Hemolysis (redirected from beta (beta) hemolysis)

hemolysis (hĭmŏl`ĭsĭs), destruction of red blood cells in the bloodstream. Although new red blood cells, or erythrocytes, are continuously created and old ones destroyed, an excessive rate of destruction sometimes occurs. The dead cells, in sufficiently large numbers, overwhelm the organ that destroys them, the spleen, so that serum pigments resulting from hemoglobin breakdown appear in the blood serum. Jaundice is caused by overloading the liver with pigment. Large-scale destruction of red blood cells, from any of a variety of causes, results in anemia. Rh disease, or erythroblastosis fetalis, is a hemolytic disease of newborns caused by an immune reaction between fetal red blood cells and maternal antibodies to them. Some hemolytic conditions, e.g., those in which red blood cells are fragile and rupture easily, are treated by removal of the spleen to slow cell breakdown or by administration of steroids. Autoimmune hemolytic conditions result from splenomegaly. The spleen not only sequesters red blood cells, but produces antibodies against the body's red blood cells. This is a potentially lethal condition that occurs more often in women than men.

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hemolysis [hē′mäl·ə·səs]

(physiology)

The lysis, or destruction, of erythrocytes with the release of hemoglobin.

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Hemolysis 

(hematolysis, erythrocytolysis), the destruction of erythrocytes, accompanied by the release of hemoglobin into the surrounding medium.

Physiological hemolysis, a process that completes the 120-day life cycle of the erythrocyte, takes place continuously in man and animals. Under normal physiological conditions 0.8 percent of all the erythrocytes—usually the “aging” ones—undergo lysis. The final decomposition of these aging erythrocytes takes place primarily in the spleen. When the erythrocytes are decomposed bilirubin, one of the bile pigments, is formed from the liberated hemoglobin through a series of complex transformations; the extent of hemolysis can therefore be judged from the amount of bilirubin in the blood and bilirubin derivatives in the feces and urine. The iron liberated in the breakdown of hemoglobin is deposited in the reticuloendothelial cells of the liver and spleen. After complex transformations, this iron is bound to the beta globulin fraction of blood albumin and then takes part in the formation of new hemoglobin.

Disruption of the balance between the lytic agent and the inhibitor may lead to the predominance of blood destruction over blood formation—in other words, to pathological hemolysis. Pathological hemolysis occurs in hemolytic anemias and hemoglobinopathies. It may result from hemolytic poisons (such as certain bacterial toxins, lead, arsenic, nitrobenzene, and morel toxin), from the formation of autoimmune and isoerythrocytic antibodies following the transfusion of incompatible blood, from Rh conflict in the newborn, from the action of certain chemical agents and cold, and, in sensitive individuals, after taking certain drugs or inhaling some types of pollen. In pathological hemolysis, erythrocytes are destroyed in all cells of the reticuloendothelial system (for example, in the liver, bone marrow, or lymph nodes) and also possibly in the bloodstream. In this case most of the hemoglobin of the destroyed erythrocytes is bound to a specific protein (haptoglobin) while the excess passes through the renal filter into the urine (hemoglobinuria). The destruction of a large mass of erythrocytes at once, such as in hemolytic anemias, may be accompanied by a serious condition (hemolytic shock) which may result in death.

Hemolysis may occur in blood that has been stored for a long time, rendering it no longer suitable for ordinary transfusions.

A. M. POLIANSKAIA