Immune Hemolytic Anemia Associated with Biclonal Cold Autoagglutinins

A 65-year-old man with bladder outlet obstruction due to prostatic hypertrophy was incidentally discovered to have cold-antibody autoimmune hemolytic anemia (cold-aggluthinin syndrome; CAS) due to autoanti-I (titer 1,024 at 4 degrees C and 64 at 30 degrees C), and a biclonal gammopathy. Immunofixation electrophoresis of serum and a red blood cell eluate revealed the patient's autoantibody to be biclonal IgM kappa and IgA kappa. No underlying cause could be determined to explain the development of either the biclonal gammopathy or the CAS. To our knowledge, this is the first reported case of CAS associated with a biclonal gammopathy and biclonal cold autoagglutinins of the IgM kappa, IgA kappa type.     

Anti-Nomifensine Antibody Causing Immune Hemolytic Anemia and Renal Failure

The relative amount of human IgG subclasses and/or subclass-specific determinants were measured in seven commercial i.v. immunoglobulin preparations and one human serum preparation - Paul Ehrlich Institute Plasma Protein Reference No, 2. Quantification was done by means of subclass-specific antisera and a human IgG subclass standard HOO-02 using the recently established rate nephelometric method. The differences between the one human serum preparation and those of normal human serum are much smaller than those between the i.v. immunoglobulin preparations, being for IgG2 the greatest and for IgG3 the smallest. This does not come as a surprise because the various treatment processes used in the manufacture of i.v. immunoglobulin preparations are likely to result in loss and/or masking of the subclass-specific determinants.
Although little is known about the genetical ramifications which could arise through the use of i.v. immunoglobulin preparations in which there is variation in the subclass distribution, attention should be given to this subject as passive immunotherapy becomes more popular.     

Hemolytic Anemia

Captopril was the first oral angiotensin-converting enzyme (ACE) inhibitor available and, as such, has been extensively studied and in clinical use for many years. Several studies have defined captopril's efficacy in the treatment of congestive heart failure (CHF) as well as determined its safety profile. The most common adverse hematologic reactions associated with captopril use include neutropenia and agranulocytosis. This paper describes an uncommon and a potentially serious hematologic side effect associated with captopril-hemolytic anemia.     

Alectinib-induced Immune Hemolytic Anemia in a Patient with Lung Adenocarcinoma

Drug-induced immune hemolytic anemia (DIIHA) is a rare condition with an increasing incidence associated with the frequent use of certain drugs. An 85-year-old woman with lung adenocarcinoma prescribed alectinib complained of dyspnea on exertion at our hospital. Based on her laboratory tests results on admission, we focused on the clinical course of anemia and hemolysis progression after alectinib administration. The patient''s anemia and hemolysis gradually improved after discontinuation of alectinib, leading to a diagnosis of alectinib-induced IHA, presented here as the first case encountered in a patient with lung adenocarcinoma. Furthermore, we discuss the importance of correlating clinical laboratory findings in DIIHA.     

Major Histocompatibility Complex Markers in Patients with Nomifensine-Induced Immune Hemolytic Anemia

To evaluate a possible role of major-histocompatibility-complex (MHC)-related immune-response genes for the selective production of drug-induced antibodies, HLA class I (ABC), class II (DR, DQ), class III (BF, C2, C4A, C4B) as well as glyoxalase-1 allotypes were investigated in 26 patients with nomifensine-induced immune hemolytic anemia. No statistically significant deviations of MHC antigen frequencies were noted. The possible implications of these findings are discussed.     

Fatal Immune Hemolytic Anemia and Hepatic Failure Associated with a Warm-Reacting IgM Autoantibody

Autoimmune hemolytic anemia (AIHA) caused by warm-reacting IgM autoantibodies is rare. We report a fatal case of primary AIHA with a warm-reacting IgM autoantibody. Recurrent episodes of intravascular hemolysis, unresponsive to all therapy and progressive hepatic dysfunction characterized the patient's clinical course. Despite corticosteroid therapy, splenectomy and multiple blood transfusions, the patient died from liver failure. The IgM autoantibody caused autoagglutination of the patient's red cells at 37 degrees C. Eluates prepared from the patient's red cells agglutinated saline-suspended test cells without the addition of antiglobulin reagent. We propose that warm-reacting IgM antibodies may lead to in vivo autoagglutination and may be associated with hepatic failure.     

