We measured C-reactive protein (CRP), a marker of systemic inflammation and risk of inflammatory disease, in 222 euthymic BD patients and 52 healthy controls.
Inflammatory disease activity was monitored monthly with measurements of serum amyloid A protein (SAA) and C-reactive protein (CRP) in symptomatic individuals.
Major controversy exists as to whether increased C-reactive protein (CRP) contributes to individual components of the metabolic syndrome or is just a secondary response to inflammatory disease processes.
CRP in the GCF appears to be of systemic origin, and therefore may be indicative of systemic inflammation from either a periodontal infection or inflammatory disease elsewhere.
There are common genetic and immunological mechanisms behind concomitant inflammation in the joints and intestinal tract.A number of blood tests, e.g. erythrocyte sedimentation rate, orosomucoid, C-reactive protein, and white cell and platelet counts, are probably the most commonly used laboratory markers of inflammatory disease, however, these tests are difficult to interpret in arthropathies associated with gut inflammation, since any increases in their blood levels might be attributable to either the joint disease or to gut inflammation.
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 GT(16) alleles, two GT(21)alleles, or GT(16/21) heterozygotes had two-fold lower serum CRP than those with other genotypes.