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At least 19 recordsLinked to original sources
PubMed1994

Transfusion therapy in autoimmune hemolytic anemia.

Autoimmune hemolytic anemias include warm and cold reactive autoimmune hemolytic anemias (WAIHA and CAD), paroxysmal cold hemoglobinuria (PCH), and drug-induced hemolytic anemias. If autoimmune hemolytic anemia is suspected, the clinical history should be communicated to the transfusion service, because specific tests to confirm these diagnoses are not routinely performed. This includes evaluation of the patient's RBCs for bound IgG and complement (direct antiglobulin test) and evaluation of the patient's serum for antibodies with RBC specificity. For warm or cold autoimmune hemolytic anemia, special procedures including autoabsorption may be necessary to identify underlying RBC alloantibodies prior to transfusion. Transfused RBCs may not have normal survival in patients with RBC autoantibodies. The decision to transfuse should consider the patient's need for oxygen-carrying capacity, the risk of withholding transfusion, and the potential benefit of alternative therapy.

Anemia, Hemolytic, Autoimmune↗
PubMedDate not supplied

Aortic valve replacement for a patient with glucose-6-phosphate dehydrogenase deficiency and autoimmune hemolytic anemia.

Autoimmune hemolytic anemia and deficiency of glucose-6-phosphate deyhdrogenase (G6PD) result in severe hemolysis with different mechanisms. In patients with both pathologies, the effects of cardiopulmonary bypass on red blood cells and thrombocytes demand special care before and after open heart surgery. We evaluated the preoperative management and postoperative care of a patient with severe aortic insufficiency associated with G6PD deficiency and autoimmune hemolytic anemia who underwent aortic valve replacement.

Adolescent↗
PubMed1981

Cellular basis of autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AIHA) is produced by the in vivo destruction of red cells coated with auto-antibodies which are produced by naturally occurring B-lymphocytes. The auto-antibody-producing cells are under the control of suppressor T-lymphocytes whose activity may be deficient in patients with AIHA. The ultimate cure of AIHA will probably reside in the reestablishment of the normal control of the autoantibody-producing cells and not in the elimination of the cells responsible for the destruction of the antibody-coated cells by splenectomy or drug therapy. The cells responsible for destruction of red cells are necessary for the removal of other antibody-coated particles (such as bacteria, etc.). The removal or inactivation of tissue macrophages predisposes the patient to other serious problems including the possibility of serve sepsis. The reestablishment of normal control of the auto-antibody-producing cells by the normalization of the patient's suppressor cell status may be a safer mode of therapy for autoimmune hemolytic anemia in the future.

Anemia, Hemolytic, Autoimmune↗
PubMed2005

Autoimmune pathogenesis and autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AIHA) is an autoimmune disorder in which autoantibodies are directed against an individual's own red blood cells (RBCs), leading to enhanced clearance through Fc receptor (FcR)-mediated phagocytosis. Although there is a large literature relating to clinical aspects of AIHA, relatively little work addresses how IgG autoantibodies are actually produced against RBC autoantigens. This review will first discuss the current understanding of autoimmunity in general and then focus on the knowledge of the immunopathogenic mechanisms responsible for autoantibody production in AIHA. Both human and animal studies will be discussed. Understanding theses mechanism is vital for developing antigen-specific immunotherapies to treat the disease.

Anemia, Hemolytic, Autoimmune↗
PubMed2000

[Autoimmune hemolytic anemia].

Autoimmune hemolytic anemias (AIHAs) are the most ancient and well known example of clinical autoimmunity. They may be still distinguished in two main groups, that is with "warm" or "cold" antibodies, according to the optimal temperature at which they react with the erythrocyte antigens in vivo and in vitro. There is also a subgroup where both kinds of autoantibodies coexist. AIHAs may be idiopathic or secondary. The immunologic techniques for the demonstration of the antibodies are well established, but one must remember that there are infrequent cases with negative DAT (Coombs) test when performed with conventional procedures. The fundamental concepts of therapy are discussed, and the detailed review of the principal procedures is performed, including blood transfusions (when and how), plasma exchanges, high-dose immunoglobulins, glycocorticosteroids, splenectomy, cytotoxic agents and stem cell transplantation, autologous and allogeneic.

Anemia, Hemolytic, Autoimmune↗
PubMed1994

Autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AHA) is characterized by the production of Coombs' antibodies, which are responsible for the destruction of red blood cells (RBCs). Analysis of both monoclonal anti-RBC autoantibodies derived from autoimmune New Zealand black mice and transgenic mice expressing a pathogenic IgM anti-RBC autoantibody has considerably improved our understanding of the B-cell responses involved in AHA, although our knowledge of T-cell immunity in AHA is still limited. The identification of the major T-cell epitope in the context of MHC class II molecules would be of paramount importance in helping to elucidate the cellular and molecular basis central to the development of AHA.

Anemia, Hemolytic, Autoimmune↗
PubMed2001

[Autoimmune hemolytic anemia].

