Auto‐Anti‐Pr<sup>a</sup>: a ‘Second’ Example in a Newborn

Three of 46 patients with autoimmune hemolytic anemia (AIHA) satisfied the diagnostic criteria for mixed-type AIHA in which both warm-type and cold-type autoantibodies against red blood cells (RBCs) are present. The specificities of these autoantibodies were analyzed. All of the warm-type autoantibodies were IgG-x, and the specificities were not serologically classified. The autoantibody of patient 1 reacted to the 41- and 80-kD peptides on immunoblotting, and the epitope corresponding to it was papain sensitive. Two warm-type autoantibodies from patients 2 and 3 resembled each other in serological analyses and reacted with a protease- and neuraminidase-resistant antigen. However, the antigen corresponding to the autoantibody of patient 3 was located on the 37-kD peptide by immunoprecipitation. All of the cold-type autoantibodies were IgM-x and showed high titer and high thermal amplitude. According to the reaction pattern with untreated and enzyme-treated RBCs, the cold-type autoantibodies of patients 2 and 3 were revealed to be anti-Om and anti-I, respectively. In patient 1, the cold-type autoantibody was characterized as having high affinity for autologous RBCs, but its specificity was unclassified. The antigens corresponding to the cold-type autoantibodies were not located by immunoblotting and immunoprécipitation. These serological and immunochemical approaches to autoantibodies in mixed-type AIHA revealed that the warm and cold components recognized the different antigens.

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“…After incubation, hemagglutination was scored visually. The 2-mercapto-ethanol (2ME) treatment was done by the method of Habibi et al [13].…”

Section: Cold-type Autoantibody Testingmentioning

confidence: 99%

Characterization of Autoantibodies in Mixed-Type Autoimmune Hemolytic Anemia

Kajii¹,

Miura²,

Ikemoto³

1991

Vox Sanguinis

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“…Our results indicate that the antibody in case 1 was not directed against any single constituent of the LIS solu- (which is further subdivided into Prlh and Prld), Pr2, Pr3 (which can also be subdivided into Pr3h and Pr3d) and Pr, [ 13,16,19,201. The antibodies to these antigens can be distinguished by their reactions with animal cells [ Most Pr antibodies are of high titer, and many have been the cause of cold agglutinin syndrome, although a few low-titer antibodies have been described [12].…”

Section: Discussionmentioning

confidence: 71%

Two Examples of Low Ionic Strength-Dependent Autoagglutinins with Anti-Pr(1) Specificity

O’Neill¹,

Shulman²,

Simpson³

et al. 1986

Vox Sanguinis

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Two low ionic strength-dependent autoagglutinins were studied and found to have anti-Pr(1) specificity. This specificity was determined by studies with enzyme-treated and neuraminidase-treated human red blood cells (RBCs), animal RBCs and chemically-modified sialoglycoproteins, all suspended in a low ionic strength solution (LISS). Both IgM complement-binding cold agglutinins had a wide thermal range and caused in vitro hemolysis of some LISS-suspended RBCs at 37°C. Compatible blood was found for these patients by using techniques that did not employ LISS.

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“…The first case was in a 19‐year‐old patient who developed acrocyanosis and mild hemolysis caused by high‐titer CAs of anti‐Pr 3 specificity 9,12 . In two other cases, an underlying rubella infection was suspected but could not be ascertained serologically 2,17 ; one of these patients was a newborn with embryopathy.…”

Section: Discussionmentioning

confidence: 99%