CRP vs ESR.pptx

CRP vs ESR

1. C-Reactive Protein and Erythrocyte Sedimentation Rate

2. Introduction CRP  was discovered by Tillett and Francis in 1930 The name CRP arose because it was first identified as a substance in the serum of patients with acute inflammation that reacted with the "c“ carbohydrate antibody of the capsule of pneumococcus CRP belongs to the pentraxin family of calcium dependent ligand-binding plasma proteins CRP  the 1 st acute-phase protein to be described and is an exquisitely sensitive systemic marker of inflammation and tissue damage The acute-phase response comprises the nonspecific physiological and biochemical responses of endothermic animals to most forms of tissue damage, infection, inflammation, and malignant neoplasia

3. Circulating CRP concentration In healthy young adult volunteer blood donors, the median concentration of CRP is 0.8 mg/l There are many factors that can alter baseline CRP levels including age, gender, smoking status, weight, lipid levels, and blood pressure A n acute-phase stimulus, values may ↑ from less than 50 m g/l to more than 500 mg/l CRP is synthesized primarily in liver hepatocytes but also by smooth muscle cells, macrophages, endothelial cells, lymphocytes, and adipocytes Hepatic synthesis starts very rapidly after stimulus, serum concentrations rising above 5 mg/l by about 6 hours and peaking around 48 hours.

4. Crp and I nflammation CRP is mainly classed as an acute marker of inflammation The main role of CRP in inflammation tends to focus around the activation of the C1q molecule in the complement pathway leading to the opsonization of pathogens CRP also initiate cell-mediated pathways by activating complement as well as to binding to Fc receptors of IgG CRP binds to Fc receptors with the resulting interaction leading to the release of pro-inflammatory cytokines

5. Crp and I nflammation Evidence suggests that CRP is not only just a marker of inflammation but also plays an active role in the inflammatory process CRP is deposited at sites of inflammation and tissue damage in both naturally occurring and experimental conditions The literature suggests that CRP binds to damaged cell membranes and contributes to the inflammatory response

6. CRP and Infection

7. CRP and Infection

8. The erythrocyte sedimentation rate (ESR) E SR)  is a nonspecific screening test indicative of inflammation It is easy to perform, widely available and inexpensive used for many years to help detect inflammation associated with conditions such as infections , cancers , and autoimmune diseases .

9. The erythrocyte sedimentation rate (ESR) Anticoagulated blood is drawn up into a tube of standardized dimensions and left in a vertical position for exactly one hour After that period the point at which the red cells have separated and settled from the plasma is recorded by reading from the scale on the side of the tube It is used as an initial screening tool and also as a follow-up test to monitor therapy and progression or remission of disease The ESR is directly proportional to red cell mass and inversely proportional to the plasma viscosity

10. Principle

11. Referance Range Adult females 0-20 mm/h Adult males 0-15 mm/hr Children(<10) 0-10 mm/hr

12. Conditions Associated With Increased Esr Kidney disease Pregnancy Rheumatic fever Rheumatoid arthritis Anemia Systemic lupus erythematosus Thyroid disease Etc

13. Some conditions with very high E S R > 100 mm/hr Multiple myeloma Connective tissue Autoimmune diseases Tuberculosis Malignancies Severe anemia

14. Decreased ESR 1. Congestive heart failure 2. Hyperviscosity 3. Decreased fibrinogen levels 4. Polycythemia 5. Sickle cell anemia < 0.5 mm/hr

15. The significance of ESR in inflammation Inflammation can cause abnormal proteins to appear in your blood. These proteins cause your red blood cells to clump together. This makes the red blood cells fall more quickly A group of RBCs that are clumped together will form a stack (similar to a stack of coins) called a rouleau (pleural is rouleaux) A n increase in plasma proteins (present in inflammatory conditions) will propagate an increase in rouleaux formations, which settle more readily than single red blood cells The fluctuating nature of the acute phase proteins in inflammation leads to the increased "stickiness" of RBC's, the formation of RBC "stacks" (rouleaux formation), and an increase in ESR

16. CONDITION OR VARIABLE CRP ESR Specimen requirements Serum or Plasma Stable in stored specimens Fresh specimen of whole blood Cannot be performed on stored specimen Method of measurement Direct quantitation of acute phase response Indirect measurement of fibrinogen elevation Magnitude and rate of rise Elevation begins within 4 to 6 hrs, closely parallels acute response with 4 to 7 hrs. half life, allowing return to normal in 3 to 7 days after stimulus is withdrawn. Peak levels 100-1000% above base line. Rises more slowly, may not return to normal for weeks, despite clinical improvement. Fibrinogen increases up to 400% above base line. Effects of anaemia, polycythemia, interaction of proteins and red blood cells, size, shape of red blood cells Unaffected False negative or false positive reactions, depending on abnormality Age and gender Minimal change from neonate to elderly Rises with age, higher values in women