This year the Platelet Immunology scientific session was divided into 4 parts: idiopathic thrombocytopenic purpura (ITP), alloimmune/isoimmune thrombocytopenia, heparin-induced thrombocytopenia and thrombocytopenia associated with GPIIb/IIIa inhibitors.

1. Idiopathic Thrombocytopenic Purpura (ITP):

For the past 10 or more years, there has been no new treatment for ITP, and in particular there is a lack of prospective randomized studies. The current treatment options for ITP are far from satisfactory,particularly for treatment of refractory ITP. Dr.J Bussel (USA) gave a brief overview on ITP clinical trials. Most are small and non-comparative studies. Among those completed and published recently, two are interesting. One showed that rhuIL-11 is not effective in refractory ITP, and another revealed that H pylori eradication led unexpectedly to improvement in the co-existing ITP. Ongoing studies which may provide clinically useful data are trials investigating the use of anti-CD 40L, rituxin, thrombopoietin, CBP1011, anti-FcR1, ATG and mycophenalate mofetil in ITP and autologous bone marrow transplant in refractory ITP.

The pathophysiology of ITP remains to be fully elucidated. Animal models may be helpful in this regard. Dr. D Bearsley described an animal model for immune thrombocytopenia using NOD SCID mice grafted with human bone marrow. She found that platelet destruction by the anti-HPA-1a antibody could be prevented by I.V. IgG.
 

2. Alloimmune and Iso-immune thrombocytopenia:

Management of neonatal alloimmune thrombocytopenia remains a very difficult problem despite many years of clinical studies in Europe and USA. Dr M. Murphy presented the results of a recent European collaborative observational study on the antenatal management of neonatal alloimmune thrombocytopenia (NAIT). The patients received (i) maternal therapy (MT); (ii) intrauterine platelet transfusion (IUT); or (iii) serial fetal blood sampling (FBS) only. 56 fetuses from 55 pregnancies were studied. 18 patients received MT consisting of IVIG + prednisolone. This treatment was successful in 12 (67%). 33 received IUT and it was successful in 19. 24 cases had only FBSinitially but 17 subsequently received other treatments. Only in 1 patient, the fetal platelet count dropped below 20x10 ⁹/L warranting early delivery. In all treatment groups, no intracranial hemorrhage (IH) occurred after the treatment had commenced but IH occurred in fetuses before commencement of treatment. One case of IH was associated with infection following cordocentesis. In conclusion, all three treatment strategies appear effective, but IUT should perhaps be reserved for 'high risk' patients as it was associated with significant mortality: three deaths in this series. Dr. J Bussel presented the results of a US multi-center study on NAIT with stratification into 4 risk groups prior to randomization and treatment with IV IgG + prednisone. The higher risk groups were given higher doses of IV IgG and at an earlier time. Like the previous US studies, IV IgG + prednisone were found to be effective.

Every few years a new platelet alloantigen is discovered. There is an urgent need for a nomenclature of human platelet alloantigens that meets the approved of most investigators in the field. A proposal was made at this meeting for the formation of a Platelet Nomenclature Committee consisting of both members of ISBT Working Party on Platelet Serology and the representatives of the SSC Platelet Immunology subcommittee. This nomenclature committee will decide on a system of naming alloantigens, probably based on the current HPA system. The committee will also decide on the membership of reference and repository laboratories.

Iso antibody associated with pregnancy poses a difficult management problem. Dr. C Kaplan presented a review of the literature and 3 pregnant women with Glanzmann's Thrombasthenia and anti-GP IIb/IIIa isoantibody. Despite regular fetal cranial ultrasound monitoring, intra- uterine death due to intracranial haemorrhage occurred in two fetuses. One mother delivered a healthy infant without thrombocytopenia. Dr. Kaplan suggested the establishment of a registry to record cases and improve clinical management.

Recently there have been many reports describing an impact of platelet alloantigen genotypes on the occurrence of coronary artery disease (CAD). Some reported an impact but others showed no impact. Dr. S. Santoso presented his data as well as others and he concluded that platelet alloantigen genotypes have only a minor influence on the occurrence of CAD.
 

3.  Heparin-induced thrombocytopenia (HIT). Although the pathogenesis of HIT has been extensively studied, some issues remained unclear. Dr. P. Visentin (USA) presented convincing data that confirmed the role of T cells in the pathogenesis of this disorder. Dr. J. Walenga presented interesting results suggesting the role of leukocytes and cytokines in HIT. Dr. M Poncz and his colleagues, using a transgenic mouse model, confirmed for the first time the pathogenetic roles of platelet factor 4(PF4) and FcgRIIa in vivo.
 
There is a growing concern that laboratory testing for HIT lacks standardization. Dr. B Chong conducted a HIT serology survey under the auspice of the SSC Platelet Immunology subcommittee. The study showed that the hospital clinical laboratories performed the functional tests, e.g., platelet aggregation test, badly although their performance of the ELISA was excellent. In contrast, the referral or expert laboratories performed both the functional tests and ELISA very well. These findings suggest that functional tests are technically difficult. Unless there are properly trained staff to do the functional tests, clinical laboratories should use the ELISA or refer the HIT test to an expert laboratory.

Management of HIT patients with 'isolated thrombocytopenia' remains controversial. Drs T. Warkentin and A. Greinacher presented data from their studies to show that these patients are at very high risk of developing thrombosis subsequently. Anticoagulant therapy is strongly recommended in these patients.
 

4. Thrombocytopenia associated with GP IIb/IIIa inhibitors: With the increasing use of GP IIb/IIIa inhibitors in cardiac patients, more and more cases of thrombocytopenia associated with the use of these drugs have been reported; however, there is little data on its pathogenesis, diagnosis and management. Drs. R. Aster, A. Greinacher and H. Kroll presented their preliminary data on this "new disorder." The thrombocytopenia usually occurs abruptly, even on the first exposure to the drug, suggesting the presence of a natural occurring antibody. > 90% of patients had antibodies that would bind to platelets coated by the drug, but 70% of normal individuals also have the antibody, though a weaker form. The antibody can be detected by flow cytometry and the M.A.I.P.A., but treatment options are limited.