Elly Huiskes

A new bead‐based human platelet antigen antibodies detection assay versus the monoclonal antibody immobilization of platelet antigens assay

The performance of a newly developed Luminex bead‐based platelet (PLT) antibody detection method (PAKLx) was compared with the monoclonal antibody immobilization of PLT antigens (MAIPA) assay and the LifeScreen Deluxe Luminex bead‐based HLA Class I antibody detection method (LMX).

Alloantibodies against low-frequency human platelet antigens do not account for a significant proportion of cases of fetomaternal alloimmune thrombocytopenia: evidence from 1054 cases

BACKGROUND: Maternal alloantibodies against the five common human platelet antigen (HPA) systems (HPA‐1 to ‐3, ‐5, and ‐15) are found in only 20% of cases referred for fetal and neonatal thrombocytopenia (FMAIT) investigations. The question asked was whether mismatches for the remaining 11 low‐frequency HPAs (HPA‐4 and ‐6bw to ‐17bw) might in part explain the remaining 80% of cases.

Neonatal alloimmune neutropenia due to immunoglobulin G antibodies against human neutrophil antigen-5a

BACKGROUND: Neonatal alloimmune‐mediated neutropenia (NAIN) due to maternal alloantibodies directed against one of the human neutrophil antigens (HNAs) can cause severe infections. NAIN has been described as caused by antibodies against HNA‐1a, ‐b, ‐c, ‐2a, ‐3a, or ‐4a, but not by antibodies against HNA‐5a.

Acquired Glanzmann's thrombasthenia caused by glycoprotein IIb/IIIa autoantibodies of the immunoglobulin G1 (IgG1), IgG2 or IgG4 subclass: a study in six cases.

Background  Acquired Glanzmanns thrombasthenia (GT) is an uncommon bleeding disorder caused by glycoprotein (GP) IIb/IIIa‐specific autoantibodies. Covering of the fibrinogen binding site of GPIIb/IIIa results in a moderate‐to‐severe bleeding tendency.

Management and outcome of 35 cases with foetal/neonatal alloimmune neutropenia

The aim of this study was to provide an overview of foetal/neonatal alloimmune neutropenia (FNAIN), together with advice on the clinical management.

Lack of detectable platelet autoantibodies is correlated with nonresponsiveness to rituximab treatment in ITP patients

To the editor: Rituximab, a chimeric CD20 monoclonal antibody that causes depletion of B cells, shows short-term treatment efficacy in 40% to 60% of immune thrombocytopenia (ITP) patients.[1][1],[2][2] Our recently published multicenter randomized open-label phase 2 trial comparing 3 rituximab

A multicenter validation of recombinant β3 integrin–coupled beads to detect human platelet antigen‐1 alloantibodies in 498 cases of fetomaternal alloimmune thrombocytopenia

Fetomaternal alloimmune thrombocytopenia (FMAIT) is caused by human platelet (PLT) antigen (HPA) incompatibility. Beads coupled with recombinant β3 integrins, displaying the biallelic HPA‐1 epitopes (rHPA‐1), have been shown to detect HPA‐1a alloantibodies implicated in FMAIT. This report describes a multicenter validation of the beads using the results of well‐characterized samples to define the optimum parameters for analysis of a large cohort of 498 clinical samples.

Protection against immune haemolytic disease of newborn infants by maternal monocyte-reactive IgG alloantibodies (anti-HLA-DR)

Human ovarian l’l-letosteroid oxidoreductase: Unique characteristics of the gramdosa-Meal cell and stromal enzyme Barbieri R.L. USA AM J OBSTET GYNECOL 1992 16614 (1117-1126) Objectives: We attempted to test the hypothesis that distinct forms of the I7-ketosteroid oxidoreductase exist in the human ovary and to compare its activity in stroma obtained from normally cycling women and from hyperandrogenic women. Study design: Human ovarian granulosa-luteal cell and stromal 17ketosteroid oxidoreductase were examined in cell incubations and subcellular homogenates. Results: In subcellular homogenates of granulosa-luteal cells 17-ketosteroid oxidoreductase activity was greater in the cytosol fraction than in the membrane fraction. In contrast, in homogenates of both ovarian stroma and Leydig cells its activity was greater in the membrane fraction than in the cytosol fraction. At the substrate concentrations used estrone was a better substrate than androstenedione for the granulosa-luteal cell 17ketosteroid oxidoreductase. In contrast androstenedione was a better substrate than estrone for that in ovarian stromal and Leydig cell membranes. In incubations of ovarian stroma from hyperandrogenic women, significantly more testosterone accumulated in the medium per milligram of tissue than in the medium of incubations of ovarian stroma from normally cycling women (142 f 48 vs. 7.9 f 7.5 pg testosterone per milligram of tissue per 48 h, mean f SD, P < 0.05). The ratio of testosterone to androstenedione was significantly higher in the medium of incubations of ovarian stroma from hyperandrogenic women than in that from normally cycling women (0.61 vs. 0.25, mean, P < 0.05). The ratio of serum testosterone to androstenedione was significantly greater in hyperandrogenic women than in normally cycling control women (0.31 f 0.11 vs. 0.20 * 0.03, mean f SD, P < 0.05). Conclusion: The localization (cytosol fraction) and substrate specificity (estrone) of the granulosa-luteal cell 17-ketosteroid oxidoreductase enzyme resembles that seen in human placenta. The localization (membrane fraction) and substrate specificity (androstenedione) of the ovarian stromal Ill-ketosteroid oxidoreductase enzyme resembles that seen in Leydig cells. It may be one enzyme that exists in multiple forms or it may be two (or more) enzymes. In some hyperandrogenic women the ovarian stromal 17-ketosteroid oxidoreductase may be more active than in normally cycling women, contributing to an abnormally increased testosterone production rate.

Detection of platelet autoantibodies to identify immune thrombocytopenia: state of the art

Immune Thrombocytopenia (ITP) is diagnosed by exclusion of other causes for thrombocytopenia. Reliable detection of platelet autoantibodies would support the clinical diagnosis of ITP and prevent misdiagnosis. We optimized our diagnostic algorithm for suspected ITP using the direct monoclonal antibody immobilization of platelet antigens assay (MAIPA), which evaluates the presence of platelet autoantibodies on the glycoproteins (GP) IIb/IIIa, Ib/IX and V bound on the patient platelets. The direct MAIPA was shown to be a valuable technique for the detection of platelet autoantibodies and could possibly become a guide for optimizing therapy towards a more personalized treatment of ITP.