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Title: | Lesson Learned: Immune-Mediated Hemolytic Anemia In Dogs |
Authors: | Maylina, Leni |
Issue Date: | May-2023 |
Abstract: | Immune-mediated hemolytic anemia (IMHA) is a type II immune reaction in which circulating red blood cell (RBC) destruction is antibody-mediated (cytotoxic) (Day 2014, Tizard 2013, Chabanne 2006, Day in Fieldman et al. 2000). Antibody attachment to erythrocyte surface depends on two main causes: 1. The majority of primary IMHA are idiopathic or associated with other autoimmune diseases in the autoimmune form of the disease, antibodies (auto-antibodies) recognize a self-antigen of the erythrocyte membrane. Hemolysis dominates the clinical picture in the absence of any other coexisting disorder. Autoimmune hemolytic anemia may occur as a single clinical entity (idiopathic), may be recognized concurrently with autoimmune thrombocytopenia (Evans syndrome), or maybe part of a multisystemic autoimmune disease like systemic lupus erythematosus (SLE). The development of autoimmunity results from a failure of the normal control mechanisms of the immune system. Autoimmune diseases are multifactorial disorders in which clinical expression relies on the presence of an optimum array of predisposing factors. Genetic factors are key determinants of disease susceptibility that explain breed or familial predispositions. Other predisposing factors must be important: hormonal background, age, and environmental factors (infectious agents, drugs and chemicals, etc.). The aim in the treatment of IMHA as with all autoimmune diseases is to manipulate (to down-regulate or suppress) the immune response that causes the disease so that the process is reduced or abolished (Berentsen 2011, Petz and Garratty 2004, Gehrs and Friedberg 2002). ... |
URI: | http://repository.ipb.ac.id/handle/123456789/129377 |
Appears in Collections: | Animal Disease and Veterinary Health |
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File | Description | Size | Format | |
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Lesson Learned Immune Mediated Hemolytic Anemia in Dogs_Leni Maylina.pdf | Article | 242.39 kB | Adobe PDF | View/Open |
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