Hemolytic anemia HA is a complex and serologically challenging subject, requiring specialized knowledge and lab experience. The information provided is intended only as an introduction to the subject. When treatment options are listed, they are for information only and in no way suggest to clinicians that such options should be taken.

Hemolytic Anemia Increased destruction of red blood cells in the peripheral blood without evidence of ineffective erythropoiesis is known as hemolytic anemia. Such anemias are generally classified into either inherited or acquired types.

Hemolysis溶血 The term hemolysis refers to red cell destruction in general and should not be interpreted as referring to intravascular red cell destruction only. It may mean that red cells are removed from the bloodstream and hemolysed extravascularly. HA may be defined as primary or secondary disease. There may be no identifiable cause of the anemia, in which case the disease is also termed “idiopathic”.

Hemolysis Hemolysis is the premature destruction of RBCs due to intrinsic inherited defects in the RBCs or because of acquired intravascular abnormalities. RBCs normally live about 120 days following bone marrow release as reticulocytes. When the RBCs become senescent they are removed from the peripheral blood by macrophages in the spleen and liver.

Hemolysis may be either intravascular or extravascular In intravascular hemolysis RBCs lyse in the circulation releasing hemoglobin into the plasma. Causes include mechanical trauma, complement fixation, and other toxic damage to the RBC. The fragmented RBCs are called schistocytes

In extravascular hemolysis RBCs are phagocytized by macrophages in the spleen and liver. Causes include RBC membrane abnormalities such as bound immunoglobulin, or physical abnormalities restricting RBC deformability that prevent egress from the spleen. Extravascular hemolysis is characterized by spherocytes.

Intravascular hemolysis releases hemoglobin which is immediately bound by haptoglobin. Hemoglobin-haptoglobin is cleared almost immediately from the plasma by hepatic reticuloendothelial cells. As intravascular hemolysis with binding to haptoglobin generally overwhelms the rate of haptoglobin synthesis, haptoglobin levels decrease. After haptoglobin is saturated, excess hemoglobin is filtered in the kidney and reabsorbed in the proximal tubules where the iron is recovered and converted into ferritin or hemosiderin.

Hemoglobinuria indicates severe intravascular hemolysis overwhelming the absorptive capacity of the renal tubular cells. Urine hemosiderin is another indicator that intravascular free hemoglobin is being filtered by the kidneys. Lactic dehydrogenase (LDH) is greatly elevated in patients with intravascular hemolysis. Note: Haptoglobin, synthesized by the liver, is decreased in patients with hepatocelIular disease.

In extravascular hemolysis spleen and liver macrophage Fc receptors bind immunoglobulin attached to RBCs and then either ingest small portions of the RBC membrane creating spherocytes or phagocytizing the RBCs.

Amino acids from the globin chains are recycled and the Fe removed from the heme and reused. The heme is degraded into the tetrapyrrole, bilirubin. Note: Because little hemoglobin escapes into the plasma in extravascular hemolysis, haptoglobin does not generally decrease.

Extravascular hemolysis

Free unconjugated bilirubin is transported to the liver where it is conjugated to glucuronic acid. In extravascular hemolysis plasma levels of unconjugated bilirubin increase because the hepatocytes cannot process the excess bilirubin. Conjugated bilirubin is excreted into the gastrointestinal tract where it is converted to urobilinogen and eventually excreted in the feces as stercobilinogen. Conjugated bilirubin levels are usually normal in hemolysis.

