Association between baseline levels of C-reactive protein (CRP) and a dinucleotide repeat polymorphism in the intron of the CRP gene

Alex J. Szalai, M. A. McCrory, G. S. Cooper, J. Wu, R. P. Kimberly

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129 Scopus citations


Elevation of baseline C-reactive protein (CRP) is associated with increased risk of cardiac disease. This increase might reflect low-grade inflammation, but differences in CRP serum levels might also have a genetic component. To test this possibility, we investigated whether a polymorphic GT-repeat in the intron of the CRP gene contributes to variation in baseline CRP. We found that the polymorphism was associated with differences in baseline CRP in both normal individuals and in patients with the inflammatory disease systemic lupus erythematosus, viz. donors carrying two GT16 alleles, two GT21 alleles, or GT16/21 heterozygotes had two-fold lower serum CRP than those with other genotypes. The frequency of GT16 and GT21 was two-fold higher in Caucasians than in African-Americans, but there was no difference in allele distribution between patients and controls. It is not yet known how this genetic polymorphism mediates its effect on CRP expression, and it probably is not a systemic lupus erythematosus susceptibility factor. Rather, the CRP intron polymorphism likely modifies the disease phenotype. On the other hand, the fact that baseline CRP does have a genetic component suggests that in coronary disease, stratification of risk assessment based on CRP levels might be enhanced by consideration of this polymorphism.

Original languageEnglish (US)
Pages (from-to)14-19
Number of pages6
JournalGenes and Immunity
Issue number1
StatePublished - Feb 2002

Bibliographical note

Funding Information:
This work was supported by: the intramural research program of the National Institute of Environmental Health Sciences and National Center for Minority Health and Health Disparities of the NIH (GSC), NIH Grant R29 AI42183 (AJS), and the Specialized Center of Research in Genetics of SLE P50 AR45231 (RPK). Received 20 August 2001; revised 11 October 2001; accepted 12 October 2001


  • Acute phase proteins
  • Inflammation
  • Risk factors


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