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PubMed1988

GPIIIa-related PLA1 antigens with different molecular weights: studies in platelets, endothelial cells, and megakaryocytes.

The mol wt of the glycoprotein(s) carrying the PLA1 antigen was examined on platelets, megakaryocytes and endothelial cells by immunoblotting with a human polyclonal anti-PLA1 antibody (BE), as well as on four different monoclonal antibodies (MoAbs; DEK-1, DEK-2C, DEK-10, and DEK-16) raised against GPIIIa, the 100,000-mol wt platelet glycoprotein known to carry the PLA1 antigen. BE reacted with PLA1 positive but not with PLA1 negative platelets. DEK-1 reacted strongly with PLA1 positive platelets but weakly with PLA1 negative platelets. The remaining three MoAbs reacted equally with PLA1 positive as well as negative platelets. BE, DEK-1, DEK-10, and DEK-16 reacted with a 120,000- as well as 100,000-mol wt band on immunoblot of PLA1 positive platelets. The 120,000-mol wt band copurified with affinity purified 100,000-mol wt GPIIIa. Megakaryocytes had a prominent 120,000- as well as 105,000-mol wt band that reacted with BE on immunoblot (the 100,000-mol wt band was not detectable). Umbilical cord endothelial cells from presumed PLA-positive infants had a prominent 100,000-mol wt band that reacted with BE, DEK-16, and DEK-1 (the 120,000-mol wt band was not visualized). The 120,000- and 100,000-mol wt PLA1-positive bands could be digested with proteolytic enzymes to 55,000- to 65,000-mol wt-resistant fragments that retain PLA1 epitopes. Further digestion with endoglycosidase-H lowered the apparent mol wt by approximately 2,000 to 6,000 daltons without affecting PLA1 reactivity. We conclude that the PLA1 antigen is present on a 120,000- as well as 100,000-mol wt glycoprotein of platelets and megakaryocytes, a 105,000-mol wt band of megakaryocytes, and a 100,000-mol wt glycoprotein of endothelial cells. We postulate that the 120,000-mol wt glycoprotein, which shares three or more epitopes with the 100,000-mol wt GPIIIa, may be a post-translational precursor of this species.

Animals↗
PubMed1988

Management of alloimmune thrombocytopenia: antenatal diagnosis and in utero transfusion of maternal platelets.

Neonatal alloimmune thrombocytopenia (NAIT) can cause severe bleeding in the central nervous system (CNS) and death or severe neurologic sequelae. The expression of the PLA1 antigen is detectable as early as 19 weeks of gestation. Alloimmunization can therefore lead to fetal thrombocytopenia very early in pregnancy. Until recently, we have had no means of detecting and assessing the severity of fetal thrombocytopenia during pregnancy. The level of the maternal antibody is not of a predictable value since 20% of the mothers had no circulating antibodies in our series. An alternative approach is to carry out investigations on fetal blood samplings. This management leads to an exact knowledge of the fetal status and antenatal diagnosis is feasible as early as the 21st week of gestation. Early diagnosis facilitates appropriate management and makes possible such therapeutic options as in utero maternal platelet transfusions. We report our experience in the antenatal diagnosis and management of nine cases with in utero transfusion in the six cases with severe thrombocytopenia. All neonates did well, with no signs of bleeding at birth. No side effects of therapy were noted after a period ranging from 6 months to 3 years.

Antigens, Human Platelet↗
PubMed1986

Studies on the pathophysiology of posttransfusion purpura.

Posttransfusion purpura typically occurs in PLA1 negative blood recipients who have been previously immunized to the PLA1 antigen. Following transfusion, severe thrombocytopenia develops with the formation of anti-PLA1. Since the patients' platelets lack the PLA1 antigen, one would not expect this antibody to destroy autologous platelets. In this study we show that PLA1 antigen exists in stored blood and can absorb to PLA1 negative platelets making them PLA1 reactive. Incubating PLA1 (-) platelets with ultracentrifuged plasma from PLA1 (+) blood donors allowed anti-PLA1 to bind to PLA1 (-) platelets. Control plasma from PLA1 (-) blood donors did not lead to anti-PLA1 binding. Using an inhibition assay, we showed that stored blood contains PLA1 material that was not removed by ultracentrifugation. The material absorbing to PLA1 (-) platelets represented the PLA1 antigen, which was confirmed by Western blotting. After incubating plasma containing PLA1 antigen with PLA1 (-) platelets, reactivity at 95,000 D was observed. Native PLA1 (+) platelets showed a similar band. When PLA1 (-) platelets were incubated with plasma from a PLA1 (-) donor, this band was not present. These studies show that a soluble form of PLA1 antigen exists in stored blood that can absorb to PLA1 (-) platelets. Consequently, anti-PLA1 can bind to these platelets leading to thrombocytopenia. These observations may explain the autologous destruction of platelets in posttransfusion purpura.

Antigens, Human Platelet↗
PubMed1986

[Immunization against the ZWa (PLA1) platelet antigen: group at risk, prevention of complications. Apropos of 132 cases].