Peripheral smear schistocytes spherocytes Haptoglobin decrease/absent mild decrease Urine hemosiderin ++ negative Urine hemoglobin Direct DAT usually negative ++++ LDH increase Intravascular Extravascular

There are two main categories of hemolytic anemia Autoimmune Red cell deficiency or abnormality

Auto-immune hemolytic anemia (AIHA)自身免疫性溶血性贫血 自身抗体（Autoantibody)：指能与自身成分特异性结合的具有免疫功能的球蛋白。正常人血清中含有autoantibody,但效价很低，无自身破坏作用。 自身免疫（Autoimmunity）：机体抗原特异性淋巴细胞发生异常，对自身正常组织发生的免疫应答状态；或抗原特异性淋巴细胞正常，而自身组织成分发生改变而引起的免疫应答状态。

发病机理Etiology 几种可能的机制： 病毒感染：可改变机体自身红细胞的抗原性；或作为多克隆激活刺激B细胞分裂增殖，并发展为浆细胞，产生自身抗体。也可直接损害免疫系统。 遗传因素：人类群体和家谱分析及动物试验模型等资料支持这种观点。 由抗原特异性淋巴细胞引起：A。淋巴细胞改变了识别能力；B。耐受性T细胞的消失，B细胞得到大力辅助产生自身抗体；C。 Ts细胞功能异常，功能低下，使Th细胞活性相对增高，而使B细胞多克隆激活，产生大量自身抗体。 AIHA is often secondary to an existing condition such as lymphoma, SLE, viral infection or untreated syphilis.

诊断原则和标准 诊断AIHA要将临床表现和实验室诊断相结合。 临床表现和实验室诊断的共同特点： 部分自身免疫疾病有明显诱因，而另一部分属于”自发“。 患者以女性多见，发病率随年龄而增高，有遗传倾向。 血清中球蛋白增高。 血清中有自身抗体和（或）针对自身抗原的致敏淋巴细胞，自身抗体在不同自身免疫病中有交叉或重叠现象。

5. 病程慢性发作和缓解交替(例如SLE）。 6. 组织损害部位有淋巴细胞和浆细胞浸润，常见嗜酸性粒细胞增多。 7. 免疫抑制剂（包括肾上腺皮质激素）或手术切除淋巴组织有一定疗效。 确定溶血性贫血的血液学检查： 一般为简单试验-----RBC count; reticulocytes count; 血清结合珠蛋白(Haptoglobin) ；血清总胆红素；LDH；Hb; 细胞形态学观察等。

AIHA指征：DAT阳性 当在输血前配血过程中偶尔可能意外发现一个DAT阳性，如果其他的试验检查结果不支持溶血性贫血，就无必要进一步进行血清学检查。因为临床无意义阳性DAT有8%的患者。 如果患者近数周输过血，须进行RBC洗脱（吸收放散）以确定洗脱下的抗体属否具有临床意义的同种抗体。

AIHA的实验室诊断 AIHA的诊断是建立在临床患者有明显溶血的特征性血清学基础上，需要一个详细的实验室检测评估。 DAT能提供患者的红细胞是否被IgG、补体或两者同时包被，以及RBC被致敏的程度。 进一步试验是确定存在于患者血清和RBC洗脱液中抗体的性质。

常规首先使用含有抗-IgG和抗-C3d的“多特异性”抗人球蛋白血清进行DAT。 如果AIHA患者DAT试验阳性，表明其RBC被IgG、C3d或者两者同时包被。进一步使用DAT标准化的抗-IgG和抗-C3（包括C3d）单特异性抗人球蛋白试剂区分RBC是否被IgG或C3致敏。 DAT结果阳性并不能诊断AIHA,同样阴性也不能排除（8%阴性AIHA患者），需要进行综合分析。

在AIHA实验室诊断中，DAT效价滴定评分是至关重要的，RBC膜上抗体数量一般是和溶解的RBC数量成正比，但是例外情况是常见的。所以不能夸大其重要性。 对于DAT阳性结果患者，要检查患者血清中的抗体并确定其特异性，以及反应温度范围，是否具有溶血活性，是否是凝集素还是不完全抗体。一般通过IAT和酶处理RBC凝集方法检测RBC放散液的反应性。

AIHA fall into three major categories Warm autoantibodies: majority of cases Cold autoantibodies: minority of cases Drug induced hemolytic anemia: responsible for a small percentage of cases.

