Correlation of Lipid Profile & Acute Inflammatory Markers in Rheumatoid Arthritis
DOI:
https://doi.org/10.48165/f65wcy04Keywords:
LDL, HTL, ESR, CRP, RAAbstract
Background: Rheumatoid arthritis (RA) primarily affect the synovium and is a chronic inflammation disease, which leads to joint damage and bone destruction. Causes of significant morbidity are due to result of synovial inflammation, joint destruction and associated disability. Many pieces of evidence suggest that proatherogenic disease associated with increased cardiovascular (CV) mortality is rheumatoid arthritis (RA). Addition to genetic and conventional CV risk factors, chronic inflammation has emerged as a key component of this process. Cardiovascular concerned demises shown a preferment in CRP among RA cases who have ongoing active inflammation that's why CRP can be self-sufficient pointer for cardiovascular disease. Subjects and Methods: Current study has been conducted in Teerthanker Mahaveer hospital, Teerthanker Mahaveer medical college. Data has been collected in duration of 12 months. After obtaining consent, data has been collected from 60 consecutive established case of rheumatoid arthritis. Almost equal number of participants were belonging to 30-39 years (16, 26.7%), 40-49 years (15, 25.0%), and 50-59 years (16, 26.7%) age groups. Very few participants were belonging to 20-29 years (4, 6.7%) and 60-69 years (9, 15.0%). Range of age was from 25 years to 69 years. Results: Pearson correlation coefficient of CPR with Total cholesterol, HDL-C, Triglyceride, LDL-C and VLDL-C were -0.326, -0.269, -0.307, -0.310 and -0.307 respectively. All the correlation coefficients were statistically significant (<0.05). Correlation coefficient of ESR with Total cholesterol, HDL-C, Triglyceride, LDL-C and VLDLC were -0.294, -0.311, -0.226, -0.253 and -0.226 respectively. Among them correlation coefficient of ESR with total cholesterol (p-value=0.023) and HDL-C (p-value=0.016) were statistically significant (<0.05). Conclusion: General population danger of atherosclerosis surmount with increment in LDL and wane of HDL but in RA population there is wear off in HDL LDL and total cholesterol, when present in its inflammatory condition. There is a difference in the lipid trend in RA patient then the general population. Rheumatoid arthritis is a disease with lipid paradox. A high inflammatory burden determined by the mean values of ESR and CRP in active disease is associated with low lipid levels but more risk of CV events.
References
1. Gravallese EM. Bone destruction in arthritis. Ann Rheum Dis 2002; 61 (Suppl 2) : ii84-ii86.
2. Gabriel SE, Crowson CS, Kremers HM, Doran MF, Turesson C, O'Fallen WM, Matteson EL. Survival in rheumatoid arthritis: a population-based analysis of trends over 40 years. Arthritis Rheum: 2003; 48: 54-58.
3. Isomaki HA, Mutru O, Koota K. Death rate and causes of death in patients with rheumatoid arthritis. Scand J Rheumatol 1975; 4: 205-208. 4. Mutru O, Laakso M, Isomaki H, Koota K. Ten year mortality and causes of death in patients with rheumatoid arthritis. Br Med J (Clin Res Ed) 1985; 290: 1797-1799.
5. Watson DJ, Rhodes T, Guess HA. All-cause mortality and vascular events among patients with rheumatoid arthritis, osteoarthritis, or no arthritis in the UK General Practice Research Database. J Rheumatol: 2003; 30: 1196-1202.
6. Pinals RS. Survival in rheumatoid arthritis. Arthritis Rheum 1987; 30: 473-475.
7. Mitchell DM, Spitz PW, Young DY, Bloch DA, McShane DJ, Fries JF. Survival, prognosis, and causes of death in rheumatoid arthritis. Arthritis Rheum 1986; 29: 706-714.
8. Wolfe A.M. The epidemiology of rheumatoid arthritis: A review, I: Surveys. Bull Rheum Dis 1968; 19: 518-523.
9. Engel A., Roberts J., Burch T.A. Rheumatoid arthritis in adults in the United States, 1960-1962. In Vital and Health Statistics, Series 11, Data from the National Health Survey, Number 17. Washington, DC, National Center for Health Statistics, 1966.
10. Mikkelsen W.M., Dodge H.J., Duff I.F., et al. Estimates of the prevalence of rheumatic disease in the population of Tecumseh, Michigan, 1959-1960. J Chronic Dis 1967; 20: 351-369.
11. Fleming A., Crown J.M., Corbett M.: Early rheumatoid disease, I: Onset. Ann Rheum Dis 1976; 35: 357-360.
12. Joshi VR. Rheumatology, Past, Present and Future. JAPI. 2012;60:21- 24.
13. Gonzalez-Gay MA, Gonzalez-Juanatey C, Martin J. Rheumatoid arthritis: a disease associated with accelerated atherogenesis. Semin Arthritis Rheum 2005;35:8–17.
14. Aviña-Zubieta JA, Choi HK, Sadatsafavi M, et al. Risk of cardiovascular mortality in patients with rheumatoid arthritis: a metaanalysis of observational studies. Arthritis Rheum 2008;59:1690–7.
15. Dessein PH, Joffe BI, Veller MG, et al. Traditional and nontraditional cardiovascular risk factors are associated with atherosclerosis in rheumatoid arthritis. J Rheumatol 2005;32:435–42.
16. López-Mejías R, García-Bermúdez M, González-Juanatey C, et al. NFKB1–94ATTG ins/del polymorphism (rs28362491) is associated with cardiovascular disease in patients with rheumatoid arthritis. Atherosclerosis 2012;224:426–9.
17. Gonzalez-Gay MA, Gonzalez-Juanatey C, Piñeiro A, et al. Highgrade C-reactive protein elevation correlates with accelerated atherogenesis in patients with rheumatoid arthritis. J Rheumatol2005;32:1219–23.
18. Gonzalez-Gay MA, Gonzalez-Juanatey C, Lopez- Diaz MJ, et al. HLA DRB1 and persistent chronic in flammation contribute to cardiovascular events and cardiovascular mortality in patients with rheumatoid arthritis. Arthritis Rheum 2007;57:125–32.