Which mechanism explains ESR elevation in inflammatory states?

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Multiple Choice

Which mechanism explains ESR elevation in inflammatory states?

Explanation:
In inflammation, acute‑phase proteins like fibrinogen and certain immunoglobulins rise in the plasma. These proteins reduce the normal negative charge on red blood cells, allowing the cells to stack together in loose aggregations called rouleaux. This rouleaux formation makes the red cells sediment more quickly when whole blood is left standing in a tube, so the erythrocyte sedimentation rate increases. While higher protein levels can also raise plasma viscosity, the key driver of a faster ESR is the tendency of red cells to form rouleaux due to increased acute‑phase proteins. Decreased plasma viscosity or protein levels would slow or lessen ESR, and red blood cell lysis does not promote the orderly aggregation that accelerates sedimentation.

In inflammation, acute‑phase proteins like fibrinogen and certain immunoglobulins rise in the plasma. These proteins reduce the normal negative charge on red blood cells, allowing the cells to stack together in loose aggregations called rouleaux. This rouleaux formation makes the red cells sediment more quickly when whole blood is left standing in a tube, so the erythrocyte sedimentation rate increases. While higher protein levels can also raise plasma viscosity, the key driver of a faster ESR is the tendency of red cells to form rouleaux due to increased acute‑phase proteins. Decreased plasma viscosity or protein levels would slow or lessen ESR, and red blood cell lysis does not promote the orderly aggregation that accelerates sedimentation.

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