Characteristics of antibodies capable of causing hemolytic anemia The autoantibody has an optimum reaction temperature of +37℃. The immunoglobulin class is usually IgG, and subclasses IgG3 or IgG1. The larger the amount of cell bound antibody, the greater the chance of red cell elimination. Cold autoantibodies may not react at + 37℃, but when they lead to complement fixation, red cells are more likely to be eliminated.

Warm antibodies WAIHA温抗体 Warm autoantibodies are the most common cause of hemolytic anemia of an immune nature. The disease may be primary and idiopathic (of no identifable cause), or secondary to some underlying condition such as lymphoma or SLE, or secondary to treatment with some medicinal drugs.

Lab findings in WAIHA Classically, the DAT is strongly positive. However, when the DAT is positive, it does not always mean that red cells will be eliminated. Antibodies are usually IgG and may be complement-binding. Most antibodies react at + 37℃ by enzyme and IAT methods. When the autoantibody has strong affinity for the antigen, there may be only weak evidence of antibody in the serum. This is because when cells are strongly auto-sensitized, there may be little or no free antibody.

Underlying alloantibodies may become detectable following removal of autoantibodies from patient’s serum by adsorption of the autoantibody with the patient’s own cells.

Antibody elusions may be carried out with the following results The antibody detected in an eluate may be stronger than that in the serum/plasma caused by concentration of antibody as a result of the elution procedure. If the DAT was strongly positive and there is no evidence that antibodies were eluted, an alternative elution technique should be considered, or there is a possibility that the AIHA is drug induced.

Cold autoantibodies Cold antibodies of a benign (harmless) nature are frequently encountered in blood specimens that have been cooled. On rare occasions, a cold autoantibody may have clinical significance, and cause hemolytic anemia. The disease may be primary and idiopathic or secondary to some underlying condition.

Lab findings in cold autoantibodies It may prove impossible to perform a DAT or any other red cell tests on a specimen which becomes agglutinated as it cools. Specimen taken from patients having a cold type hemolytic anemia should then be maintained at +37℃ and kept at this temperature for the duration of all testing, in order to prevent adsorption of antibody and complement in vitro.

Red cells used for the DAT should be washed in +37℃ saline. The DAT may be performed on blood collected into EDTA, which prevents the in vitro uptake of complement. Causative antibodies usually have extremely high titers and are IgM. They sometimes cause hemolysis in vitro. All compatibility tests should be performed at +37℃. The main danger of transfusion is that potent cold agglutinins may mask other clinically significant alloantibodies and that as a result, allo- as well as auto-incompatible blood is transfused.

Specific categories of cold autoantibodies Cold hemagglutinin diesease (CHAD) Acute CHAD is secondary to disease (such as lymphoma) or infection (such as Mycoplasma pneumoniae or infectious mononucleosis, i.e. glandular fever). Chronic CHAD is usually found in aged patients, and sometimes linked to diseases such as lymphoma.

Characteristics of CHAD Children are rarely affected----patients are usually elderly. The condition may be self-limiting and flare up only in cold conditions, when the patient’ extremities (ears, nose, fingers and toes) become cold. When it occurs with febrile illness, haemolysis can be increased, but usually remains extravascular.

In chronic disease, the autoantibody is usually a monoclonal IgM (but sometimes IgG or IgA) that agglutinates red cells in the cold. When the nature of the antibody is biphasic (reacts at two different temperatures, in two different ways, i.e. agglutination at cold temperatures, and haemolysis when the temperature is raised) it usually leads to a more severe condition.

Complement fixation leads to extravascular red cell destruction and because of the consumption of complement, may transiently limit further haemolysis. Complement-binding antibody dissociates in vivo from red cells when they warm up in the central circulation. The antibody then becomes available again, to rebind with unsensitized red cells in vivo.

