Summary The alpha‐2‐globulin previously reported as 'PAG' has been renamed Pa 1. It appears to be inherited by means of an autosomal gene, possibly recessive. There is no evidence indicating a genetic relation to 16 other independent grouping systems. The appearance of this protein seems to be under hormonal control. Résumé L'alpha‐2‐globuline précédemment appelée »PAG« a été renommée Pa 1. Il semble que cette alpha‐2‐globuline soit conditionnée par un gène autosomal, peut‐être récessif. Il n'y a aucune manifestation permettant de déduire qu'il y ait une relation génétique avec 16 autres systèmes de groupes indépendents. Cette protéine semble être sous contrôle hormonal. Zusammenfassung Das früher als »PAG« bezeichnete Alpha‐2‐Globulin wird in Pa 1 umbenannt. Es handelt sich offensichtlich um ein autosomales, möglicherweise rezessives Erbmerkmal. Es fehlen Hinweise für eine genetische Beziehung zu 16 anderen gruppen‐spezifischen Merkmalen. Das Auftreten dieses Eiweißes steht offenbar unter hormonaler Kontrolle.

Five examples of a “new” blood group antibody, anti‐Rd (Radin), are reported. The corresponding antigen, Rd, is infrequent and does not correspond to any other known “low‐incidence” antigen. Family studies indicate that Rd is an autosomal dominant character which does not belong to the ABO, MNSs, Rh, Lutheran, Kell or Kidd blood group systems. Furthermore, the gene determining Rd is not closely linked to either the haptoglobin or red cell acid phosphatase loci. Anti‐Rd caused mild to moderate hemolytic disease of the newborn in all five families and has appeared with the first pregnancy.

Questions have been raised by statements of the American College of Obstetricians and Gynecologists that Rh immune globulin should be given to all Rh positive, Du variant, mothers who have recently delivered Rh positive infants. This practice is not recommended. However, blood banks must assure that a positive Du test on a mother's blood sample is not caused by a massive fetal-maternal hemorrhage. Failure to recognize this cause of a positive Du test may result in the administration of an inadequate dose of Rh immune globulin.

Summary:mately 5 years after completing all treatment, he developed pancytopenia. Extensive workup ruled out relapsed Hodgkin's disease. Myelodysplasia was diagnosed by bone A 38-year-old man developed idiopathic thrombocytopenic purpura (ITP) 8 months following allogeneic marrow biopsy and he underwent successful marrow transplantation from his HLA-matched sister in August BMT while being treated for cGVHD with corticosteroids and tacrolimus (FK506). He received two courses 1994. Transplantation was complicated by pneumonia, veno-occlusive disease, hemolytic-uremic syndrome from of high-dose intravenous immunoglobulin (IvIG) which resulted in transient improvement. A single dose of cyclosporine and mild acute graft-versus-host disease. The hemolytic uremic syndrome resolved on reduced doses of intravenous anti-D immunoglobulin induced a durable response. Anti-D immunoglobulin is better tolerated, cyclosporine, and this medication was eventually discontinued. He later developed extensive chronic graft-versusless complicated to administer, and less expensive than a course of IvIG.host disease involving eyes, mouth, esophagus, liver and skin documented by liver biopsy and clinical findings. Keywords: idiopathic thrombocytopenic purpura; bone marrow transplantation; anti-D immunoglobulin; chronicIn April 1995, 8 months after transplantation, he developed ITP with a platelet count of 10 000/l and graft-versus-host disease mucosal bleeding. Bone marrow biopsy and cytogenetics confirmed trilineage engraftment with female metaphases. Megakaryocytes were abundant and appeared normal. PlatPersistent thrombocytopenia following allogeneic bone elet transfusions did not increase his platelet count. Direct marrow transplantation has been associated with an overall and indirect antiplatelet antibodies were detected. Penicillin poor prognosis.1,2 Such patients usually have extensive and trimethoprim-sulfamethoxazole were stopped without graft-versus-host disease and are at risk for infectious comimprovement in his platelet counts, and he received two plications. True ITP post-BMT has been reported occasioncourses of high-dose gammaglobulin (2.5 g/kg over several ally and has been treated with increased immunodays) with transient effect (Figure 1). Although he had suppression, splenectomy and androgens.3 Antiplatelet antiundergone a splenectomy, and his peripheral blood smear bodies of donor origin were shown in one study. 4 Concomirevealed Howell-Jolly bodies, we performed a liver-spleen tant medical problems in the post-transplant population may scan which documented a splenule. He was treated with make effective treatment of ITP particularly difficult.one intravenous dose of 25 g/kg anti-D immunoglobulin with immediate response and achieved a remission lasting 6 months ( Figure 1). No complications were observed and Case report his hematocrit remained stable.A 38-year-old man with secondary myelodysplasia from alkylating treatment for nodular sclerosing Hodgkin's disDiscussion ease underwent bone marrow transplantation from...