BACKGROUND:Current guidelines recommend that platelets (PLTs) from D- donors should be given to D- patients. However, such evidence comes from studies with a limited number of included patients that reported an incidence of anti-D alloimmunization to be up to 19%. We thus decided to extend these findings by examining anti-D alloimmunization at our institution, where PLT transfusions from D+ donors are transfused to D- patients because of logistic constraints.STUDY DESIGN AND METHODS:From April 1999 to December 2009, we retrospectively reviewed the clinical and transfusion records of all D- patients who received PLT transfusions from D+ donors at our hospital. PLT concentrates (PCs) were obtained from apheresis and from whole blood donations. RhIG was not administered after the transfusion of PCs from D+ donors. The antibody screen test to detect anti-D was performed by low-ionic-strength solution indirect antiglobulin test using the gel test.RESULTS:Our series comprises 1014 D- patients who received 5128 PLT transfusions from D+ donors (89% were pooled PCs). We had 315 (31.1%) patients who had a blood sample to analyze the presence of anti-D 4 or more weeks after the first D+ PLT transfusion with a median follow-up of 29 weeks (range, 4-718 weeks). Anti-D developed in 12 (3.8%) of these 315 patients.CONCLUSIONS:The frequency of anti-D alloimmunization of D- patients after receiving pooled PCs from D+ donors is low. The transfusion of D-incompatible pooled PCs without immunoprophylaxis to D- men or D- women without childbearing potential seems a reasonable and safe alternative.

BACKGROUND: Amotosalen plus ultraviolet A light photochemical treatment (PCT) inactivates high titers of bacteria, and other pathogens, in platelet concentrates (PCs) potentially allowing the storage of platelets (PLTs) for up to 7 days. Adhesion and aggregation of PLTs to injured vascular surfaces are critical aspects of PLT hemostatic function.STUDY DESIGN AND METHODS: Two ABO-identical leukoreduced huffy coat-derived PCs in additive solution were mixed and divided: one-half underwent PCT (PCT-PCs) and the other was kept as a control (C-PCs); both were stored under standard conditions. The total number of paired PCs studied was nine. Samples were taken on Day 1 (before PCT) and after 5 and 7 days of storage. The adhesion and aggregation capacities were evaluated under flow conditions in a ex vivo perfusion model.RESULTS: Compared to control, PCT resulted in a decrease in PLT count of 6.5 percent (p = 0.004) and 10.2 percent (p = 0.008) after 5 and 7 days' storage, respectively (n = 9). PLT interaction with subendothelium was mainly in form of adhesion. The surface covered by PCT PLTs on Day 1 was 26.0 4.2 percent (mean SEM). On Day 5, PCT-PCs showed a covered surface of 20.9 2.2 percent, and the C-PCs, 20.6 1.6 percent. After 7 days, PCT-PCs produced a nonsignificant higher PLT deposition compared to control (27.1 2.9% vs. 21.2 2.8%, p = 0.06).CONCLUSION: PCT of PCs and storage up to 7 days was associated with a 10.2 percent decrease in PLT count due to processing losses compared to C-PC. PLT adhesive and aggregating capacities under flow conditions of PCT-PCs were similar to C-PCs and remained well preserved for up to 7 days of storage.