Lab findings in CHAD CHAD is caused by IgM antibody, usually with Anti-I specificity, so it reacts with all adult red cells. Sometimes the causative antibody is anti-I (which may be identified using cord red cells which are I negative, i positive and react more strongly with anti-i).

The antibody may react at +37℃ in the presence of albumin. The DAT is positive using an antiglobulin reagent specific for complement (anti-C3). The causative antibody is usually of high titer, agglutinating red cells up to a titer of 1000 or higher at +4℃.

Clinical manifestation of CHAD Anemia Reynaud’s syndrome (discolouration of the fingers and toes) Treatment options: Transfusion is seldom needed. If transfusion is required, blood should be warmed and washed cells are sometimes preferred. Keeping the patient warm at all times is important.

Paroxysmal cold hemoglobinuria PCH 阵发性冷血红蛋白尿PCH is a rare condition caused by a biphasic (active at two different temperatures) auto anti-P. The antibody binds to red cells when the individual becomes cold during the night. As a result of antibody binding, complement also becomes cell bound. When the blood warms as the temperature rises in the morning, the coated red cells are hemolysed. Hemoglobinuria follows, and occurs in episodes related to exposure to cold temperatures.

Characteristics of PCH PCH usually occurs secondary to infection in children, when antibodies are produced that cross-react with P antigen. PCH may be seen post M. pneumoniae infection (or other infections such as measles, mumps, chicken pox, CMV, Epstein Barr virus and syphilis). Sufferers are highly susceptible when environmental temperature is low. Disease is usually transient and self-limiting, especially in children.

Lab findings in PCH The cause is usually a polyclonal IgG antibody, that reacts as a biphasic hemolysin using the Donath-Landsteiner test (this is carried out at cold and then warm temperatures to demonstrate the biphasic nature of the antibody; red cells are sensitized at +4℃, and bind complement which hemolyses the red cells when the test is warmed to +37℃). The Donath-Landsteiner test is not carried out in blood transfusion service labs, but could be performed in a pathology lab with a hematology department.

Blood grouping and compatibility testing is complicated by autoantibodies. IgG anti-P is usually the responsible antibody. DAT is positive using antiglobulin reagent with anti-C3 specificity only.

Clinical manifestation in PCH Hemoglobinuria Anemia-usually mild but may be severe Treatment options: Transfusion may be needed, using the least incompatible red cells. Corticosteroids may be given to treat severe anemia. Patients should avoid exposure to cold temperature.

Drug induced hemolytic anemia 药物诱发的溶血性贫血DIHA has the potential to be extremely serious and may be life-threatening. Many theories have been postulated on how drugs induce hemolytic anemia. Certain medicinal drugs-either prescribed or over-the-counter, may have the side effect of triggering AIHA. This may also apply to certain chemnical and insecticides.

服用青霉素、非那西丁、氨基比林、磺胺、甲基多巴等药物后，可以引起体内产生抗体。产生的抗体可以与药物本身反应，也可以与固有的红细胞抗原反应，从而引起DAT阳性。 免疫和细胞破坏，粒细胞、血小板减少等现象导致溶血性贫血。

In drug induced hemolytic anemia, the DAT is usually positive using an anti-IgG antiglobulin reagent. The sensitizing antibody is usually IgG with Rh specificity. Individuals with glucose-6-phosphate dehydrogenase (G6PD) deficency may experience a hemolytic episode if given drugs containing aspirin. Anti-malaria drugs are also a potential cause of acute hemolysis. So the drug is the trigger for an intrinsic deficiency.

Process of drug autoimmune hemolytic anemia Drugs can induce AIHA in various ways, including the following: Antibody to the drug: drugs may be immunogenic in themselves and antibodies formed against them cross-react with the patient’s red cells. Antibody to the red cell membrane: drugs may have the potential to bind loosely to red cells, initiating an immune response that then auto-sensitizes the red cells.