Autoimmune hemolytic anemia (AIHA) is subclassified according to the character of the autoantibodies, however, its clinical pictures are highly heterogenous even in a given subclass. In this article, we reviewed pathogenesis, clinical and laboratory characteristics of AIHA, exemplifying data of 26 patients with autoimmune hemolysis with warm-type autoantibodies (13 AIHA, 10 Evans' syndrome, 3 systemic lupus erythematosus), and recent advances in this field. White blood cell and platelet counts varied among patients at presentation. Six of 13 AIHA patients had low reticulocyte production index (RPI) indicative of inappropriate reticulocyte response with considerable erythroblasts in the bone marrow, suggesting that ineffective erythropoiesis contributes the pathogenesis of warm-type AIHA. Ten patients were judged to require red cell transfusion. Their RPI did not differ from that of patients who did not require transfusion, indicating that the degree of hemolysis is the major determinant of the severity of the disease. No significant side effects of transfusion were observed.

Anemia, Hemolytic, Autoimmune↗
PubMed2006

Rituximab therapy for chronic lymphocytic leukemia-associated autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AIHA) is a well-known complication of chronic lymphocytic leukemia (CLL). In recent years the anti-CD20 monoclonal antibody rituximab has been used for the therapy of steroid-refractory AIHA and autoimmune thrombocytopenia, either idiopathic or in association with CLL. We report the results of rituximab treatment for 14 patients suffering from CLL-associated AIHA. They developed a direct antiglobulin test positive AIHA at a mean time of 47 months (range 0-135 months) from the diagnosis of CLL. In 3 cases AIHA was diagnosed at the same time as CLL. Only 1 patient had fludarabine-related AIHA. All patients received steroids as first-line treatment. At a mean time of 46 days (range 1-210 days) from the diagnosis of AIHA all patients received rituximab at a dosage of 375 mg/m(2)/weekly for 4 weeks. All patients except 3 (2 died of cardiac failure or sepsis soon after the third cycle and 1 HCV-positive patient experienced a rise in serum amino transferases) completed the scheduled four programmed cycles. First injection side effects of rituximab were minimal. All but 2 patients showed an increase in hemoglobin levels in response to rituximab (mean value 3.6 g/dl; range 0.7-10 g/dl) and a reduction in the absolute lymphocyte count and lymph nodes and spleen volume. Nine patients required packed red cell transfusions before starting rituximab; 5 no longer needed transfusions just after the second cycle and another patient after the fourth cycle. Three patients (22%) were considered to fully respond and 7 (50%) only responded partially. At a mean follow-up of 17 months, 8 patients were still alive, 6 of them transfusion-free. Our results prove that the anti-CD20 monoclonal antibody is an effective and well-tolerated alternative treatment for CLL-associated AIHA.

Aged↗
PubMedDate not supplied

Infantile cytomegalovirus-associated autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AIHA) is a hematologic disorder that is rarely seen in infants and young children. Most cases are associated with viral or bacterial infection, but the immunologic events leading to hemolysis are poorly understood. We describe two infants with severe cytomegalovirus (CMV)-associated warm antibody AIHA. One case was immunohematologically analyzed and showed suggestive evidence that endogenous anti-CMV IgG antibodies were the pathogenic antibodies leading to hemolysis, implicating a possible causal relationship between AIHA and CMV infection. Both patients were ultimately treated with intravenous CMV immune globulin, with subsequent improvement. These cases suggest that investigation for the presence of CMV in infantile AIHA is warranted and that CMV immune globulin should be considered as a therapeutic option.

Anemia, Hemolytic, Autoimmune↗
PubMed2006

Sirolimus rescue for tacrolimus-associated post-transplant autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AIHA) has been reported to occur after renal transplantation, and typically does so in the first few weeks post-transplant. We report on a 3-yr-old child who developed cold AIHA nearly 1 yr after an ABO identical, living donor renal transplant from his mother. Numerous transfusions, pulse steroids, repeat plasma exchange treatments, and IVIG were unsuccessful. Nearly 3 wk into his illness, tacrolimus was changed to cyclosporine, and then to sirolimus, and resulted in a prompt response. He currently has a normal renal function and a normal hemoglobin level on sirolimus monotherapy.

Anemia, Hemolytic, Autoimmune↗
PubMed2005

CD4+CD25+ regulatory T cells control induction of autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AIHA) is the result of increased destruction of red blood cells (RBCs) due to the production of autoantibodies, and it can be life-threatening. To study the mechanisms that trigger AIHA, we used the Marshall-Clarke and Playfair model of murine AIHA, in which mice repeatedly immunized with rat RBCs develop erythrocyte autoantibodies as well as rat-specific alloantibodies. We analyzed the role of CD25(+) T-regulatory subsets in controlling AIHA in C57/Bl6 mice using antibody depletion studies. Treatment with anti-CD25 antibody but not isotype control prior to immunization with rat RBCs increased the incidence of AIHA from 30% to 90%. Adoptive transfer of purified splenic population of CD4(+)CD25(+) but not CD4(+)CD25(-) cells from immunized mice into naive recipients prevented the induction of autoantibody production. Altogether, our data establish a critical role for CD4(+)CD25(+) cells for control of AIHA, which may help to establish therapeutic strategies for treatment of AIHA.

