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Blood transfusion and rhesus disease
Published in Michael J. O’Dowd, The History of Medications for Women, 2020
Further research revealed that Rh antibodies did not occur naturally in the blood and that they were found only as a result of the introduction of the Rh antigen into the body of a susceptible individual. Soon after the discovery of the new agglutinin, Wiener and Peters studied the blood of patients who had suffered severe transfusion reactions. They demonstrated the presence of antibodies whose action paralleled that of the antibodies in the anti-Rh serum. They thus proved that the substance first revealed by the use of the serum from monkeys actually existed in human blood and that it was capable of exerting an antigenic action. They also discovered that the Rh factor was inherited as a Mendelian dominant (Potter, 1947).
Candidiasis
Published in Rebecca A. Cox, Immunology of the Fungal Diseases, 2020
Judith E. Domer, Emily W. Carrow
A number of different serologic tests, including whole cell agglutination,191 double-immunodiffusion,192 counter immunoelectrophoresis (CIE),193 co-counterimmunoelectropho- resis,194 latex agglutination,195 crossed immunoelectrophoresis (XIE),196 ELISA,197,198 passive hemagglutination,198 and radioimmunoassay199 have been proposed at one time or another as diagnostic or prognostic aids in candidiasis. It became clear early,191 however, that agglutinins, i.e., antibodies to the surface antigens of Candida, were present in a relatively large percentage of normal individuals, and, while the concentration of such antibodies was usually greater in patients with candidiasis, the differential was not great enough to make the agglutinin response a reliable indicator of disease status.
The Hematologic System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Different types of blood can be classified on the basis of cell membrane proteins that normally cause antibody reactions. Thus, blood may be grouped as type O, A, B, or AB, These four groups are based on the presence or absence in blood cells of the type A and type B proteins that may cause transfusion reactions. Called agglutinogens because they lead to agglutination (clumping) and hemolysis (rupture) of blood cells exposed to specific antibodies, these proteins react with agglutinins in the plasma to cause the cells to clump. Those people without a specific agglutinogen usually do have the complementary agglutinin in their plasma.
COVID-19 and Anemia: What Do We Know So Far?
Published in Hemoglobin, 2023
Luai Abu-Ismail, Mohammad J. J. Taha, Mohammad T. Abuawwad, Yaqeen Al-Bustanji, Khayry Al-Shami, Abdulqadir Nashwan, Mohamed Yassin
A significant number of cases of hemolytic anemia have been documented in the context of COVID-19, mostly due to the development of auto-antibodies, despite the fact that AIHA has an estimated incidence of 13/100,000 in the normal population annually [14]. It has been hypothesized that this might contribute to thrombosis and adverse outcomes in COVID-19 patients, considering the known risk of thrombosis in individuals with cold agglutinin hemolytic anemia [15]. Hemolysis may also be brought on by viral infection-induced changes in their shape and functions [16]. This is crucial when hemoglobinopathies or hereditary anemias are present [17]. Severance et al. found that the SARS-CoV-2 infection caused oxidative stress, which is what caused hemolytic anemia in children with hereditary spherocytosis [18]. However, oxidative stress contributes to hemolysis in other inherited hemolytic anemias, including hemoglobinopathies and not only in congenital spherocytosis. On the other hand, due to diminished immune response without cytokine storm and decreased T cell-mediated immunity, finally, the degree of anemia in AIHA is a factor in predicting the prognosis in COVID-19 patients [19]. As a result, the National Haemoglobinopathy Panel (NHP) has produced recommendations on how to treat anemic patients with reference to planned blood transfusions and outpatient visits in order to lower the risk of exposure to SARS-CoV-2 and related COVID-19 severity in the patient population at risk [17].
Autoimmune hemolytic anemia: causes and consequences
Published in Expert Review of Clinical Immunology, 2022
In all patients, the clinical evaluation is completed by the investigation of underlying alloantibodies in patient’s serum (indirect agglutinin test, IAT), reported in about one-third of AIHA patients [22]. The latter may cause severe hemolytic reactions in the case of transfusion. In complex cases, allo- and autoantibody may be distinguished by immune-absorbance techniques and extended RBC genotyping [3]. Additionally, autoantibodies may be eluted from the washed patient’ RBCs to determine the class, specificity, titer, and thermal range. As regards specificity, in wAIHA autoantibodies are mainly directed against RBC membrane proteins including Band 3, glycophorin A, and Rh system, while in CAD the polysaccharide regions of glycoproteins, such as I/i or Pr antigen, are the most common target.
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
Upon admission, the patient’s skin was highly jaundiced with a measured bilirubin of 43.8 mg/dL and a blood pressure of 104/50 mm Hg. Acute diffuse abdominal pain was present on palpation. Some shortness of breath was noted with rhonchi and abdominal distention. A rectal exam was guaiac positive and showed occult blood. His hemoglobin was 6.3 g/dL, resulting in the immediate transfusion of 4 units of packed red blood cells on his first day of admission. His total bilirubin of 43.8 mg/dL was fractionated, and direct bilirubin measured 32.7 mg/dL. The blood bank laboratory tests also had several findings; an antibody screen was positive and was confirmed with a direct Coombs test. The lab then discovered a warm agglutinin IgG antibody through a direct antiglobulin test. Other notable laboratory data included a lipase level of 390 U/L, elevated lactate dehydrogenase, decreased haptoglobin, and 1+ schistocytes (Supplemental Table).