Autoimmune hemolytic anemia pathophysiology: Difference between revisions
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{{Autoimmune hemolytic anemia}} | {{Autoimmune hemolytic anemia}} | ||
{{CMG}} '''Assosciate Editor(s)-In-Chief:''' [[User: Prashanthsaddala|Prashanth Saddala M.B.B.S]] {{shyam}} | {{CMG}} '''Assosciate Editor(s)-In-Chief:''' [[User: Prashanthsaddala|Prashanth Saddala M.B.B.S]]; {{shyam}} | ||
==Overview== | ==Overview== | ||
Revision as of 22:09, 16 March 2018
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Autoimmune hemolytic anemia Microchapters |
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Differentiating Autoimmune hemolytic anemia from other Diseases |
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Diagnosis |
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Autoimmune hemolytic anemia pathophysiology On the Web |
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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
Pathophysiology
Warm autoimmune hemolytic anemia
The pathophysiology of Warm autoimmune hemolytic anemia involves immunoglobulin G (IgG) antibodies binding to red blood cells at a temperature of 37 degrees Celcius. [1] Macrophages bind to the antibody-coated red blood cells via the Fc receptors and result in extravascular destruction.Warm autoimmune hemolytic anemia.
References
- ↑ 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.