Hemolytic anemia in the elderly

Introduction to hemolytic anemia in the elderly Hemolytic anemia refers to anemia that occurs when red blood cells are prematurely destroyed and their speed exceeds the compensatory capacity of bone marrow. Due to the abnormality of the red blood cells themselves, it is easy to be destroyed, and hemolysis occurs; or the red blood cells themselves are not abnormal, and the red blood cells are largely destroyed due to the action of the hemolytic factors, and the hemolytic anemia occurs more than the compensatory action of the bone marrow hematopoietic function. basic knowledge The proportion of illness: 5-10%, common in patients with folic acid, vitamin B12 deficiency and liver enlargement. Susceptible people: the elderly Mode of infection: non-infectious Complications: jaundice, renal failure

The cause of hemolytic anemia in the elderly

(1) Causes of the disease

The causes of hemolysis are: due to the abnormality of red blood cells themselves, it is easy to be destroyed, hemolysis occurs; or the red blood cells themselves are not abnormal, and the red blood cells are destroyed by the action of hemolytic factors, and the hemolytic anemia occurs more than the compensatory effect of bone marrow hematopoietic function. .

Lymphatic proliferative diseases (such as lymphoma, chronic lymphocytic leukemia, multiple myeloma and macroglobulinemia), immune diseases (rheumatoid arthritis, Sjogren's syndrome, etc.) It causes immune dysfunction in the body and loses recognition ability to its own red blood cells, resulting in abnormal autoantibodies. Such autoantibodies can be IgG, IgA, IgM or C3. According to the temperature required for the antibody to act on red blood cells, it can be divided into warm antibody type (mainly IgG, IgM, IgA is rare, most active at 37 °C) and cold antibody type (mainly IgM, 20% most effective) Active) is an incomplete antibody. The adsorption of the incomplete antibody on the erythrocyte membrane can change the performance of the erythrocyte membrane, making the red blood cells spherical, easily destroyed by mononuclear-macrophage phagocytosis, and is extravascular hemolysis. Secondary autoimmune hemolytic anemia in the elderly is mostly in this form.

There are many mechanisms by which drugs induce immune hemolytic anemia. The drug-induced immune hemolytic anemia in the elderly is mostly:

1. Autoantibody mechanism: represented by a-methyldopa, generally considered to be due to a decrease in autoimmune function caused by a decrease in T suppressor cells by a-methyldopa drugs. The erythrocyte surface-coated antibodies in these patients are mostly IgG antibodies, and about 10% of patients have positive anti-human globulin test (Coombs test) and last longer (3-6 months). This type of hemolytic anemia occurs only in 0.5% of patients taking the drug, the onset is slow, only 3 to 4 months after taking the drug, the symptoms are mild, and there is a tendency to self-limiting, the blood picture can be recovered after stopping the drug, and a few people need steroids. treatment. In addition to a-methyldopa, drugs that cause such autoimmune hemolytic anemia include levodopa, procainamide, mefenamic acid, and chloronitrogen.

2. Semi-antigen mechanism: A hapten refers to an antigen having a molecular weight of <10 KD. Such antigens generally do not induce an immune response. When a patient intravenously injects some immunogenic drugs, such as intravenous injection of large doses (more than 1 million U per day) of penicillin for more than 1 week, penicillin can act as a hapten and on normal erythrocyte membranes. The protein binds firmly to produce an IgG antibody. This kind of antibody only destroys red blood cells with penicillin binding. The anemia is mostly mild to moderate. Very few patients can take long-term use of intravascular hemolysis and hemoglobinuria, and may have severe anemia. During the treatment with penicillin, the patient's direct Coombs test and the indirect Coombs test (ie, the serum of the patient and the red blood cells sensitized by penicillin in vitro) were also positive, and such hemolysis was quickly terminated after the withdrawal of penicillin. Steroid treatment does not reduce anemia, the most important thing is to stop penicillin, otherwise anemia can be aggravated or even life-threatening. Cephalosporin can cause this type of immune hemolysis. Generally speaking, it is mild.

(two) pathogenesis

The life span of normal red blood cells is 100 to 120 days. Due to the defects of red blood cells (cell membrane, red blood cell energy metabolism related enzymes and hemoglobin molecules), the lifespan of red blood cells is shortened, so that they are destroyed. In addition, factors other than red blood cells are acquired, they can be abnormal immune effects, or chemical or physical. Role or biological factor. In a few cases, the above two factors can exist in the same patient at the same time. The site of hemolysis can be roughly divided into two parts: intravascular and extravascular. Blood type inconsistent blood transfusion (up to 50ml or more life-threatening), a large number of red blood cell destruction, acute hemolysis occurs in the blood vessels of the blood, may have chills, fever, low back pain, tachycardia, hemoglobinuria, severe shock, Acute renal failure. When red blood cells are abnormal or aging, the reticuloendothelial system is destroyed. Hemoglobin is not directly released into the plasma, but is metabolized by biliary pigment to become bilirubin, which is characterized by chronic hemolysis of hyperbilirubinemia due to the rate of red blood cell destruction. Slow, free hemoglobin can all bind to haptoglobin, so there is no hemoglobinuria.

Prevention of hemolytic anemia in the elderly

1. Adrenal cortical hormone is effective for immune hemolytic anemia, but it is ineffective for other hemolysis and avoids abuse.

2. Although the plasma can temporarily improve the general situation, but the autoimmune hemolytic anemia can aggravate the hemolysis reaction, complications caused by hemolysis should be prevented early.

Complications of hemolytic anemia in the elderly Complications, jaundice, renal failure

Accompanied by infection, jaundice, hepatosplenomegaly, liver damage, kidney failure and so on.

Symptoms of hemolytic anemia in the elderly Common symptoms Hemolytic anemia jaundice lymph node enlargement Skin purpura immune hemolytic red blood cell volume increase

The onset of the disease is mixed, the clinical manifestations will be covered by the manifestations of the primary disease, hemolytic anemia can also be the earliest symptoms, and the primary disease occurs only months or even years later, in addition to anemia, patients Most have mild to moderate jaundice and splenomegaly, but also have hepatomegaly and lymphadenopathy or skin purpura. If it is caused by chronic lymphocytic leukemia or lymphoma, splenomegaly is often more obvious.

Examination of hemolytic anemia in the elderly

Hemoglobin is reduced to varying degrees, and reticulocytes are increased. However, if there is a hemolytic crisis or a deficiency of folic acid, the reticulocytes will not increase, but will be lower than normal. When hemolysis is severe, nuclear red blood cells or spheres can be seen in the blood. Red blood cells, white blood cell counts vary, often increase in acute hemolysis, normal platelet count, elevated serum bilirubin, mainly indirect bilirubin increase, plasma haptoglobin reduction and hemoglobinuria in blood vessel hemolysis, anti-human The globulin test is often positive.

The elderly have low immune function and are susceptible to infection, such as pulmonary infection, and X-rays may be abnormal.

Diagnosis and diagnosis of hemolytic anemia in the elderly

diagnosis

The typical manifestations of hemolytic anemia and positive anti-human globulin test are the basis for diagnosis. The diagnosis of primary disease is mainly based on medical history and related examinations. Drug-induced autoimmune hemolytic anemia should have a corresponding history of drug use.

Differential diagnosis

Clinical consideration should first consider the differentiation of immune hemolysis with hemoglobin disease and hemolytic anemia caused by genetic enzyme deficiency.

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