BackgroundPotent anti‐inflammatory rheumatoid arthritis (RA) treatments are associated with reduced cardiovascular risk as well as increases in low‐density lipoprotein (LDL) cholesterol. This apparent paradox may be explained by favorable changes in other lipid measurements. The objective of this study was to determine the longitudinal association between changes in inflammation with advanced lipoprotein measurements and high‐density lipoprotein (HDL) cholesterol efflux capacity.Methods and ResultsWe conducted this study in a longitudinal RA cohort from a large academic center, including subjects with high‐sensitivity C‐reactive protein (hs‐CRP) reduction ≥10 mg/L at 2 time points 1 year apart. Subjects receiving statins during the study period or preceding 6 months were excluded. We compared total cholesterol, LDL cholesterol, HDL cholesterol, apolipoprotein B, and apolipoprotein A1 levels and HDL cholesterol efflux capacity at baseline and 1‐year follow‐up by using the paired t test. We also assessed the correlations between reductions in hs‐CRP with percentage change in lipid parameters. We studied 90 RA subjects (mean age 57 years, 89% female), all of whom were receiving disease‐modifying antirheumatic drugs. We observed a 7.2% increase in LDL cholesterol levels (P=0.02) and improvement in efflux capacity by 5.7% (P=0.002) between baseline and follow‐up, with a median hs‐CRP reduction of 23.5 mg/L. We observed significant correlations between reductions in hs‐CRP with increases in apolipoprotein A1 (r=0.27, P=0.01) and HDL cholesterol efflux capacity (r=0.24, P=0.02).ConclusionAmong RA subjects experiencing reductions in hs‐CRP, we observed increased LDL cholesterol levels and concomitant improvements in HDL cholesterol efflux capacity. These findings provide further insight into lipid modulation and the beneficial effect of reduction in inflammation on lipids in vivo.
Patients with RA experienced flares more often when noted to be in higher disease activity states than when in remission and reported changes in disease-modifying antirheumatic drugs or biologics more frequently when flares were of longer duration. There is a need to prospectively study symptom intensity and duration of flare in relation to disease activity and consider self-management strategies in the development of a measure of flare.
Serum Vitamin B12 levels were determined on 378 patients ranging in age from 56 to 104 years with a median age of 77 for both males and females. A radiodilution method was employed for these determinations. This screening procedure identified 26 patients with low serum B12 levels. Nineteen of these patients had no other symptoms and were hematologically normal. The B12 binding proteins, transcobalamins (TC) I, II, and III were quantitated employing QUSO and DEAE cellulose batch separations. The total number of TC II binding/affinity sites for B12 were elevated in both the normal and low B12 elderly groups. About 17% of the total serum B12 was carried by TC II in the control group while only 4% of the total was carried on TC II in both the normal and low B12 elderly. This was accompanied by an increase in unsaturation in TC II for these two groups. The findings suggest that an alteration in the TC II-B12 delivery system has occurred in the elderly.
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