationship between serum leptin level and disease activity in patients with systemic sclerosis (SSc). Leptin can be used as an activity marker in SSc and further studies should be carried out to clarify this relationship. PubMed, Clin Rheumatol, 2013 Dec 27. (Also see Hormones)
Increased intrarenal arterial stiffness may predict the occurrence of new digital ulcers (DU) in systemic sclerosis. Doppler indices could be used in association with the capillaroscopic and clinical findings or serological tests for the identification of patients at high risk of developing DUs. PubMed, Arthritis Care Res (Hoboken), 2014 Feb 10. (Also see Digital Ulcers)
Early systemic sclerosis (SSc): Analysis of the disease course in patients with marker autoantibody or capillaroscopic positivity or both. The data demonstrate faster progression of SSc in autoantibody-positive patients, particularly in those with preclinical internal organ involvement at baseline, than in autoantibody-negative patients. PubMed, Arthritis Care Res (Hoboken), 2014 Feb 10. (Also see Scleroderma Autoantibodies and Capillaroscopy)
Patients with Systemic Sclerosis (SSc) Present Increased DNA Damage Differentially Associated with DNA Repair Gene Polymorphisms. Polymorphic sites of the XRCC1 and XRCC4 DNA repair genes may differentially influence DNA damage and the development of autoantibodies. PubMed, J Rheumatol, 2014 Feb 1. (Also see Causes of Scleroderma: Genetics)
Reconciling Healthcare Professional and Patient Perspectives in the Development of Disease Activity and Response Criteria in Connective Tissue Disease-related Interstitial Lung Diseases (CTD-ILD). Efforts described here demonstrate unequivocally the value and influence of patient involvement on core set development. PubMed, J Rheumatol, 2014 Feb 1. (Also see Pulmonary Fibrosis and Connective Tissue Disease)
Disease progression in systemic sclerosis (SSc)-overlap syndrome is significantly different from limited (IcSSc) and diffuse cutaneous systemic sclerosis (dcSSc). SSc-overlap syndromes should be regarded as a separate SSc subset, distinct from lcSSc and dcSSc, due to a different progression of the disease, different proportional distribution of specific autoantibodies, and of different organ involvement. PubMed, Ann Rheum Dis, 2014 Jan 3. (Also see Systemic Scleroderma in Overlap)
Autoantibodies to angiotensin (AT1R) and endothelin (ETAR) receptors in systemic sclerosis (SSc) induce cellular and systemic events associated with disease pathogenesis. Anti-AT1R and anti-ETAR autoantibodies could provide novel targets for therapeutic intervention in the treatment of SSc. PubMed, Arthritis Res Ther, 2014 Jan 28;16(1):R29. (Also see Scleroderma Autoantibodies)
Reading Voices of Scleroderma Books: Diana Kramer.
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Thanks to UNITED WAY donors of Central New Mexico and Snohomish County!
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