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Abbreviations: CRP: C-reactive protein ESR: erythrocyte sedimentation rate IL: interleukin RBC: red blood cell
| The first 300 words of the full text of this article appear below. |
| Introduction |
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| The ESR |
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Numerous factors affect the ESR. In the blood of healthy patients, gravity causes RBCs to settle. However, as they fall, the upward displacement of plasma balances the downward force, resulting in little settling. When RBCs aggregate, forming rouleaux, the downward forces exceed upward forces, and the ESR increases. Plasma proteins have the greatest effect on RBC aggregation, which is directly proportional to the protein's molecular weight and degree of asymmetry.
Needle-shaped fibrinogen, a large and asymmetric molecule, has the greatest effect of all plasma proteins on ESR. When fibrinogen increases, as in various inflammatory states, the ESR increases concomitantly. For this reason, many clinicians view the ESR as an indirect measure of fibrinogen. Because it is affected by plasma proteins, the ESR tends to rise slowly after the onset of inflammation and can stay elevated for days to weeks after resolution of the inflammation.
Importantly, noninflammatory conditions also affect the ESR. RBCs that have abnormal morphology, as in sickle cell disease, have less of a tendency to form rouleaux, thereby producing lower ESRs. Anemia tends to increase rouleaux formation, and polycythemia decreases it. Understandably, hyperviscosity states slow the ESR, and hypoviscosity states speed the ESR.
| The CRP |
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