Donor screening for hepatitis B virus infection in a cell and tissue bank.

BACKGROUND AND OBJECTIVES: Hepatitis B virus (HBV) has been transmitted by tissue transplantation. In order to reduce the risk of HBV transmission, testing for antibody to HBV core antigen (anti-HBc) is used in addition to testing for hepatitis B surface antigen (HBsAg) in many blood centers and tissue banks. DESIGN AND METHODS: We retrospectively analyzed the results of HBV assays in tissue donors. All tissue donors were tested for HBsAg and anti-HBc. All anti-HBc positive sera were tested for the antibody to HBsAg (anti-HBs). From July 2006, an HBV nucleic acid testing (NAT) assay was also performed. RESULTS: A total of 6855 tissue donors from January 1999 till July 2007 were tested for HBV assays: 4756 women and 2099 men. Positive HBsAg was found in 23 (0.36%) living donors, while no multiorgan or cord blood (CB) donor was found to be positive for HBsAg. Positive anti-HBc was found in 80 multiorgan donors (12.94%), 599 living donors (17.84%), and 103 CB donors (3.57%) (P<0.005), while isolated anti-HBc was found in 12 multiorgan (1.94%), in 126 living tissue donors (3.75%), and in 8 CB donors (0.28%). A total of 1310 donors were analyzed for single-sample DNA HBV NAT assay. DISCUSSION: We consider that anti-HBc and NAT assays must both still be performed in addition to HBsAg assay for HBV screening in tissue donors. All these tests will be useful in order to define an algorithm for safe and efficient management of the tissue bank.

Post-transfusion purpura as the main manifestation of a trilineal transfusion reaction, responsive to steroids: flow-cytometric investigation of granulocyte and platelet antibodies.

We report a typical case of post-transfusion purpura (PTP) due to anti-PlA1 in a 65-year-old woman. Serological studies were carried out using flow cytometry (FCM). The patient also developed red cell alloantibodies that produced a delayed hemolytic transfusion reaction (DHTR) and broad HLA antibodies. Treatment with high-dose intravenous IgG (HDIgG; a first-generation preparation) was ineffective, but a course of steroids resulted in a rapid increase in the the platelet count.

Isoimmune neonatal neutropenia caused by Fc gamma RIIIb antibodies in a Spanish child.

BACKGROUND: Fc gamma RIIIb deficiency is a rare defect in which neutrophils do not express Fc gamma RIIIb and therefore the individuals with this defect have an NA null phenotype. Soluble Fc gamma RIII in plasma is severely decreased and almost undetectable. During pregnancy, Fc gamma RIIIb deficiency may cause the formation of maternal Fc gamma RIIIb antibodies, which leads to an isoimmune neonatal neutropenia. The first known case of isoimmune neonatal neutropenia caused by these antibodies in a Spanish child was identified. CASE REPORT: A newborn infant was severely affected by omphalitis; analysis of his blood showed an absolute neutropenia, but he responded well on intravenous immunoglobulin therapy. The maternal antiserum reacted strongly with all tested Fc gamma RIIIb-positive neutrophils. A family study showed that the infant's mother, one of the mother's sisters, and her mother were Fc gamma RIIIb deficient. No neutrophil antibodies were found in the plasma from these other Fc gamma RIIIb-negative women, although both had had numerous pregnancies. The three women were healthy, but one had recurrent otitis. DNA analysis of the family showed the absence of both Fc gamma RIIIB genes in the three Fc gamma RIIIb-negative women. The father of the child and all the children of the Fc gamma RIIIB gene-deficient women were shown to lack one of the Fc gamma RIIIB genes. CONCLUSION: A new case of isoimmune neonatal neutropenia caused by anti-Fc gamma RIIIb is identified. The family study indicates that the Fc gamma RIIIb deficiency is a hereditary genetic defect. In accordance with the location of Fc gamma RIIIB on chromosome 1, an autosomal pattern of inheritance of the Fc gamma RIIIB-deficient allele was observed.