China
Africa
Explore chapters and articles related to this topic
Hemolytic Anemia Associated with Red Cell Membrane Defects
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Numerous clinical disorders are associated with morphologic acanthocytosis and/or echinocytosis. These include uremia (echinocytosis), malnutrition (acanthocytosis), hypothyroidism (acanthocytosis), postsplenectomy (both), and others. Clinically significant hemolysis, however, is unusual in these disorders. However, acquired hemolytic anemia associated with acanthocytosis is encountered in a few clinical situations.
Miscellaneous Forms of Acquired Red Cell Aplasia and Erythropoietic Failure in Childhood
Published in Stephen A. Feig, Melvin H. Freedman, Clinical Disorders and Experimental Models of Erythropoietic Failure, 2019
Melvin H. Freedman, Stephen A. Feig
The most common viral-induced red cell aplasia is due to parvovirus B19,30 the agent that causes erythema infectiosum (fifth disease). This virus replicates preferentially in rapidly dividing erythroid precursors and is directly toxic to CFU-E progenitors and to erythroblasts.30 Erythropoietic failure due to parvovirus is usually transient and the development of anemia is usually related to the need for increased erythropoiesis to compensate for shortened red cell survival in chronic hemolytic anemia.2 In normal individuals short periods of erythropoietic failure go unnoticed, but in patients with an underlying congenital or acquired hemolytic anemia, a severe and rapidly progressive decrease in hemoglobin may develop.31–36 Usually these patients only require one or two transfusions to maintain an adequate hemoglobin until erythropoietic compensation recovers in 10 to 14 days.
The Influence of Pituitary-Adrenal Axis on the Immune System
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
Several clinical observations suggest that in man therapeutic doses of ACTH seldom affect antibody levels. Thus, the production of protective antibody against pneumococcal polysaccharide was unaltered during treatment with ACTH and cortisone,21 and precipitin formation to the same antigen in patients receiving cortisone treatment for rheumatoid arthritis was not inhibited.22 Similarly ACTH and cortisone did not reduce the development of diphtheria antitoxin following toxoid injections.23 However, it has been reported repeatedly that the course of acquired hemolytic anemia improved significantly with ACTH and cortisone treatment; this was associated with a reduction in antibody titers.24,25 Several investigators have established in both clinical and in experimentally induced serum sickness that ACTH or cortisone inhibit the disease at doses that produce no alternation in the response of skin to test dose of antigens.26,31 Cortisone and ACTH in dosages sufficient to inhibit the tuberculin reaction were without effect on the titer of hemagglutinating antibodies.32,33
Ultrastructural analysis of nucleated erythrocyte in patients with autoimmune hemolytic anemia (AIHA)
Published in Ultrastructural Pathology, 2023
Jing Liu, Shuxu Dong, Yongxin Ru
Autoimmune hemolytic anemia (AIHA) is a group of divergent diseases caused by autoantibody (Ab)-induced destruction of red blood cells (RBCs) with or without complement (C) activation.1 As a subtype of acquired hemolytic anemia (HA), it can be idiopathic (primary AIHA) or secondary to diseases that induce immune dysregulation (secondary AIHA). The pathogenesis of AIHA involves several factors, including production of serous Abs, activation of complement, the engulfing of RBCs by the monocyte/macrophage system and compensatory mechanisms of the bone marrow (BM).2 The pathogenic anti-RBC antibody is detected through direct antiglobulin test (DAT) and categorized into warm AIHA (wAIHA), cold AIHA (cAIHA), mixed type AIHA (mixed AIHA) and atypical AIHA based on the optimal reactive temperature of the Ab.3,4
Papilledema from gain-of-function mutations in the STAT3 gene
Published in Ophthalmic Genetics, 2019
Young-Woo Suh, Jonathan C. Horton
In 1951 Evans and colleagues described a cohort of 29 patients with a spectrum of acquired hemolytic anemia and primary thrombocytopenic purpura (11). Patients with Evans Syndrome also manifest neutropenia, hepatosplenomegaly, immunodeficiency, recurrent infections, interstitial lung disease, and eczema (12,13). Autoimmune lymphoproliferative syndrome has been included as a feature of Evans Syndrome (14). Before genetic testing revealed STAT3 mutations, our first patient received a diagnosis of Evans Syndrome and our second patient received a diagnosis of the autoimmune lymphoproliferative syndrome.
Iron metabolism abnormalities in autoimmune hemolytic anemia and Jianpishengxue keli can ameliorate hemolysis and improve iron metabolism in AIHA mouse models
Published in Annals of Medicine, 2023
Manjun Zhao, Yan Wang, Jin Yang, Yi Wang, Yingying Feng, Lei Chen, Zonghong Shao, Huaquan Wang, Limin Xing
AIHA is a predominant form of acquired hemolytic anemia that is mediated by the immune system. Autoantibodies against red blood cells (RBCs) produced and secreted by hyperactive B lymphocytes with or without complement system activation, lead to hemolysis [1].