Antibody to the drug-membrane complex: a single specificity antibody may be formed against the immunogen created by cell bound drug + red cell membrane together. Drug metabolites: the antibody may be formed against a chemical produced by the drug rather than the drug itself.

Lab findings in drug related AIHA The DAT may be strongly positive with or without complement involvement. If an eluate is prepared from the patient’s cells, the eluate will not react with routine reagent cells but only with cells coated with the specific drug. Routine antibody screening tests may be negative.

Some drug induced antibodies show blood group specificity (e. g Some drug induced antibodies show blood group specificity (e.g. Rh and Duffy) Penicillin-induced hemolytic anemia: -positive DAT with or without cell destruction -penicillin-bound red cells are sensitized by the autoantibody Cephalosporin-induced hemolytic anemia: -this drug is related to penicillin and has a similar pattern as above. -cephalosporin-induced HA is becoming more prevalent.

Treatment options for drug induce AIHA If the clinical condition persists unnoticed and drugs continue to be administered, the situation may become debilitating and could lead to fatalities. When the AIHA is the result of the production of anti-drug antibodies, discontinuation of the drug leads to eventual resolution of the hemolytic anemia and the DAT becomes negative quite rapidly.

If the drug associated AIHA is the result of the production of red cell autoantibodies, removal of the drug may not halt the autoimmune process. Various drugs may cause this, e.g. α-methyldopa.

Red cell abnormalities/deficiencies Conditions caused by the malfunction of inherited genes can result in red cell membrane deficiencies, or in enzyme or hemoglobin malfunctions. For example: thalassemia is a hemoglobin deficiency in which red cells have a shortened lifespan. Sickle cell anemia is caused by structural abnormal within the hemoglobin molecule. Red cells with abnormal shapes, such as the spherical cells seen in hereditary spherocytosis, are also prone to hemolysis. Red cells from patients with paroxysmal nocturnal hemoglobinuria (PNH) are susceptible to hemolysis because of a red cell membrane defect.

Paroxysmal nocturnal hemoglobunuria This is an acquired intrinsic defect of the red cell membrane. The cells have an increased sensitivity to traces of complement and become hemolytic readily. Patients with bone marrow failure may develop PNH.

Characteristics of PNH Ongoing hemolysis is more commonly seen than hemolytic episodes. PNH can be life-threatening.

Lab findings in PNH Red cells may lyse in a low ionic strength saline medium. The Ham’s acid hemolysis test is positive. In the Ham’s acid test, red cells are tested for their resistance to lysis in an acidified serum; lowering the pH causes complement lysis in PNH. (This test is not carried out in blood transfusion service labs, but could be performed in a pathology lab with a hematology department).

Clinical manifestation in PNH Anemia Complications: hepatic portal vein thrombosis and/or cerebral thrombosis Hemoglobinuria

Treatment options for patients with PNH Transfusion may modulate the production of PNH cells by the bone marrow. PNH responds to corticosteroids. Prophylactic use of anticoagulants (such as Warfarin) may be beneficial. In very severe forms of PNH, bone marrow transplantation may be considered.

THE DIRECT ANTIGLOBULIN TEST The DAT should be performed as part of a differential diagnosis on every patient in whom the presence of hemolysis has been established. The predictive value of a positive DAT is 83% in a patient with hemolytic anemia, but only 1.4% in a patient without hemolytic anemia.

Small amounts of IgG and complement appear to be present on all red cells. Healthy individuals can have 5 to 90 IgG molecules/red cell and 5 to 40 C3d molecules/red cell; these levels are below the threshold of detection in routine testing. Depending on the technique and reagents used, the DAT can detect 100 to 500 molecules of IgG/red cell and 400 to 1100 molecules of C3d/red cell. Positive DATs are reported in 1:1000 up to 1:14,000 blood donors and 1% to 15% of hospital patients. Most blood donors with positive DATs appear to be perfectly healthy and most patients with positive DATs have no obvious signs of hemolytic anemia although, after careful evaluation, some may show slight evidence of increased red cell destruction.