Auto-Immune Hemolytic Anemia Caused by Anti-U

Abstract. A case of warm antibody auto-immune hemolytic anemia is described in which the serum antibody, and an eluate from the patient's red cells, both had anti-U specificity. The antibody did not react with Rh_null red cells, and gave weaker reactions with -D- red cells than with other U-positive red cells. Five other anti-U sera were tested in comparative titrations and some of these also reacted more weakly against -D- red cells than against red cells having common Rh phenotypes.     

Donath-Landsteiner Autoimmune Hemolytic Anemia in Children

During the last 4 years, we have studied a total of 531 adults and 68 children with clinically and serologically well-defined forms of immune hemolytic anemias. Among these, Donath-Landsteiner (DL) hemolysis was the underlying disease in 22 of the 68 children (32.4%), but was not observed in adults. All children with DL hemolysis suffered from acute infections presumably of viral origin. In none of the cases was the DL hemolysis suspected clinically. Boys were more often affected than girls. The hemolytic episodes were severe, but resolved within few weeks. Serologically, all patients had a strongly positive direct antiglobulin test (DAT) using anti-C3d reagents, but a weak (n = 6) or negative (n = 16) IgG-DAT. DL hemolysins were always weak and transient, detectable with enzyme-treated red blood cells (RBC) in all, with untreated RBC in 12 of 22 sera. To explore the reason why these weak antibodies can cause extensive hemolysis in vivo, we compared the action of DL antibodies and of cold agglutinins (anti-I) on RBC by several reincubations at 4 and at 37 degrees C. The data obtained from this experiment demonstrate a stronger aggravation of hemolysis by DL than by anti-I antibodies, presumably due to low-affinity interaction between the cells and DL antibodies.     

The Hemolytic Anemia of Human Bartonellosis

A study of the processes of formation and destruction of blood has beencarried out, in addition to other investigations of the physiopathology of theanemia of human bartonellosis. From the results obtained the following conclusions may be drawn:

1. The life-span of the red cells parasitized by Bartonella bacilliformis isgreatly shortened. However, not all the parasitized red cells are prematurelydestroyed.

2. Red cells from normal subjects are partially destroyed when they are injected into infected patients. More than 50 per cent of them survive normally.

3. The mechanical fragility of the red cells is increased in the majority ofthe cases.

4. The index of sequestration of red cells by the liver and spleen was increased in the three patients studied. Also, the products of catabolism of hemoglobin were increased in all the patients studied.

5. The increased production of red cells as a response to the great destructionwas prevented at first, but later it reached its peak, being in some cases fivetimes greater than normal.

6. The search for agglutinins and hemolysins was negative.

7. The amount of free protoporphyrins in the red cells was increased, indicating that there was some interference to the synthesis of hemoglobin thatwould also explain the hypochromia of the red cells.

8. The increase in the diameter of the red cells was independent of the actualamount of reticulocytes.

Submitted on November 23, 1960 Accepted on February 12, 1961     

Heparin Therapy in Autoimmune Hemolytic Anemia

1. Although a few previous reports suggest a beneficial effect of heparinin autoimmune hemolytic anemia, there has been no general recognition ofthis form of treatment. Therefore, its striking benefit in a patient with severeautoimmune hemolytic anemia refractory to usual therapeutic measures hasbeen reported.

2. The mechanism of action of heparin in autoimmune hemolytic anemiaremains unknown; it does not appear to be due to any anticomplementaryactivity.

3. Heparin should be tried more widely in autoimmune hemolytic anemia,particularly in situations in which response to corticosteroids and splenectomyhas been disappointing.

     

Megaloblastic Erythropoiesis in Acquired Hemolytic Anemia

1. A case of auto-immune hemolytic anemia complicated by megaloblasticerythropoiesis is described. The possible mechanism is discussed.

2. The direct Coombs test is a useful adjunct in the diagnosis of megaloblastic anemias.

Submitted on June 7, 1960 Accepted on December 10, 1960     

Autoimmune Hemolytic Anemia Associated with Autoanti-Ge

The first reported example of autoimmune hemolytic anemia due to an autoanti-Gerbich is described. The patient's red blood cells exhibited a strongly positive direct antiglobulin test with both IgG and complement antiglobulin reagents. The serum contained a potent antibody which produced agglutination of red blood cells as well as a positive indirect antiglobulin test. Treatment of the serum with 2-mercaptoethanol demonstrated that the antibody contained both IgG and IgM components. The serum antibody and the antibody eluted from the patient's red blood cells had anti-Gerbich specificity. The patient's cells typed as Gerbich-positive with saline-agglutinating anti-Gerbich sera. Of great interest was the fact that the patient's mother also has acquired immune hemolytic anemia, but the IgG antibody in her serum and eluted from her red blood cells had anti-pdl specificity.