China
Africa
Explore chapters and articles related to this topic
Immunohematology
Published in Gabriel Virella, Medical Immunology, 2019
Gabriel Virella, Armand Glassman
Pathogenesis. Warm autoimmune hemolytic anemia is due to the spontaneous emergence of IgG antibodies that may have a simple Rh specificity such as anti-e, or uncharacterized specificities common to almost all normal red cells (“public” antigens, thought to be the core of the Rh substance). In many patients, one can find antibodies of multiple specificities. The end result is that the serum from patients with autoimmune hemolytic anemia of the warm type is likely to react with most, if not all, of the red cells tested. These antibodies usually cause shortening of red cell life due to the uptake and destruction by phagocytic cells in the spleen and liver.
Systemic loxoscelism induced warm autoimmune hemolytic anemia: clinical series and review
Published in Hematology, 2022
Brandon Calhoun, Andrew Moore, Andrew Dickey, D. Matthew Shoemaker
Envenomation by a brown recluse spider, L. reclusa, can result in systemic loxoscelism which can cause warm AIHA. The diagnosis of warm AIHA is confirmed by the direct antiglobulin/Coomb’s test. Warm AIHA can be a life-threatening disease process and should be managed urgently/emergently. Hemodynamic support with intravenous fluids and RBC transfusion is the initial step in the management of these patients. Corticosteroids are the mainstay of current management. The first-line treatment for warm AIHA is corticosteroids, which has a response rate of approximately 70–85%. Second line treatments include rituximab (response rate: 73%). Rarely patients require splenectomy (response rate: 82%) for refractory disease. Corticosteroids should be tapered over a three-month period. The patient should follow-up with a hematologist/oncologist within one week after discharge and should be evaluated with a complete blood count, comprehensive metabolic panel, reticulocyte count, LDH, and haptoglobin level. In the event of refractory or relapsed warm autoimmune hemolytic anemia, the physician should consider either rituximab or splenectomy. In addition, the patient should maintain a tapering regimen of prednisone for 4–6 weeks.
Multifactorial jaundice and pigmented choledocholithiasis secondary to warm autoimmune hemolytic anemia and alcoholic cirrhosis
Published in Baylor University Medical Center Proceedings, 2022
Colten Watson, Mazen Hassan, Grant Breeland
In warm autoimmune hemolytic anemia (w-AIHA), the body creates the autoantibodies IgG1 and IgG3 that can bind and lyse red blood cells, causing anemia.1 These autoantibodies, called hemolysins, can be detected with a Coombs test and confirmed with a direct antiglobulin test. Alcoholic cirrhosis presents with several of the same features, such as extreme jaundice and constitutional symptoms. It usually presents in the fifth to sixth decade of life in the setting of excessive chronic ethanol ingestion. Most evidence supporting ethanol consumption as an etiology for cirrhosis has come from epidemiological studies. The overwhelming cause of acute jaundice in patients with alcohol abuse is acute alcoholic hepatitis. The pathogenesis of alcoholic hepatitis is attributed mainly to the expression of cytokines, oxidative stress, reactive oxygen species, and SREBPs and SREBP-1, which impair fatty acid oxidation. Abstinence remains the most effective treatment method.2 The combination of alcoholic cirrhosis with w-AIHA in patients is not well documented in the medical literature.
Severe babesiosis with associated splenic infarcts and asplenia
Published in Baylor University Medical Center Proceedings, 2021
Zachary A. Sporn, Andrew Z. Fenves, David B. Sykes, Hanny Al-Samkari
Given the known risk of warm autoimmune hemolytic anemia in patients without a spleen17 and lack of alternative explanation, our second patient’s hemolytic anemia was attributed to ongoing Babesia infection. Further work is needed to evaluate the mechanism of this Babesia-related autoimmune hemolysis, especially given the report of cases in the setting of an undetectable parasitemia despite ongoing hemolysis.17 Whether this antibody-mediated hemolysis targets antigens present on all RBCs, or the target antigens are present exclusively on infected RBCs, may have implications for future treatment regimens.