Autoimmune hemolytic anemia historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Assosciate Editor(s)-In-Chief: Prashanth Saddala M.B.B.S; Shyam Patel [2]
Overview
Historical Perspective
- In 1904, Donath and Landsteiner described the syndrome of paroxsymal cold hemoglobinuria (PCH), which is due to an IgG autoantibody that can trigger intravascular hemolysis.[1] Donath and Landsteiner described a biphasic hemolysin (IgG) that binds red blood cells and low temperatures and triggers complement-mediated intravascular hemolysis at warm temperatures. This is now known as the Donath-Landsteiner antibody.
- In 1945, Coombs described the anti-globin test, which is now known as the Coombs' test or direct anti-globulin test.[2] Coombs was able to detect antibodies coating red blood cells, but the limit of detection was poor, with the requirement that a red blood cell needed to be coated with 100-500 molecules of IgG. This threshold was later improved using the super Coombs' test, which could detect presence of autoimmune hemolytic anemia even when fewer molecules of IgG were present on the red blood cell.
- In 1958, Leslie Zieve conducted a retrospective study on patients with alcoholic liver disease who had hemolytic anemia.[3]
- In 1968, Balcerzak confirmed the phenomenon of hemolytic anemia in conjunction with cholestatic jaundice and hypercholesterolemia.[3] This condition was known as Zieve syndrome, named after Leslie Zieve.
- In 1970, Zuelzer and colleagues from Wayne State School of Medicine in Detroit described the nature and proposed etiologies of autoimmune hemolytic anemia [4] They noted that autoantibodies could be produced by transient viral infections, such as CMV infection.[4] It was noted that there was a close correlation between the onset of infection and presence of hemolysis. Zuelzer and colleagues proposed in their manuscript that the etiology for autoimmune hemolytic anemia was an immunologic handicap predisposing to occult viral infections.
- In 1973, Playfair and Marshall-Clarke developed a murine model of autoimmune hemolytic anemia. In this murine model, the mice developed autoantibodies against their own red blood cells upon injection of rat red blood cells. The rat red blood cells triggered antibody production, since the rat antigens were foreign, but the antibodies also reacted against self antigens (murine antigens) also [5] Clinically, the mice developed anemia, elevated reticulocyte count, and positive direct antiglobulin test (Coomb's test). The mice had decreased survival.[5]
- In 1985, P.D. Issit described the molecular events leading to the development of autoimmune hemolytic anemia.[2] He proposed that an autoantibody was first made due to failure of self-recognition and failure of T cell regulation. The production of the autoantibody was less likely related to changes in the red blood cell itself. Other factors that Issit proposed as contributing factors for autoantibody production were drugs, systemic inflammation, infections, and genetic factors. Next, he proposed that this autoantibody could eliminate red blood cells. He proposed that anemia was a result of excess red blood cell destruction by the autoantibody, and this could not be compensated by increased marrow production of red blood cells.
- In 2001, Ikeda and colleagues noted an association between autoimmune hemolytic anemia and multiple other autoimmune conditions.[6] He reports on Evan's syndrome (the combination of immune thrombocytopenia purpura and autoimmune hemolytic anemia in a patient with Grave's disease (an autoimmune condition of the thyroid gland characterized by the presence of thyroid-stimulating antibodies.
- In 2001, M. Zecca and colleagues reported on the use of rituximab and intravenous immunoglobulin (IVIg) in the treatment of autoimmune hemolytic anemia and pure red cell aplasia. Among 15 children with warm autoimmune hemolytic anemia treated with rituximab, 13 showed a favorable response.[7]
- In 2007, G. D'Arena and colleagues showed that rituximab at a dose of 375mg/m2 IV weekly was effective in cohort of 11 patients with steroid-refractory autoimmune hemolytic anemia.[7]
References
- ↑ Akpoguma AO, Carlisle TL, Lentz SR (2015). "Case report: paroxysmal cold hemoglobinuria presenting during pregnancy". BMC Hematol. 15: 3. doi:10.1186/s12878-015-0023-7. PMC 4334594. PMID 25699184.
- ↑ 2.0 2.1 Chaudhary RK, Das SS (2014). "Autoimmune hemolytic anemia: From lab to bedside". Asian J Transfus Sci. 8 (1): 5–12. doi:10.4103/0973-6247.126681. PMC 3943148. PMID 24678166.
- ↑ 3.0 3.1 Liu MX, Wen XY, Leung YK, Zheng YJ, Jin MS, Jin QL; et al. (2017). "Hemolytic anemia in alcoholic liver disease: Zieve syndrome: A case report and literature review". Medicine (Baltimore). 96 (47): e8742. doi:10.1097/MD.0000000000008742. PMC 5708965. PMID 29381966.
- ↑ 4.0 4.1 Zuelzer WW, Mastrangelo R, Stulberg CS, Poulik MD, Page RH, Thompson RI (1970). "Autoimmune hemolytic anemia. Natural history and viral-immunologic interactions in childhood". Am J Med. 49 (1): 80–93. PMID 4194012.
- ↑ 5.0 5.1 Mqadmi A, Zheng X, Yazdanbakhsh K (2005). "CD4+CD25+ regulatory T cells control induction of autoimmune hemolytic anemia". Blood. 105 (9): 3746–8. doi:10.1182/blood-2004-12-4692. PMC 1895013. PMID 15637139.
- ↑ Hegazi MO, Ahmed S (2012). "Atypical clinical manifestations of graves' disease: an analysis in depth". J Thyroid Res. 2012: 768019. doi:10.1155/2012/768019. PMC 3206356. PMID 22132347.
- ↑ 7.0 7.1 Fozza C, Longinotti M (2011). "Use of rituximab in autoimmune hemolytic anemia associated with non-hodgkin lymphomas". Adv Hematol. 2011: 960137. doi:10.1155/2011/960137. PMC 3087411. PMID 21547266.