Although a positive DAT in a patient with hemolytic anemia indicates the most likely diagnosis is one of the immune hemolytic anemias, the DAT can be positive, coincidentally, in patients with hemolytic anemia that is not immune-mediated. Conversely, some patients with immune hemolytic anemia have a negative DAT .

Positive DATs due to elevated levels of IgG or complement, with no clear correlation with anemia, have been noted on the red cells of patients with sickle cell disease, β-thalasemia, renal disease, multiple myeloma, auto-immune disorders, AIDS, and other diseases with elevated serum globulin or blood urea nitrogen (BUN) levels. Interpretation of positive DATs should include the patient’s history, clinical data, and the results of other laboratory tests.

When investigating a transfusion reaction, performance of the DAT on postreaction specimens is part of the initial transfusion reaction investigation. The DAT may be positive if sensitized red cells have not been destroyed or negative if hemolysis and rapid clearance have occurred.

Evaluation of a Positive DAT A positive DAT alone is not diagnostic. The interpretation of the significance of this positive result requires knowledge of the patient’s diagnosis; recent drug, pregnancy, and transfusion history; and information on the presence of acquired or unexplained hemolytic anemia. Dialogue with the attending physician is important. Clinical considerations together with laboratory data should dictate the extent to which a positive DAT is evaluated.

Patient History The following situations may warrant further investigation of a positive DAT. History of recent transfusion. When a patient has recently been transfused, a positive DAT may be the first indication of a developing immune response. The developing antibody sensitizes the transfused red cells that have the corresponding antigen and the DAT becomes positive; the antibody may not be of sufficient quantity to be detected in the serum. Antibody may appear as early as 7 to 10 days after transfusion in primary immunization or as early as 1 to 2 days in a secondary response; these alloantibodies could shorten the survival of red cells already transfused or given in subsequent transfusions. A mixed-field appearance in the posttransfusion DAT (ie, agglutination of donor red cells and no agglutination of the patient’s red cells), may or may not be observed.

2. Administration of drugs previously associated with immune-mediated hemolysis. Many drugs have been reported to cause a positive DAT and/or immune-mediated hemolysis, but the occurrence is rare. 3. History of hematopoietic progenitor cell or organ transplantation. Passenger lymphocytes of donor origin produce antibodies directed against ABO or other blood group antigens on the recipient’s cells, causing a positive DAT.

4. Administration of IVIG or IV anti-D. Intravenous immunoglobulin (IVIG) may contain ABO antibodies, anti-D, or, sometimes, other antibodies. Intravenous Rh Immune Globulin used to treat immune thrombocytopenic purpura causes Rh-positive patients to develop a positive DAT.

If an anemic patient with a positive DAT does show evidence of hemolysis, testing to evaluate a possible immune etiology is appropriate. Reticulocytosis, spherocytes observed on the peripheral blood film, hemoglobinemia, hemoglobinuria, decreased serum haptoglobin, and elevated levels of serum unconjugated bilirubin or lactate dehydrogenase (LDH), especially LDH1, may be associated with increased red cell destruction. If there is no evidence of immune hemolysis, no further studies are necessary, unless the patient requires red cell transfusion and the serum contains incompletely identified unexpected antibodies to red cell antigens; an eluate may be helpful with antibody identification

直接抗人球蛋白试验阳性的类型鉴别及临床意义

抗人球蛋白试验(Coombs Test)在血液免疫学中是经常使用的一种方法 ,尤其在自身免疫性溶血性贫血(AIHA)的诊断和血库的交叉配血试验中是传统的一种“金标法”。 但是由于很多疾病如慢性肝炎、肝癌、 SLE和慢性阻塞性肺疾病(COPD)等等 ,有时其红细胞的直接抗人球蛋白试验(DAT)也出现阳性 ,为了区别 DAT是否由于红细胞的真正抗体引起 ,有必要对 DAT 进行类型鉴别 ,有利于临床对AIHA 的早期诊断和指导血库对交叉配血不合进行输血会诊的处理