Adoptive Transfer↗
PubMed1977

Grand rounds: autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AHA) may be either primary (ie, "idiopathic," one third of all patients) or secondary (ie, associated with underlying illness, two thirds of all patients). A positive Coombs antiglobulin test is the most important criterion for diagnosis of AHA, and characterization of RBC coating (as to whether it is by IgG alone, by IgG plus complement, or by complement alone) may be valuable in ruling out certain underlying illnesses as causative in selected patients. Many limitations to the antiglobulin test must be kept in mind. As routinely performed, a positive result requires greater than 500 molecules of IgG per RBC. Red blood cells from normal subjects have less than 35 molecules of IgG per RBC. Up to 2% to 5% of patients with AHA will have RBC coating in the 50 to 500 molecules per cell range and may therefore have "false"-negative antiglobulin tests. Apparent failures of strength of antiglobulin reactions to correlate with severity of in vivo RBC destruction may result from technical factors or may reflect intrinsic differences among autoantibodies (eg, IgG subclass, affinity). A likely mechanism of in vivo RBC destruction in AHA has been demonstrated in immune-mediated in vitro RBC "rosette" formation about macrophages and lymphocytes bearing specific receptors for subclasses of IgG and for subcomponents of complement. Increased avidity of macrophages for coated RBCs in response to such stimulus as infection may play an additional role. Treatment involves control of underlying disease and the judicious use of adrenal steroids, splenectomy, and immunosuppressive agents. Transfusions, while life-saving in life-threatening anemia, carry substantially increased risks in AHA patients. Their use should be strictly limited.

Aged↗
PubMed1988

[Autoimmune hemolytic anemia].

Autoimmune hemolytic anemias are a heterogenous group of disorders as evidenced by the multiple forms and classifications they have been commonly subjected to: acute or chronic, idiopathic or symptomatic, clinically latent or expressed, due to warm or cold autoantibodies. This work attempts to give an overview and synthesis of recent achievements in the knowledge of these syndromes within clinical, immunohematologic and pathophysiologic fields. In contrast, little progress has been made in the therapeutic measures the efficacy of which depends on the same variables as more than a decade ago.

Anemia, Hemolytic, Autoimmune↗
PubMed2001

Chronic hepatitis C virus infection associated with primary warm-type autoimmune hemolytic anemia.

Autoimmune hematologic abnormalities are not well recognized in chronic hepatitis C virus infection. We demonstrate an unusual association between primary autoimmune hemolytic anemia and chronic hepatitis C virus infection. A 69-year-old woman who had a history of hepatitis C virus-related liver cirrhosis was found to have deteriorating anemia with reticulocytosis when admitted to the hospital. Laboratory work revealed both positive direct and indirect Coombs' tests, and warm-type immunoglobulin G against surface antigens of red blood cells. After prednisolone therapy, her anemia improved dramatically. To our knowledge, this is the first reported case of chronic hepatitis C virus infection linked with autoimmune hemolytic anemia in its natural course, not related to prior interferon treatment. Our report suggests that isolated autoimmune hemolytic anemia may be one of the unusual hematologic manifestations of chronic hepatitis C virus infection.

Aged↗
PubMed1993

Clinical features and splenic pathologic changes in patients with autoimmune hemolytic anemia and congenital hemolytic anemia.

We characterized the pathologic changes in 50 spleens from patients with autoimmune hemolytic anemia and in 13 spleens from patients with congenital hemolytic anemia. The major pathologic findings in autoimmune hemolytic anemia were mild to pronounced cord congestion and variable white pulp area, erythrophagocytosis in conjunction with an increased polymorphonuclear neutrophil reaction, and increased deposition of hemosiderin and extramedullary hematopoiesis. In contrast, both the severity and the frequency of polymorphonuclear neutrophil reactions, deposition of hemosiderin, and extramedullary hematopoiesis were less in patients with congenital hemolytic anemia, and prominent cord congestion associated with an empty or collapsed sinus was noted in patients with hereditary spherocytosis. The activity of erythrophagocytosis in the sinus was more distinct in patients with congenital hemolytic anemia, especially those with nonspherocytic congenital hemolytic anemia, than in patients with autoimmune hemolytic anemia. These findings are consistent with the existence of different mechanisms of trapping and destruction of erythrocytes in autoimmune hemolytic anemia and congenital hemolytic anemia.

Adolescent↗
PubMed1977

Refractory sideroblastic anemia secondary to autoimmune hemolytic anemia.

A 75-year-old woman was hospitalized with autoimmune hemolytic anemia. During a period of 22 months the patient had six hemolytic crises which responded to treatment with prednisone and azathioprine. During the last admission the patient presented a sideroblastic anemia with 98% of 'ring sideroblasts' in the bone marrow. This association has never, to our knowledge, been reported before. It is possible that the immunosuppression played a definite role in the development of this sideroblastic anemia.

Aged↗