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At least 361 records · Page 20Linked to original sources
PubMed1988

[Drug-induced thrombopenias and neutropenias. An in vitro study by the indirect immunofluorescence test].

The sera from 38 patients with suspected drug-induced thrombocytopenia (22) or neutropenia (16) were tested with the indirect immunofluorescence test on platelets or granulocytes for the presence of drug-dependent antibodies. Three drug-induced antibodies with reactivity against platelets and 5 with reactivity against granulocytes were detected. In 3 sera antibodies were found which reacted already with target cells without adding the drug to the test system. These data show that drug-induced blood dyscrasias often have an immunological cause and that in vitro tests can be helpful in detecting the responsible drug. Different mechanisms can be involved. In many sera circulating antibodies were not found, but an immunological mechanism is likely to be involved in some of these cytopenias: the antibody could be entirely absorbed by the target cells, a metabolite of the drug could be the immunogen and finally the test may not be sensitive enough.

Agranulocytosis↗
PubMed1988

[Thrombopenia and disseminated intravascular coagulation during treatment with heparin: 2 cases with neurological complications].

We report two cases of heparin-induced thrombocytopenia (H.T.) associated with a disseminated intravascular coagulopathy (DIC). Heparin was prescribed after a cerebral infarct in the first case and after an orthopedic surgical procedure in the second case. The DIC induced neurological complications and the death of both patients. Heparin-induced thrombocytopenia is common but is exceptionally associated with neurological symptoms. Heparin-induced DIC is quite uncommon, since only 20 cases have been reported but neurological complications (focal deficits or disturbances of consciousness) are noted in about one third of the cases and the outcome is fatal in 60 percent of the cases. The treatment of heparin-induced DIC and thrombocytopenia is disappointing. Monitoring of the platelets count is warranted during heparin treatment to prevent this severe complication.

Disseminated Intravascular Coagulation↗
PubMed1986

[EDTA-dependent pseudo-thrombopenia].

Pseudothrombocytopenia, a term used to define a spuriously low platelet count produced by automatic cell counters, is most often due to platelet clumping induced by EDTA. In a period of two years we have observed 8 patients with a mean platelet count of 46,000/mm3 in the presence of EDTA. When samples of capillary blood (without EDTA) were tested, the mean platelet count was 202,000/mm3. A further patient had platelet adherence to neutrophils with normal platelet counts. This rare finding can also lead to pseudothrombocytopenia. In the event of unexpected thrombocytopenia a smear from EDTA-blood samples reveals the presence of platelet clumping or adherence to neutrophils. Counts of capillary blood samples reveal the true platelet number.

Adult↗
PubMed1987

[Major thrombopenia induced by heparin. Practical approach to cardiac surgery under extracorporeal circulation].

Major heparin-induced thrombocytopaenia (HIT) is a condition which is feared more for its thrombotic complications than for the risk of haemorrhage. The platelet count is part of routine surveillance of patients receiving this treatment which must be withdrawn if HIT occurs. The use of heparin remains essential for cardio-pulmonary bypass surgery. There are two possible scenarios: The thrombocytopaenia occurs in the postoperative period: the standard heparin may be relayed by oral anti-vitamin K anticoagulants, platelet antiaggregant drugs or by low molecular weight heparin (LMWH). The diagnosis of HIT is made before surgery: three therapeutic attitudes are discussed with respect to the urgency of surgery: surgery is deferred for 6 to 8 weeks to allow the platelet count to return to normal and the responsible circulating antibody to disappear; the use of LMWH providing the tests of platelet aggregation are negative with this product; in addition, there are other problems specific to their use in cardiopulmonary bypass to be considered; blood exchange at the beginning of cardiopulmonary bypass to eliminate the circulating factor responsible and so allow the use of standard heparin during and after the operation: this is the only possible solution in cases with in vitro aggregant activity of LMWH.

Cardiac Surgical Procedures↗
PubMed1985

[Neonatal alloimmune thrombopenia. Clinical and biological study of 84 cases].

Eighty-four patients with neonatal alloimmune thrombocytopenia (NAT) were investigated clinically and by biological laboratory methods. The condition appeared at birth, usually as an isolated thrombocytopenic purpura, but in about 20% of the neonates the haemorrhagic syndrome was associated with signs of infection or with jaundice and hepatosplenomegaly. Considerable variations were observed in the severity of the purpura; in 3 cases the thrombocytopenia was clinically silent. Haemorrhagic brain lesions were present in 7% of the neonates, and severe neurological sequelae in 14 of the 59 children on long-term follow-up. The overall mortality rate was 9.2%. The PLA1 system was involved in 56 of the 59 families studied, with PLA1-negative mothers developing immunization against the foetus' PLA1 antigen. In 20% of these mothers the antibody was not demonstrable, and the diagnosis relied on the mother's phenotype and on a history of previous NAT. The strong association demonstrated between the HLA-DR3 antigen and the ability to develop anti-PLA1 antibodies is of extreme importance. It may be helpful to confirm the diagnosis in mothers without detectable anti-PLA1 antibodies and to identify mothers at risk of alloimmunization. Neurological sequelae, which were due to post-natal haemorrhage in at least 70% of the cases, could now be avoided by an early diagnosis, modern transfusional techniques and caesarian section. However, antenatal lesions cannot be avoided, except by preventive measures, yet to be developed, against alloimmunization or the cytopenic effect of the platelet antibody.

Blood Group Incompatibility↗
PubMedDate not supplied

[Vascular headache, thrombopenia and serotonin metabolism].

The role of platelet serotonin in migraine remains a subject of controversy. However, the frequency of association of migraine with antibody-mediated thrombocytopenia would suggest that platelet dysfunction or impaired serotonin metabolism might play a role in migrainous attack. We report three new cases, two involving chronic idiopathic thrombocytopenia and one lupus. The observation of high levels of anti-platelet antibodies in close correlation with the occurrence of attacks suggests that the Serotonin Releasing Factor (SRF) could be concerned. This was suspected previously on the basis of in vitro studies. The hypothesis that other forms of migraine might be linked to an immunopathological process involving other immunoglobulins is proposed (Acta neurol. belg., 1988, 88, 290-296).

Adult↗
PubMed1987

Autoantibodies to nuclear lamin B in a patient with thrombopenia.

We report the characterization of novel nucleus specific autoantibodies in the serum of a patient with systemic lupus erythematosus. Immunofluorescent staining of cycling cells and absorption experiments localized the antigen to the nuclear envelope. Two-dimensional gel electrophoretic analysis of immunoprecipitated nuclear proteins show the antigen to be an acidic polypeptide (IP approximately 5.4) of 68 kDa molecular mass. It has been identified as lamin B, one of the three major nuclear envelope polypeptides of mammalian cells. Antibodies shown to be polyclonal immunoglobulin Gs, were directed against determinant(s) of the protein that have apparently been conserved during evolution. They do not appear to be related to other autoantibodies present in the serum (anti-DNA and anti-platelet). The nuclear specificity shown by these antibodies further demonstrates the antigenicity of proteins related to intermediate filament proteins in patients with autoimmune disorders.

Adult↗