Low-density lipoprotein (LDL) apheresis is well-established in selected patients with uncontrolled LDL levels. As such treatment affects biomarkers important in atherosclerosis and acute coronary syndromes, we systematically compared the inflammatory response induced by three LDL apheresis columns. Three patients with heterozygous familial hypercholesterolemia participated in a cross-over study with six consecutive treatments with three different LDL apheresis columns: DL-75 (whole blood adsorption), LA-15 (plasma adsorption), and EC-50W (plasma filtration). Biochemical parameters and inflammatory biomarkers, including complement activation products and 27 cytokines, chemokines, and growth factors were measured before and after treatment. Complement was activated through the alternative pathway. The final end product sC5b-9 increased significantly (P < 0.01) and equally with all devices, whereas the anaphylatoxins C3a and C5a were lower by use of the adsorption columns. Hs-CRP was reduced by 77% (DL-75), 72% (LA-15), and 43% (EC-50W). The cytokines were consistently either increased (IL-1ra, IP-10, MCP-1), decreased (IFN-gamma, TNF-alpha, RANTES, PDGF, VEGF), or hardly changed (including IL-6, IL8, MIP-1alphabeta) during treatment. The changes were in general less pronounced with the adsorption columns. All columns reduced LDL significantly and to the same extent. In conclusion, three LDL-apheresis devices with equal cholesterol-lowering effect differed significantly with respect to the inflammatory response.
ObjectiveThe tender joint count (TJC) is included in composite disease activity scores (CDAS) (the Disease Activity Score in 28 joints, the Clinical Disease Activity Index, and the Simplified Disease Activity Index). The impact of having predominantly tender joints was explored by use of the Tender‐Swollen Joint Count Difference (TSJD), and ultrasound (US) provided a measure of joint inflammation. The current study aimed to explore the cross‐sectional and longitudinal associations between the TSJD and a spectrum of outcome measures, including US scores in patients with established rheumatoid arthritis (RA) during follow‐up and while receiving treatment with biologic disease‐modifying antirheumatic drugs (bDMARDs).MethodsThis was an observational study of 209 patients with established RA consecutively included upon initiation of bDMARD treatment and followed‐up with clinical, laboratory, and comprehensive US examinations at 0, 1, 2, 3, 6, and 12 months. Patients were categorized into 2 groups: those with predominantly tender joints (TSJD >0) and those with predominantly swollen joints (TSJD ≤0). Statistical analyses included Pearson's correlation coefficient, an independent samples t‐test, and regression analyses.ResultsThe TJC had high correlations only with patient‐reported outcomes (PROMs) (P < 0.001). Levels from CDAS and PROMs were significantly higher (P < 0.001) at all visits in patients with TSJD >0 compared to those with TSJD <0. Laboratory markers and assessor's global visual analog scale scores were similar, and US sum scores were significantly lower (P < 0.001–0.03). The baseline TSJD positively predicted levels of all CDAS at 6 months (P < 0.001–0.019) but was a negative predictor of US sum scores (gray‐scale and power Doppler) at 6 and 12 months (P < 0.001).ConclusionPatients with predominantly tender joints had higher CDAS but lower levels of inflammation as defined by US. These findings indicate that inclusion of the TJC in the CDAS may contribute to misleading information about inflammatory activity.
Objective To examine the association of body mass index (BMI) with pain in people with hand osteoarthritis (OA), and explore whether this association, if causal, is mediated by systemic inflammatory biomarkers. Methods In 281 Nor‐Hand study participants, we estimated associations between BMI and hand pain, as measured by the Australian/Canadian Osteoarthritis Hand Index (AUSCAN; range 0–20) and Numerical Rating Scale (NRS; range 0–10); foot pain, as measured by NRS (range 0–10); knee/hip pain, as measured by the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC; range 0–20); painful total body joint count; and pain sensitization. We fit natural‐effects models to estimate natural direct and natural indirect effects of BMI on pain through inflammatory biomarkers. Results Each 5‐unit increase in BMI was associated with more severe hand pain (on average increased AUSCAN by 0.64 [95% confidence interval (95% CI) 0.23, 1.08]), foot pain (on average increased NRS by 0.65 [95% CI 0.36, 0.92]), knee/hip pain (on average increased WOMAC by 1.31 [95% CI 0.87, 1.73]), generalized pain, and pain sensitization. Mediation analyses suggested that the effects of BMI on hand pain and painful total body joint count were partially mediated by leptin and high‐sensitivity C‐reactive protein (hsCRP), respectively. Effect sizes for mediation by leptin were larger for the hands than for the lower extremities, and were statistically significant for the hands only. Conclusion In people with hand OA, higher BMI is associated with greater pain severity in the hands, feet, and knees/hips. Systemic effects of obesity, measured by leptin, may play a larger mediating role for pain in the hands than in the lower extremities. Low‐grade inflammation, measured by hsCRP, may contribute to generalized pain in overweight/obese individuals.
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