检测对象 　一组为 8 例本院住院患者:按文献[1 ]确诊的AIHA ,血标本均在激素治疗前采集; 另一组43例在交叉配血中出现DAT阳性患者 ,肝癌 9例、 COPD 7例、肺癌5例、食道癌 5 例、淋巴瘤 4 例、SLE 3例、结肠癌4例、类风湿关节炎1例、慢性重型肝炎5例。

方法 　所有标本利用 DiaMed2ID 反应卡进行红细胞的DAT测定和患者血浆与抗体筛查细胞的间接抗人球蛋白试验( IAT) ,操作按 DiaMed2ID 说明书。 同时所有标本分别与单特异抗 C3 和抗 IgG血清反应 ,然后把 IgG或 IgG+ C3 型标本的红细胞压积进行56 ℃热放散试验 ,放散试验按《输血技术手册》操作[2 ],提取放散液同抗体筛查细胞进行 IAT。

结果　 2.1 AIHA组与非AIHA组患者的 Coombs试验及免疫分型显示 ,8 例 AIHA 中 2 例为 IgG,6 例为 IgG+C3 ,IAT中只有 5 例阳性;而非 AIHA 组免疫分型均为 IgG+ C3 , IAT全部阴性

2.2　患者红细胞放散液与抗体筛查细胞反应 ,AIHA组全部阳性 ,而非 AIHA 组只有一例 SLE患者阳性 ,其余均阴性 ,经χ2检验校正公式统计处理 ,两者有显著性差别(χ2= 37.81 , P < 0101) ,见表2。

3 　讨论 直接抗人球蛋白试验(DAT)是自身免疫性溶血性贫血(AIHA)的常用实验室诊断指标。但是很多疾病均可以出现患者红细胞 DAT阳性的结果。究其原因是红细胞的自身抗体或者免疫复合物黏附在红细胞膜上 CR1 受体引起的[3 ],因此鉴别二者的类型显得极其重要。 自身抗体是由于致病因素引起自身抗原的变异及免疫稳定性破坏 ,致使免疫调节功能紊乱而产生的。自身抗体大部分同 Rh 阳性红细胞有高度亲和性 ,显示抗体的血型抗原特异性[4 ],而免疫复合物中的抗体不会对红细胞产生特异的凝集作用。

所以利用抗原抗体在适当温度下的可逆反应原理 ,把DAT阳性患者红细胞在 56 ℃放散洗脱 ,当患者放散液中有自身抗体存在时 ,它与 Rh 阳性的抗体筛查细胞一般均可出现凝集反应 ,以区别是真实的自身抗体还是免疫复合物引起的。

本文通过随机AIHA组和非 AIHA 组的免疫血清学对比试验已经充分证实这一理论 本文通过随机AIHA组和非 AIHA 组的免疫血清学对比试验已经充分证实这一理论 ! 同时本文 8 例AIHA 有 3 例IAT是阴性的 ,说明以传统的 DAT结合 IAT方法来鉴别红细胞上吸附的是抗红细胞抗体还是免疫复合物存在明显不足[3 ]。 笔者认为对 DAT阳性的标本利用放散试验可以非常准确的进行类型鉴别 ,帮助临床上对 SLE、慢性肝炎、 COPD、肿瘤等各种DAT阳性的初诊患者的鉴别诊断 ,以免造成误诊。

同时对DAT阳性的AIHA患者进行免疫分型也是指导临床治疗的非常重要一环。据有关资料显示免疫分型中IgG+ C3 型溶血较严重 ,不同免疫亚型对临床选择治疗方案、判断预后有很重要价值.