The identification of anti-ZWa (-PLA1) alloimmunisation is not very frequent. It can be observed in most perinatal alloimmune thrombocytopenias (PAT) and rare post transfusional purpuras (PTP). On the other hand, the clinical consequences of these immunisations are often dramatic, particularly for the foetuses for which there has been no prevention so far. The retrospective study of 132 cases, 123 PAT and 9 PTP, shows the possible irreversible complications for 18% of the newborns with PAT, but especially for 10% of the foetuses which will show PAT at birth. HLA markers are very useful to detect the people who are likely to develop an anti-PLA1 immunization for they are PLA1 negative and HLA DR3. Then, it becomes possible to prevent the complications of these immunisations. It is what we tried to do through the diagnosis and the treatment of PAT in 3 foetuses.

Antigens, Human Platelet↗
PubMed1987

Antigenic differences between human platelets and megakaryocytes.

To investigate the apparent paradox in the observation that most patients with immune thrombocytopenias have normal or increased numbers of megakaryocytes (MKs), the extent of antigenic cross-reactivity between normal platelets and MK was examined. Indirect immunofluorescence and ultrastructural studies were carried out by means of four antisera specific for platelets: anti-GpIb, anti-GpIIb/IIIa, anti-PLA1, and an antiserum from a patient with quinidine-induced thrombocytopenia. Following incubation of freshly collected marrow with these antisera, MK were first identified by phase-contrast microscopy and then inspected for fluorescence. Almost all MKs were found reactive with the last three antisera, albeit to a variable extent. In contrast, only 24% reacted with anti-GpIb. The pattern of fluorescence, ie, rim, partial or cytoplasmic, appeared to be related to the extent of MK fragmentation. Only rim fluorescence of living MKs could be interpreted to indicate that the platelet epitope was exposed on the surface of the precursor cell. The observations suggest that platelet antigens are variably expressed on the plasma membranes of MKs. In a clinical setting, the heterogeneity among platelet target antigens and the extent to which these are exposed on MKs at various stages of maturation may dictate the severity of the thrombocytopenia and degree of ineffective thrombocytopoiesis.

Antigens, Human Platelet↗
PubMed1987

[Intracerebral hemorrhage at 2 different times in neonatal alloimmune thrombocytopenia].

We demonstrate the sonographic and computer-tomographic findings in a newborn with neonatal alloimmune thrombocytopenia (NAITP). Initial examination on the third day of life showed an extensive old and already partially resolved haematoma as well as a new perinatal haematoma in the left cerebral white matter. Follow-up investigations revealed enlargement of the cystic defect, midline-shift to the right and progressive dilatation of the right lateral ventricle caused by compression of the Foramina Monroi. Peritoneal drainage of the cyst resulted in prompt diminution of the enlarged right lateral ventricle. The case report emphasises that in patients with NAITP intracranial haemorrhage may occur in utero and during the perinatal period as well. In pregnant women suspected to produce antibodies against PLA 1 positive thrombocytes, we recommend regular ultrasonic cranial examinations of the fetus. Delivery should be as careful as possible.

Adult↗
PubMedDate not supplied

[Pregnancy monitoring and labor planning in PLA1-induced neonatal alloimmunothrombocytopenia].

Alloimmune thrombocytopenia in newborns may lead to severe bleeding. Most often this thrombocytopenia is caused by incompatibility in the PlA system (mother PlA1 negative, child PlA1 positive). If the mother produces antibodies against PlA1 which cross the placenta, they will then destroy the child's platelets. Recent investigations have shown a strong correlation between HLA-DR3 and production of antibody. Since no screening for such antibodies is performed during pregnancy the resulting thrombocytopenia in the newborn will always be a sudden event. The best therapy is transfusion of PlA1 negative platelets; if no PlA1 negative donor can be found (2.25% of all donors) platelet concentrates of the mother may be used. After diagnosis of PlA related thrombocytopenia the relatives of the mother should be tested for PlA for the following reasons: 1. to determine PlA1 negative relatives to be used as possible donors in future pregnancies, and 2. to detect PlA1 negative women of child bearing age. If pregnant these women should be HLA-DR typed and followed for anti PlA1 antibodies to estimate the risk for the child and to determine further procedures, for instance sectio caesarea to avoid intracranial bleeding during birth.

Adult↗
PubMed1985

Intracranial hemorrhage in utero due to isoimmune neonatal thrombocytopenia.

A case is presented of isoimmune neonatal thrombocytopenia complicated by spontaneous intracranial hemorrhage in utero. Maternal platelets were found to be negative for the PLA1, Baka, and HLA-A2 antigens. The present case demonstrates that the classical conservative approach of elective cesarean section can not guarantee against this crippling event.

Adult↗
PubMed1983

[Neonatal thrombopenia caused by antiPLA1 and HLA-DR3 antigen alloimmunization].

The HLA typing of mothers alloimmunised against the PLA1 antigen of their thrombocytopenic neonate shows that the A1, B8, DR3 haplotype is involved. The very strong association found with DR3 (20/21) suggests that an immune response gene located in the D region of the major histocompatibility complex might be responsible for the ability to develop an anti PLA1 antibody.

Adult↗