Apolipoprotein-defined lipoprotein abnormalities in rheumatoid arthritis patients and their potential impact on cardiovascular disease

• Published in: Scandinavian journal of rheumatology Vol. 41; no. 3; pp. 165 - 169
• Main Authors: Knowlton, N, Wages, JA, Centola, MB, Alaupovic, P
• Format: Journal Article
• Language: English
• Published: Colchester Informa Healthcare 01-05-2012; Taylor & Francis; Informa
• Subjects: Aged; Apolipoprotein A-I - blood; Apolipoprotein C-III - blood; Apolipoproteins B - blood; Arthritis, Rheumatoid - blood; Biological and medical sciences; Biomarkers - blood; Cardiovascular Diseases - blood; Case-Control Studies; Cholesterol - blood; Cholesterol, VLDL - blood; Cohort Studies; Diseases of the osteoarticular system; Female; Humans; Immunoassay; Immunoprecipitation; Inflammatory joint diseases; Lipoprotein(a) - blood; Male; Medical sciences; Middle Aged; Nephelometry and Turbidimetry; Triglycerides - blood; Human; Immunopathology; Chronic; Rheumatoid arthritis; Diseases of the osteoarticular system; Rheumatology; Autoimmune disease; Cardiovascular disease; Inflammatory joint disease; Apolipoprotein; Lipoprotein
• ISSN: 0300-9742; 1502-7732
• DOI: 10.3109/03009742.2012.654815

Objectives: The aim of this study was to explore apolipoprotein-defined lipoproteins for abnormalities when comparing non-rheumatological controls to rheumatoid arthritis (RA) patients.
Methods: Apolipoprotein and lipoprotein profiles were measured on 94 RA patients and 79 controls by immunoturbidimetric procedures, electroimmunoassays, and immunoprecipitation. Differences between means were tested with a two-sided Student t test with Satterthwaite adjustment. p-values were adjusted for multiple comparisons using the Bonferroni procedure.
Results: RA patients had significantly higher levels of total cholesterol (TC), triglycerides (TG), and very low density lipoprotein cholesterol (VLDL-C) than controls, but no significant differences in the levels of high density lipoprotein cholesterol (HDL-C) and LDL-C. RA patients had significantly lower levels of apolipoprotein (apo)A-I and lipoprotein (Lp)A-I:A-II, but no difference in levels of LpA-I than normal controls. There was a significant difference in the levels of LpB:C but not in LpB:C:E between RA patients and controls. The main abnormality among apoB lipoproteins was the significantly increased concentration of the LpA-II:B:C:D:E subclass in RA patients in comparison with controls. The high levels of LpA-II:B:C:D:E are also reflected in significantly increased levels of apoC-III, and apoC-III bound to apoB lipoproteins.
Conclusion: The LpA-II:B:C:D:E subclass has potential as a new marker for cardiovascular disease (CVD) in RA patients.