No significant changes in arterial stiffness in patients with ankylosing spondylitis after tumour necrosis factor alpha blockade treatment for 6 and 12 months.

OBJECTIVE: The increased cardiovascular risk associated with AS is attributable to multiple factors: disease activity, systemic inflammation, traditional risk factors and NSAIDs. This study aimed to investigate the effects of 24 and 52 weeks of TNF-α inhibitor treatment on arterial stiffness and cardiovascular risk factors. METHODS: Arterial stiffness was measured using the augmentation index (AIx) and pulse wave velocity (PWV), while other cardiovascular risk factors [lipid profile, blood pressure (BP) and BMI] were collected for active AS patients. RESULTS: In total, 49 patients, comprising 30 men, were included in the study, with a mean age of 46.9 (12.1) years. Of these, 20 (40.8%) patients were current smokers, while 10 were treated for hypertension. Patients had long-standing [11.9 (9.2) years] and active AS, with a high initial BASDAI [55.0 (18.2)]. Regarding treatment, 26 patients received etanercept, 17 adalimumab and 6 infliximab. No changes were observed in PWV and AIx after 6 or 12 months following TNF-α blockade [PWV 6.97 (2.03) m/s, 6.92 (1.81) m/s and 7.10 (1.95) m/s at baseline, 6 months and 1 year, respectively, P = 0.64; AIx 19.5 (13.1%), 20.2 (12.8%), 18.3 (13.5%), respectively, P = 0.87]. Lipid profiles and other cardiovascular risk factors were unchanged. However, BASDAI, BASFI and biological inflammation were significantly improved. CONCLUSION: Arterial stiffness was not improved after 6 and 12 months of anti-TNF-α therapy. However, treatment decreased biological inflammation and disease activity without causing any changes in lipid profiles and other traditional cardiovascular risk factors.

Plasma or serum? A qualitative study on rodents and humans using high-throughput microRNA sequencing for circulating biomarkers.

microRNAs are small non-coding RNAs gaining interest for their potential roles as reliable biomarkers for the diagnosis and therapeutics of numerous pathologies, ranging from cancer to neurodegenerative or psychiatric disorders. Indeed, microRNAs are present in various accessible biofluids, including peripheral blood, and specific dysregulation of their expression may be associated with these different pathological conditions. microRNAs can be isolated from plasma or serum for sequencing with commercial kits. However, these two biofluids might exhibit some differences in their microRNA contents, due notably to the coagulation process occurring during serum collection. It remains unclear from previous studies and commercial recommendations which blood fraction is preferable. Because of the small amount of circulating microRNAs in a given blood volume, this question appears crucial for qualitative and quantitative optimization of microRNA profiling, especially in animal models used for investigating the pathophysiological relevancy of this approach. We therefore evaluated the efficiency of RNA isolation and microRNA levels from plasma and sera isolated from rats and humans, with a widely used extraction kit (QIAGEN miRNeasy), and assessed microRNA quality and quantity with high-throughput sequencing. Fewer reads with length corresponding to non-miRNAs sequences were observed in plasma than in serum, both from rats and humans. Moreover, rat plasma produced twice as many aligned reads compared to sera, as well as more aligned reads corresponding to microRNAs (84.6% against 38.7%), differences that were not find in human samples. Our results, therefore, clearly indicate that plasma should be preferred for miRNA investigations, particularly for translational studies.