Haptoglobin (HPT)
TECHNICAL UPDATE

DESCRIPTION/BACKGROUND INFORMATION:

Haptoglobin (HPT) is an alpha-2-glycoprotein synthesized by the liver. Haptoglobin is present in the blood waiting to bind released hemoglobin (Hgb). During extracellurar hemolysis, Hgb is released from the erythrocytes and free Hgb dimers bind almost immediately to HPT.

HPT-Hgb complexes are large enough to prevent or greatly reduce renal loss of Hgb and its iron. The complexes are removed very rapidly by the hepatic Kuppfer cells, where the proteins are degraded and the iron and amino acids reutilized. In addition, HPT-Hgb complexes may be important for the control of local inflammatory processes; the HPT-Hgb complex is a potent peroxidase, capable of hydrolyzing peroxides released during phagocytosis at sites of inflammation.

CLINICAL APPLICATION:

Haptoglobin binds hemoglobin and is taken up by the liver, the liver recycles the iron heme, and amino acids contained in the Hgb protein. This process destroys HPT as well as Hgb. In the presence of active hemolysis, the rate of HPT destruction will outpace the rate at which new HPT is created. Consequently, the concentration of HPT in the blood will decrease. HPT depletion usually is the most sensitive laboratory indicator of hemolysis. Other causes of red cell destruction also decrease HPT: a blood transfusion reaction; mechanical heart valve, abnormally shaped red cells; or abnormal Hgb such as thalassemia or sickle cell anemia.

HPT is known as an acute phase reactant. Its level increases during acute conditions such as infection, injury, tissue destruction, some cancers, burns, surgery, or trauma. Its purpose is to remove damaged cells and debris and rescue important material such as iron. HPT levels can be used to monitor the course of these conditions. HPT levels are increased by corticosteroid hormones and many NSAIDS.

Estrogens decrease synthesis of HPT. Most forms of acute or chronic hepatocellular disease, including acute viral hepatitis and cirrhosis with jaundice, are associated with decreased level of HPT due to altered estrogen metabolism in addition to increased red cell breakdown secondary to erythrocyte membrane lipid alterations. Genetic absence (ahaptoglobinemia) and hypohaptoglobinemia have been reported in many populations, especially in individuals of African descent.

Normal results vary based on the laboratory and test method used. HPT is not present in newborns at birth, but develop adult levels by 6 months. Normal results vary widely from person to person. Unless the level is very high or very low HPT levels are most valuable when the results of several tests done on different days are compared.

METHODOLOGY:

Nephelometry

TEST NAME & NUMBER:

• 2607 Haptoglobin (HPT)
  

REFERENCES:

1. Putnam FW. Haptoglobin. In The Plasma proteins, 2nd ed, vol 2. FW Putna, ed. 1975; New York: Academic Press, 2-51.
   
2. Silverman LM and Christenson RH. Amino acids and proteins. In Tietz textbook of clinical chemistry, 2nd ed. CA Burtis and ER Ashwood, eds. 1994; Philadelphia; W.B. Saunders Co., 707-708.
   
3. Gale Encyclopedia of Medicine, Gale Research. 1999.
   
4. Rebecca Elstrom, M.D. Division of Hematology-Oncology, University of Pennsylvania Medical Center, Philadelphia, PA; VeriMed Healthcare Network, a118/01.