- Email: [email protected]
Early pregnancy loss: Mechanisms and treatment
293 JIM 05568 Beard, R.W. and F. Sharp (Eds.), Early Pregnancy Loss: Mechanisms and Treatment, XVIII + 442 pp., Springer-Verlag, Berlin-Heidelberg, 1988. D M 150,-, ISBN 3-540-19530-0 This book contains reports of a study group of researchers and clinicians set up by the Royal College of Obstetricians and Gynaecologists in the U.K. for the investigation of problems encountered in the first three months of pregnancy and of the ways to tackle them. The reports deal with various aspects of recurrent miscarriages including their epidemiology, pathology, and the possible genetic or immunological causes. Evidence based on both experimental and clinical studies is presented. A great deal of attention is directed at the exploration of the role of maternal immune responses to foetal M H C antigens in the maintenance of pregnancy. Data are presented on the expression of different antigens by cells of the conceptus before, during and after implantation, as observed in rodents and humans. These indicate that the human villous trophoblast shows no H L A class I or II antigens, whereas the extravillous trophoblast bears class I but not class II antigens. Moreover the allotypic trophoblastlymphocyte cross-reacting antigen (TLX) has been described. Anti-trophoblast antibodies could be demonstrated regularly in murine pregnancy and occasionally during normal human pregnancy. Immunoregulation studies in mice reveal suppressor cell activity in the uterine decidua after implantation; this activity is deficient in abortions due to rejection of the foetus but may be normal in abortions caused by a genetic lesion. In murine recurrent spontaneous abortions (RSA) N K cells rather than specific immune effectors play a key role. In the rat placenta three suppression mechanisms have been found to control the synthesis of class I and II antigens and thereby prevent the immune rejection of the foetal allograft. Some study group members view the human foetalmaternal interaction as resembling more closely the tumour-host than the graft-recipient relationship. The association of anti-phospholipid autoantibodies with foetal loss is also discussed. On the basis of the foregoing it has been suggested that maternal recognition of incompatible TLX antigens could lead to the production of protective
factors (e.g., blocking antibodies) beneficial to pregnancy. Thus therapeutic regimes have been devised for the treatment of RSA of apparently immunological origin (excluding patients aborting due to genetic causes), involving immunization with paternal lymphocytes, pooled donor lymphocytes, or syncytiotrophoblast membrane preparations. In a special section of the book immunotherapy trials, performed over the past several years in different countries are described and the results of others reported in hterature are reviewed. In most of them women with a history of RSA, sharing a number of H L A antigens with their partners and devoid of serum factors blocking M L R to the partner's cells, were immunized with various doses of paternal lymphocytes, a single intravenous injection being preferred for the induction of blocking antibodies. Alternative immunizing materials have included leukocyte-rich erythrocyte concentrates and sterile trophoblast membrane vesicles from term placentae of normal pregnancies. Most of the trials resulted in ca. 80% success for the next pregnancy and correlated with the appearance of antipaternal blocking antibodies in the sera of women giving birth to healthy babies (no consistent relation was found between the incidence of leukocytotoxic antibodies and the therapy outcome). Some participants in the project criticize the therapy protocols for the lack of adequate controls and caution against interpreting the results as indicative of immune aetiology of the treated cases. On the other hand the immunotherapy is characterized as harmless during the pregnancy, at birth and for the child's health; the risk of viral contamination associated with donor lymphocyte transfusion is considered to be absent in trophoblast membrane inoculation. Recommendations for the future stress the need for improved patient selection and follow-up of children born after the intervention. The remaining section is devoted to other methods of treatment - cervical cerclage, preventive administration of exogenous human chorionic gonadotrophin, and psychotherapy. Each presentation is followed by a record of the discussion among the participants. Regrettably missing are a general summary and an index that would facilitate the reading and comprehension of this informative text.
F. BOREK
factors (e.g., blocking antibodies) beneficial to pregnancy. Thus therapeutic regimes have been devised for the treatment of RSA of apparently immunological origin (excluding patients aborting due to genetic causes), involving immunization with paternal lymphocytes, pooled donor lymphocytes, or syncytiotrophoblast membrane preparations. In a special section of the book immunotherapy trials, performed over the past several years in different countries are described and the results of others reported in hterature are reviewed. In most of them women with a history of RSA, sharing a number of H L A antigens with their partners and devoid of serum factors blocking M L R to the partner's cells, were immunized with various doses of paternal lymphocytes, a single intravenous injection being preferred for the induction of blocking antibodies. Alternative immunizing materials have included leukocyte-rich erythrocyte concentrates and sterile trophoblast membrane vesicles from term placentae of normal pregnancies. Most of the trials resulted in ca. 80% success for the next pregnancy and correlated with the appearance of antipaternal blocking antibodies in the sera of women giving birth to healthy babies (no consistent relation was found between the incidence of leukocytotoxic antibodies and the therapy outcome). Some participants in the project criticize the therapy protocols for the lack of adequate controls and caution against interpreting the results as indicative of immune aetiology of the treated cases. On the other hand the immunotherapy is characterized as harmless during the pregnancy, at birth and for the child's health; the risk of viral contamination associated with donor lymphocyte transfusion is considered to be absent in trophoblast membrane inoculation. Recommendations for the future stress the need for improved patient selection and follow-up of children born after the intervention. The remaining section is devoted to other methods of treatment - cervical cerclage, preventive administration of exogenous human chorionic gonadotrophin, and psychotherapy. Each presentation is followed by a record of the discussion among the participants. Regrettably missing are a general summary and an index that would facilitate the reading and comprehension of this informative text.
F. BOREK