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Introduction autoimmune hemolytic anemia Autoimmune Hemolytic Anemia as red blood cells produced antibodies against their own, leaving their red blood cell destruction resulting hemolysis. Hemolytic anemia is the most common type. When someone's immune surveillance function abnormalities and changes in the antigenicity of red blood cells or red blood cells external infections such as mycoplasma and when the same antigen will produce its own antibodies. The optimum temperature according to antibody, the disease is divided into two categories: (a) warm antibody type: IgG antibodies induced by the temperature, the role of optimum temperature 37 , can occur at any age, 20% to 30% of the cases, said due to unknown causes primary, the rest is secondary, often secondary to malignant cell proliferative disease, rheumatism, and chronic inflammation and certain infections such as ovarian tumor, anti-human globulin test is positive and the diagnosis of corticosteroid treatment is effective help. In addition to aggressive treatment of primary disease, but is mainly used corticosteroids, immunosuppressive agents and splenectomy treatment. (B) of the cold antibody type: is divided into two types: (1) cold agglutinin syndrome and paroxysmal cold hemoglobinuria. Cold agglutinin syndrome caused by the cold IgM antibodies, because the optimum temperature is 0 ~ 5 when red blood cells and produce direct agglutination named Raynaud's phenomenon, in addition to primary herein, may be secon


dary to infection, such as Mycoplasma lymphocyte proliferative pneumonia or malignant disease, cold agglutinin titer test has diagnostic value increased, in addition to treating the primary disease, the available immunosuppressive agents, severe cases can lose washed red blood cells and plasma exchange. (2), paroxysmal cold hemoglobinuria is rare. Overdysfunction of the disease produced by the immune antibodies, combined with the red blood cell surface or free in serum, the sensitized red blood cells, or activation of complement, premature destruction of red blood cell hemolytic anemia situation. Diagnosis (a) medical history and symptoms (1) a history of questions: Note: without jaundice, blood transfusion; have painful foot cyanosis; the lymphatic system is suffering from cancer, myeloma, stomach cancer, autoimmune disease (systemic lupus erythematosus, rheumatoid arthritis, etc.) mycoplasma, virus infection and syphilis and other diseases. whether to apply penicillin, quinidine, quinine, methyl dopa and other drugs. (2) Clinical symptoms: dizziness, fatigue, shortness of breath, palpitations; chills, fever, back pain, chest tightness (acute hemolysis). (B) physical examination found that the appearance of anemia, skin, sclera jaundice, enlarged spleen and mild, some patients with hand, foot and hair (cold antibody type). (C) of the auxiliary examination blood: hemoglobin less positive cells are pigmented anemia; white blood cells, platelets normal; increased reticulocytes, small spherocytosis, showing immature red blood cells. Bone marrow: hyperplasia to marked hyperplasia of immature red blood cells. Myeloid, megakaryocytic cell lines to normal. Red pigment of blood indirectly increased jaundice, serum haptoglobin decreased or disappeared, plasma free hemoglobin increased. Urine hemosiderin was negative. Positive direct antiglobulin test, indirect antiglobulin test positive or negative (warm antibody type autoimmune hemolytic anemia). Cold agglutinin test was positive (cold agglutinin syndrome.) Hot and cold hemolysis test positive test positive in urine hemosiderin (paroxysmal cold hemoglobinuria). (D) the differential diagnosis 1. Hereditary spherocytosis: a family history; peripheral small spherical red blood 10%; red blood cell osmotic fragility test was positive; since the dissolution test: hemol 5%. 2. Paroxysmal nocturnal hemoglobinuria: Acid hemolysis test, venom factor hemolysis test positive test positive in urine hemosiderin. 3. Glucose -6- phosphate dehydrogenase deficiency: methemoglobin reduction test was positive; fluorescent spot test, nitro tetrazolium basket paper method: G6PD activity decreased. Treatment (a) warm antibody type autoimmune hemolytic anemia, cause clearly identified, the primary disease should be actively treated. Glucocorticoids: hydrocortisone: 400 ~ 600mg / d, intravenous infusion, 3 ~ 5d after the switch to prednisone: 1mg/kg/d, oral, 7 ~ 10d improvement in condition, near normal hemoglobin, each weeks of prednisone decreasing dosage of 10 ~ 15mg, until the prednisone 20mg / d, regularly check hemoglobin and reticulocyte count 2 to 3 weeks, if the steady reduction of prednisone every 2.5mg, to 5 ~ 10mg / d, or every other day application of 10 ~ 20mg prednisone maintenance therapy for 6 months. Splenectomy: application of high-dose glucocorticoid treatment and hemolytic anemia after 2 weeks no improvement; or need a large daily dose of prednisone (> 15mg) to maintain the improvement of hematology; or can not tolerate prednisone, immunosuppressive agent therapy, or have contraindications should consider splenectomy treatment. Splenectomy done before the best test 51Cr red blood cell life and detention to determine efficacy of splenectomy. Immunosuppressive drugs: on glucocorticoid therapy and splenectomy can not be achieved remission; a splenectomy contraindications; daily dose of prednisone to be larger (> 15mg) to maintain hematological improvements. Application of azathioprine: 50 ~ 200mg / d; cyclophosphamide: 50 ~ 150mg / d. Hematologic remission, the first reduction of corticosteroid dose, and then decreased to a maintenance dose of immunosuppressive agents, maintenance therapy 3 to 6 months. Observe during the treatment side effects such as bone marrow suppression. Other: (1) high-dose intravenous gamma globulin: 0.4 ~ 1.0g/kg, used in conjunction 5d, a small part of the IgG-mediated autoimmune hemolytic anemia have a certain effect, but the effects are short-lived. (2) plasma exchange: for high antibody titers, glucocorticoid treatment of poor patients. (3) Blood transfusion: hemolytic crisis or severe anemia patients can lose the whole amount of blood or washed red blood cells. (B) Cold antibody autoimmune hemolytic anemia, looking for underlying disease, treatment of primary disease. Avoid cold stimulation, keep warm. Immunosuppressive drugs: the warmth and support of patients with ineffective treatment can be applied, chlorambucil: 2 ~ 4mg / d, treatment for 3 to 6 months (or cyclophosphamide: 100 ~ 150mg / d, treat 3 months .) Efficacy criteri. Ease: Clinical symptoms disappeared. RBC count, hemoglobin and reticulocyte percentage were in the normal category. Determination of serum protein in the normal range of red pigment. Direct and indirect Coomb `s test were converted to negative. 2. Partial remission: Clinical symptoms disappeared. Hemoglobin 80g / L or more, the number of reticulocytes in 5% or less, serum total bilirubin not more than 34 £ mol / l (2mg/dl), Coomb negative or remained positive but the titer significantly lower than before treatment. 3. No significant effect: After treatment, there are varying degrees of hemolytic anemia or symptoms, laboratory tests failed to meet the partial response standards. Prevention of common sense autoimmune hemolytic anemia occurring human body immune disorder, resulting in the destruction of red blood cells for their own factors (complement, antibodies), leading to premature accelerated destruction of red blood cells the body to the clinical symptoms of anemia. The clinical manifestations of this disease has no specific diagnosis mainly depends on laboratory tests, as most of the disease secondary to other diseases, it is clear whether the diagnosis should continue to search for primary disease such as cancer, connective tissue disease, in order to achieve the underlying causes purpose, can actually be cured of the disease. Zunzhu medication regularly during treatment should, in particular hormone in patients with long-term use is not free to self-withdrawal or reduction, otherwise it will lead to increased disease and serious complications.


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