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The acute phase reactants are elevated in all inflammatory disorders whether acute or chronic.
These studies have stated that ESR and WBC, as well as the other acute phase reactants, are most commonly used in clinical practice to demonstrate moderate sensitivity and specificity as well as low diagnostic efficacy (22, 26-28).
This latter group, the opsonophagocytic family of C-type lectins, functions predominantly as acute phase reactants. They are calcium-dependent PRR proteins that recognise and bind to microbial carbohydrates and promote phagocytosis via complementary receptors on neutrophils and monocytes/macrophages.
Although C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), widespread and classic markers of inflammation for many years, continue to be valuable, modern studies suggest that MPV and NLR are also promising as novel acute phase reactants (21,23).
IL-6 being an acute phase reactant and inflammatory mediator acts as a possible contributor for cardiac pathology.
Several recent research studies have suggested additional markers that may have prognostic value, including acute phase reactants such as C-reactive protein.
Serum ferritin, the most specific indicator of iron deficiency, is an acute phase reactant and its level is affected by inflammation.
In conclusion, a suggested arthritis screening profile consisting of the acute phase reactant CRP, circulating cytokines (IFN-[gamma], IL-1[beta], IL-1Ra, TNF, GM-CSF, and VEGF), autoantibodies RF and anti-CCP and HLA-DRB1 high-resolution molecular typing shows promise to identify those patients who may benefit from a more aggressive treatment regimen or immediate biological biotherapy.
C-reactive protein: from acute phase reactant to cardiovascular disease risk factor.
Similar conclusions were reported in a follow-up report by the same group using serum amyloid A, another acute phase reactant, instead of hs-CRP (31).
Many studies have been published on quantitative analysis of C-reactive protein which is an acute phase reactant protein that is produced in the liver.
Secondary (AA) amyloidosis is a disorder characterized by the extracellular tissue deposition of fibrils composed of fragments of serum amyloid A protein (SAA), an acute phase reactant. AA amyloidosis can complicate a number of chronic inflammatory conditions, including rheumatoid arthritis (RA), juvenile RA, and ankylosing spondylitis1,2.

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