Autoimmune hemolytic anemia caused by IgG lambda-monotypic cold agglutinins of anti-Pr specificity after rubella infection.

BACKGROUND: In postinfection cold agglutinin (CA) disease, a relation between CA specificity and the underlying infectious agent has been observed. The induction of anti-I by Mycoplasma pneumoniae and that of anti-i by EBV are well-established examples. CASE REPORT: A 5-year-old boy developed severe hemolytic anemia after serologically ascertained rubella infection. Hemolysis was caused by high-titer CAs, which were analyzed by absorption and elution with sialidase-treated RBCs and hemagglutination-inhibition experiments. RESULTS: After elimination of normal anti-I and anti-T, the predominant CA was found to be an IgG lambda autoantibody with anti-Pr(1) specificity. CONCLUSION: This case seems to be of interest because it is the first report of severe CA-induced hemolysis after rubella infection, it is the first description of an IgG lambda-monotypic CA, and, along with previous case reports (three established and three suspected cases), it indicates a relationship between rubella infection and the CA specificity anti-PR:

[Severe neonatal alloimmune thrombocytopenia with delayed antibody detection]. / Schwere neonatale Alloimmunthrombozytopenie mit verzögertem Antikörpernachweis.

Neonatal alloimmune thrombocytopenia (NAIT) is caused by maternal immunisation against a paternal antigen on fetal platelets. The antigen involved in the majority of cases is HPA-1 a (PIA1). Usually circulating platelet alloantibodies are detectable in the mother. In this report, we present a thrombocytopenic newborn with severe hemorrhagic diathesis due to materno-fetal HPA-1 a (PIA1) incompatibility. Platelet antibodies could initially not be demonstrated in the mother's serum but became detectable after four weeks. Because of the severe and protracted course of the disease, repeated platelet substitution was necessary throughout the first two months of life.

Incidence and persistence of anti-Kell after transfusion of Kell-positive blood.

116 Kell-negative patients who had received at least one Kell-positive blood unit were tested about 3 and 12 months after transfusion. Antibody screening was performed by tube test and by gel centrifugation; both methods yielded identical results. After 3 months, anti-Kell was detected in 11 (9.5%) patients. Antibody titers using K+, k+ cells ranged from 1:1 to 1:128 with a predominance of low titers. Titers using K+, k- cells tended to be higher by one step; one anti-Kell could only be demonstrated with K+, k- cells. After about 12 months, anti-Kell could no longer be detected in 5 of the 11 patients (45.5%).

Efficient antibody screening using gel centrifugation.

In a prospective study including 6,674 sera, antibody screening was performed (1) by tube test (saline/albumin/antiglobulin), (2) by gel centrifugation (Diamed) using two tests, saline/room temperature and antiglobulin/37 degrees C, and (3) by gel centrifugation using a single test antiglobulin (IAT)/ room temperature (RT). By gel centrifugation (saline RT + IAT 37 degrees C), compared to tube test, 40% more Coombs-reactive antibodies but 60% fewer cold-reactive antibodies were detected. Similar results were obtained by gel centrifugation using a single test IAT RT instead of the two tests saline RT + IAT 37 degrees C. A case of delayed hemolytic transfusion reaction was observed caused by anti-C demonstrable only by gel centrifugation. [table: see text]

Cold agglutinins of anti-Pr specificity in rubella embryopathy.

Cold agglutinins of anti-Pr specificity were detected in two newborn infants suffering from serologically ascertained rubella embryopathy, an IgM kappa anti-Pr(a), titer 64, and an IgM lambda anti-Pr1, titer 16. The cases are rare examples of cold agglutinin production in newborns; a possible relationship between anti-Pr specificity and rubella infection is discussed.

Characterization of I/F1 glycoprotein as a receptor for Mycoplasma pneumoniae.

Serologic evidence of anti-I and anti-Fl cold agglutinins occurring in mycoplasma infections led to the isolation of I/Fl glycoprotein from human erythrocyte membranes. Mycoplasma pneumoniae bound to purified I/Fl glycoprotein in a dose-dependent fashion depending on sialylated carbohydrate determinants. This was shown by the decreased binding of mycoplasmas to either sialidase-treated I/Fl glycoprotein (dot blot analysis) or sialidase-treated erythrocytes (hemagglutination test). Structural properties of the receptor for optimal binding could be explored by hemagglutination inhibition assays. Glycophorins were excluded as receptors. These results indicate that Fl (and I) antigens are receptors for M. pneumoniae.

[Selection of HLA compatible thrombocyte donors using electronic data processing with a newly developed score]. / Auswahl HLA-kompatibler Thrombozytenspender über EDV mit einem neuentwickelten Score.

We developed a program for personal computers which selects platelet donors for a given patient according to the following criteria: 1. Anti-CMV-status, 2. ABO-compatibility of various degrees, and 3. HLA-incompatibility. For evaluation of HLA-incompatibility, we created a score which presently provides the following classification: 0 = identical antigen, 5 = same supertypic antigen or blank in the donor, 50 = very frequently cross-reactive antigen, 75 = frequently cross-reactive antigen, very rare antigen or antigen poorly expressed on platelets in the donor, 100 = mismatch.

Coexisting anti-I and anti-F1/Gd cold agglutinins in infections by Mycoplasma pneumoniae.

192 sera containing cold agglutinins of apparent anti-I specificity were reinvestigated for concomitant cold agglutinins (CA) against sialic acid-dependent antigens. 35 cases of additional anti-F1 and 3 cases of additional anti-Gd were detected. 53% of cases with coexisting anti-I and anti-F1/Gd CA had a clinical diagnosis of pneumonia, in 39% IgM antibodies against Mycoplasma pneumoniae could be demonstrated. Since F1 and Gd antigens are identical with the structures identified as receptors for M. pneumoniae, the findings support the hypothesis that postinfectious CA are directed against the receptor of the infectious agent.

Autoimmune hemolytic anemia by coexisting anti-I and anti-Fl cold agglutinins.

In association with atypical pneumonia, a patient developed acute severe autoimmune hemolytic anemia. Hemoglobin temporarily was only 7.0 g/100 ml, so that the patient needed red blood cell (RBC) transfusion. Hemolysis was found to be caused by high titer cold agglutinins (CA), which occurred transiently during the acute period of the disease. CA of two different specificities, anti-I and anti-Fl, were demonstrated in the patient's serum. Antibodies of the two specificities were clearly separated by absorption/elution experiments using neuraminidase (RDE)-treated RBC. They were distinguished by serologic means: Both anti-I and anti-Fl react more strongly with adult RBC than with newborn and i adult RBC; in contrast to anti-I, anti-Fl does not agglutinate RDE-treated cells. Inhibition experiments showed that I-active substances prepared from papainized RBC exhibited both I and Fl antigenic activity. By RDE-treatment of I-active substances, Fl-activity was markedly reduced, while I-activity was increased.