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hsCRP may be a more accessible and reliable method of indicating inflammation, a known precursor to PsA.
A recent prospective cohort study conducted in Canada has indicated that high sensitivity C-reactive protein (hsCRP) could potentially predict the development of psoriatic arthritis (PsA) in patients with psoriasis.1
Already used across several specialties to assess inflammation, hsCRP has remained relatively untested in predicting progression to PsA. Previous research has indicated the presence of inflammatory lesions, including synovitis and osteitis, in patients long before PsA diagnosis.2 Given hsCRP’s capability to identify inflammation, researchers suggest this metric could be applied to predict PsA.
“Given this growing body of evidence supporting the presence of systemic inflammation in pre-clinical PsA, a simple, affordable and accessible blood biomarker like hsCRP, could significantly enhance the identification of individuals at high-risk for progression to PsA,” wrote Lihi Eder, MD, PhD, University of Toronto, and colleagues. “We aimed to investigate the association between hsCRP levels and the risk of developing PsA in a prospective cohort of patients with psoriasis.”1
Investigators analyzed patients from the ongoing University of Toronto Psoriasis Cohort, which began in 2006 as a method of identifying risk factors for PsA. This study utilized data from 2006-2019, excluding patients who did not have follow-up visits or serum samples in the biobank.1
A total of 589 participants were included in the study; each one provided blood samples at each annual rheumatologist visit. Covariates for the study included age, sex, psoriasis duration, area, and severity index, nail lesions, and body mass index.1
Each participant’s hsCRP levels were measured from the first available serum sample. During these visits, a comprehensive assessment of PsA symptoms was conducted by a rheumatologist expert. Diagnosis was determined by two rheumatologists after reviewing all available data.1
Of the included participants, investigators noted that 57 developed PsA during the follow-up period. Mean follow-up duration was 7.5 years, suggesting a crude PsA incidence rate of 1.2 cases per 100 patient-years. Mean age of participants was 47.3 +/- 13.5, and mean psoriasis duration was 16.2 +/- 14.4 years. Mean hsCRP level was 3.1 +/- 5.5 mg/L, with those who developed PsA showing higher baseline hsCRP levels (5.4 +/- 13.1 mg/L).1
Notably, hsCRP levels were substantially higher in patients with arthralgia (4.2 +/- 8.53 vs 2.71 +/- 3.67 mg/L), those with obesity (4.75 +/- 4.95 vs 2.45 +/- 5.61 mg/L), and in females (3.92 +/- 7.13 vs 2.51 +/- 3.68 mg/L). The remaining covariate groups exhibited no significant differences in hsCRP levels.1
Eder and colleagues used univariate regression analysis to reveal that higher hsCRP levels were significantly associated with PsA development, with a 3% increase in PsA risk for each 1 mg/L increase in hsCRP (hazard ratio [HR] 1.03, 95% CI, 1.01-1.05; P =.007). The association remained consistent after multivariable regression analysis, with a 4% PsA risk increase for each 1 mg/L increase in hsCRP (HR 1.04; 95% CI 1.01-1.07; P =.007).1
Because of its use as a biomarker of systemic inflammation, investigators explained that hsCRP is independently associated with increased risk of PsA development among patients with psoriasis. Notably, this remained true regardless of potential compounding factors, which the team suggests proves its use as a biomarker for PsA.1
Additionally, hsCRP is a more sensitive assessment of the protein level at the lower end of the spectrum than the more commonly used CRP. Investigators indicated that, because CRP levels are typically lower in patients with PsA, hsCRP may be a more reliable and successful PsA predictor.1
“This finding underscores the presence of sub-clinical inflammation prior to the development of objective PsA signs and highlights the potential of hsCRP as a biomarker for identifying at-risk populations,” wrote Eder and colleagues. “This could facilitate early interventions that may prevent the progression to PsA.”1