Objective: To characterize the causes of marked elevation of C-reactive protein (CRP) levels, investigate patient outcomes, and examine factors that might influence the CRP response.
Design: Health records were used to retrospectively determine patient characteristics, diagnoses, and outcomes over a 2-year period (2012 to 2013).
Setting: A large referral centre in Moncton, NB.
Objective: To determine if ischaemia is a causal factor in the development of calcinosis in SSc.
Methods: Patients with SSc were assessed yearly. Physicians reported the presence of calcinosis, digital ischaemia (digital ulcers, digital necrosis/gangrene, loss of digital pulp on any digits and/or auto- or surgical digital amputation) and nailfold capillary dropout assessed using a dermatoscope.
Background: Systemic sclerosis (SSc)-related interstitial lung disease (ILD) has phenotypic similarities to lung involvement in idiopathic interstitial pneumonia (IIP). We aimed to assess whether genetic susceptibility loci recently identified in the large IIP genome-wide association studies (GWASs) were also risk loci for SSc overall or severity of ILD in SSc.
Methods: A total of 2571 SSc patients and 4500 healthy controls were investigated from the US discovery GWAS and additional US replication cohorts.
Objective: To examine the demographic and clinical characteristics of systemic sclerosis (SSc) patients without antinuclear antibodies (ANA) compared to ANA-positive patients.
Methods: SSc patients enrolled in the Scleroderma Family Registry and DNA Repository were included. Relevant demographic and clinical data were entered by participating sites or obtained by chart review.
Objective: The goal of this study was to determine the sensitivity of the new 2013 classification criteria for systemic sclerosis (SSc; scleroderma) in an independent cohort of SSc subjects and to assess the contribution of individual items of the criteria to the overall sensitivity.
Methods: SSc subjects from the Canadian Scleroderma Research Group cohort were assessed. Sensitivity was determined in several subgroups of patients.
In this study, 1,833 systemic sclerosis (SSc) cases and 3,466 controls were genotyped with the Immunochip array. Classical alleles, amino acid residues, and SNPs across the human leukocyte antigen (HLA) region were imputed and tested. These analyses resulted in a model composed of six polymorphic amino acid positions and seven SNPs that explained the observed significant associations in the region.
View Article and Find Full Text PDFObjective: To assess physician service use in a large sample of patients with systemic sclerosis (SSc), and to determine factors associated with physician use.
Methods: Our sample was a national SSc registry maintaining data on demographics (age, sex, race/ethnicity, education, income) and clinical factors (disease onset, organ involvement, etc.).
Objective: To assess the number of live births in women whose systemic sclerosis (SSc) onset occurred during their reproductive years, and to compare this with general population rates.
Methods: Within the Canadian Scleroderma Research Group cohort, we identified 320 women whose SSc symptoms began prior to age 50 years. We determined the number of children born in the years following first onset of symptoms.
Objective: To estimate the prevalence of elevated pulmonary arterial pressures (PAP) as a correlate for pulmonary arterial hypertension (PAH) in patients with systemic sclerosis (SSc) in rheumatology centers in Canada.
Methods: During the one-year study period (June 2002-May 2003), charts of patients with SSc were reviewed to determine demographics, SSc characteristics, percentage of patients with a PAH diagnosis, and the site criteria for such diagnosis. Subjects with no PAH that had symptoms of dyspnea and/or fatigue were invited to undergo Doppler echocardiography to estimate their systolic PAP (sPAP).
Objective: To determine if the prevalence of 2 prothrombotic genetic factors, factor V Leiden and prothrombin gene mutation, is increased in patients with antiphospholipid (aPL) antibodies with a history of venous/arterial thrombosis compared to patients with aPL antibodies with no history of thrombosis.
Methods: One hundred fifty-seven patients with aPL antibodies were studied. The occurrence of venous and arterial thrombotic events since the time of antibody detection was determined retrospectively, using appropriate clinical and diagnostic criteria.