The risk of developing liver cancer in hepatitis B virus (HBV) carriers differs across geographical areas, suggesting that exposure to other risk factors may contribute to HBV-linked cancer risk. Our study estimates the mortality due to liver disease and the role of other risk factors in a Spanish HBV cohort. 2,352 hepatitis B surface antigen (HBsAg)-positive and 15,504 HBsAg-negative subjects were identified among blood donors during 1972-1985 and were followed until December 2000 through the Mortality Registry. Clinical examination and an epidemiological questionnaire were performed on 1,000 HBsAg-positive survivors during 1994-1996. In subjects deceased from liver disease, medical records were revised and relatives were interviewed. A nested case-control analysis was conducted comparing both groups. In HBsAg-positive men, an excess mortality from liver cancer [standardized mortality ratio (SMR): 14.1; 7.7-23.6], cirrhosis (SMR: 10.5; 7.0-15.1), haematological neoplasms (SMR: 3.2; 1.2-6.9) and AIDS was detected (SMR: 5.5; 2.2-11.4). In women, an excess was found for cirrhosis (SMR: 7.2; 1.4-21.1). Progression factors to liver disease were alcohol intake [odds ratio (OR): 6.3; 3.1-12.8], diabetes (OR: 3.6; 1.3-9.6), HBV replication (OR: 50.0; 14.9-167.3) and hepatitis C virus (HCV) infection (OR: 27.4; 7.1-107.7). In conclusion, in Spain after 20 years of follow-up, chronic HBV exposure appears as a major risk factor for liver cancer among men and for cirrhosis in both sexes. The risk of death from liver disease among HBV carriers with the presence of HBV replication, HCV, alcohol consumption and diabetes was significantly increased and suggests synergism among these exposures and HBV. Mortality from haematological neoplasms was detected and could be associated to HIV coinfection. These results support screening and adequate follow-up among HBsAg-positive subjects at high risk to develop liver disease, particularly when these risk cofactors are present.

Platelet (PLT) transfusion in patients with thrombotic thrombocytopenic purpura (TTP) is usually considered to be contraindicated based on reports of clinical deterioration and death after PLT transfusion, generally before plasma exchange (PE) was started. The rationale is that the increased number of circulating PLTs after transfusion aggravates microvascular thrombosis. Notwithstanding, some communications suggest that, under an established regimen of PE, TTP patients could receive PLT transfusions, if required, without clinical consequence. We report the case of a 45-year-old woman diagnosed with TTP after a 10-day history of asthenia, malaise, and fever. PE was prescribed, but because she had no available peripheral access, a central venous catheter was required. Her PLT count was 6 × 10 per L. Insertion of a 9F, doublelumen catheter was attempted in the femoral vein in the operating room by an experienced anesthesiologist. The maneuver was unsuccessful bilaterally, and a hematoma formed in the right groin despite local pressure. A leukoreduced five buffy coat–derived PLT concentrate (PC) in additive solution, containing 5.3 × 10 PLTs, was transfused. Ten minutes after the PC was administered, the PLT count was 86 × 10 per L. The corrected count increment was 23,446. At that time, a double-lumen catheter was placed successfully in a jugular vein without complication. No adverse changes were observed in her clinical status. Before PE was initiated 10 hours later, a 13 percent decrease in her hematocrit (Hct) was noted, probably due to groin bleeding. Treatment was started with steroids and daily PEs of 110 percent of plasma volume with a cell separator (COBE Spectra, Gambro BCT, Lakewood, CO). Cryosupernatant plasma was used as the replacement solution. There was progressive normalization of previously altered laboratory values (PLT count, haptoglobin, lactate dehydrogenase, Hct, and creatinine) and clinical improvement. The right groin hematoma was resorbed without sequelae. The patient was discharged after 20 PEs. She is currently well 20 months after completing treatment. Bleeding related to central venous catheter insertion is a major cause of morbidity and mortality in TTP. In our own experience, one patient died after inserting a jugular catheter (1 of 40 TTP patients treated in our institution). We are not recommending liberal PLT transfusions to patients with TTP. Rather, we suggest that the risk of bleeding should be considered carefully when a central catheter needs to be inserted in a TTP patient before PE. Usually, we try to avoid falling under the six heads of Scylla (PLT transfusion) at the risk of plunging into the whirlpool Charybdis (bleeding complications). In the Odyssey, Odysseus chose to lose some of his crew to the monster Scylla, rather than his whole ship to Charybdis. The challenge we face is even harder, that is, transfusing PCs to TTP patients to protect them from potentially dangerous bleeding without precipitating a fatal event. This objective may be achievable if PE is performed promptly after PLT transfusion. Miguel Lozano, MD, PhD e-mail: mlozano@clinic.ub.es Abel Domingo, MD Arturo Pereira, MD, PhD Department of Hemotherapy and Hemostasis Jaime Fontanals, MD, PhD Department of Anesthesiology Roberto Mazzara, MD, PhD Department of Hemotherapy and Hemostasis Agustí Pi i Sunyer Biomedical Research Institute (IDIBAPS) Hôpital Clínic of Barcelona University of Barcelona. Villarroel 170 08036 Barcelona, Spain

We demonstrate that exposure of cultured human endothelial cells to rHuEPO resulted in a dose-dependent increase in the tyrosine kinase activity, with phosphorylation of JAK-2 followed by rapid phosphorylation of STAT-5. Simultaneously, rHuEPO induced long-lasting phosphorylation of MAPK p42/44. Activation of this signaling pathways was directly associated with an increase in the thrombogenic properties of the extracellular matrix generated by these cells, when they were exposed to flowing blood. The enhancement in the reactivity of the resulting extracellular matrix towards platelets was associated with a higher expression of tissue factor. All these effects were blocked by an antibody to the EPO receptor and by specific inhibitors of tyrosine phosphorylation. The observed action of rHuEPO on endothelial cells seemed to be specifically triggered by the subsequent events that follow receptor binding, and occurred even at pharmacological concentrations of the cytokine. Our results indicate that rHuEPO has a direct action on the endothelium, increasing the reactivity of the underlying extracellular matrix towards platelets, effect that may be attributed to an increase in the expression of TF.

TransfusionVolume 34, Issue 6 p. 542-549 The role of the Baumgartner technique in transfusion medicine: research and clinical applications G. Escolar MD, Corresponding Author G. Escolar MD Associate ProfessorFacultad de Medicina, Universidad de Barcelona; and Head of Section, Servicio de Hemoterapia y Hemostasia, Hospital Clínico y Provincial, Villarroel, 170, 08036-Barcelona, Spain.Search for more papers by this authorR. Mazzara, R. Mazzara Roberto Mazzara, MD, Head of Section, Servicio de Hemoterapia y Hemostasia.Search for more papers by this authorR. Castillo, R. Castillo Ricardo Castillo, MD, Professor of Medicine, Facultad de Medicina, Universidad de Barcelona, and Servicio de Hemoterapia y Hemostasia.Search for more papers by this authorA. Ordinas, A. Ordinas Antonio Ordinas, MD, Professor of Medicine, Facultad de Medicina, Universidad de Barcelona, and Head of Department, Servicio de Hemoterapia y Hemostasia.Search for more papers by this author G. Escolar MD, Corresponding Author G. Escolar MD Associate ProfessorFacultad de Medicina, Universidad de Barcelona; and Head of Section, Servicio de Hemoterapia y Hemostasia, Hospital Clínico y Provincial, Villarroel, 170, 08036-Barcelona, Spain.Search for more papers by this authorR. Mazzara, R. Mazzara Roberto Mazzara, MD, Head of Section, Servicio de Hemoterapia y Hemostasia.Search for more papers by this authorR. Castillo, R. Castillo Ricardo Castillo, MD, Professor of Medicine, Facultad de Medicina, Universidad de Barcelona, and Servicio de Hemoterapia y Hemostasia.Search for more papers by this authorA. Ordinas, A. Ordinas Antonio Ordinas, MD, Professor of Medicine, Facultad de Medicina, Universidad de Barcelona, and Head of Department, Servicio de Hemoterapia y Hemostasia.Search for more papers by this author First published: June 1994 https://doi.org/10.1046/j.1537-2995.1994.34694295074.xCitations: 24 Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume34, Issue6June 1994Pages 542-549 RelatedInformation

Journal Article Clinically Significant Anti-A1 in Blood Group A2 Patients Get access Arturo Pereira, M.D., Arturo Pereira, M.D. Servicio de Hemoterapia y Hemostasia Hospital Clinico de Barcelona Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar Roberto Mazzara, M.D., Roberto Mazzara, M.D. Servicio de Hemoterapia y Hemostasia Hospital Clinico de Barcelona Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar Ricardo Castillo, M.D. Ricardo Castillo, M.D. Servicio de Hemoterapia y Hemostasia Hospital Clinico de Barcelona Barcelona, Spain Search for other works by this author on: Oxford Academic Google Scholar American Journal of Clinical Pathology, Volume 92, Issue 5, 1 November 1989, Pages 709–710, https://doi.org/10.1093/ajcp/92.5.709a Published: 01 November 1989