Donors with repeated blood product discards for filtration problems, clots or hemolysis: Causes and follow-up.

INTRODUCTION: Sanquin donor medicine department is informed when donations or their components are rejected. This can occur isolated or frequently. It is undesirable because the donations cannot be used and there may be an underlying medical cause. Based on regional approaches, a uniform procedure was developed. METHODS: Information about whole blood, plasma- plateletpheresis donations from which one or more components were rejected for filtration time (>2 h), hemolysis or clots were extracted from blood bank information system. After rejection of two successive components or donations or total ≥3 the donor is contacted. Depending on the medical history and investigation by the family doctor, the donor carrier is re-evaluated. We looked for the causes of the discarded products and performed a survey among blood services regarding polices with discarded products. RESULTS: One or more components from 1742 of about 2.2 million successful donations (0.08%) were rejected. The highest percentage of rejection was seen in plateletpheresis (1.5%), all for clots. No underlying medical causes were found. 24 whole blood donors were found to have sickle cell trait (SCT) and were permanently deferred. The policies for follow-up after discarded products or acceptance of SCT donors vary between the 16 blood banks. Six organizations do not follow-up donors and seven accept SCT for blood or plasma donation. CONCLUSION: Informing donors with repeated discarded products avoids the non-use of donations. Causes of repeated discarded products can be found by follow-up of donors. The results of the survey indicate a large discrepancy in policies applied worldwide.

Donor complication rates in whole blood, plasma and platelet donors: Age versus experience.

BACKGROUND: Many blood banks use upper age limits for donors out of concern for a higher donor complication rate in older donors. Experienced donors are known to have lower donor complication rates, and older donors are often more experienced, confounding the effect of age on donor complication rate. STUDY DESIGN AND METHODS: We studied donor complication rates in whole blood, plasma, and plateletpheresis donors from 2012 to 2022. Donor complication rates were compared between age groups in inexperienced (<20th donation) and experienced (≥20th donation) donors. In addition to this direct comparison, we made use of logistic regression with finer-grained experience groups, to further quantify the effects of age, experience and other factors on donor complication rate. RESULTS: While overall rate of vasovagal reaction was lower, rate of moderate/severe vasovagal syncope was highest in 70-79 year donors, however, only reached significance for plasma donors. Furthermore, rates of failed stab were highest in this age group. Hematoma rate showed a U-shaped pattern with regard to age, where the rate was not higher in the 70-79 year age group than in the 18-23 year age group. Pain decreased with age, however, rates were higher in the 70-79 year age group than in the 65-69 year age group. DISCUSSION: When properly accounting for donor experience, donor complication rate profiles clearly change with age. The increased risk for moderate/severe vasovagal syncope in older donors should be clearly communicated. Extra caution is needed if these donors are accepted for first-time donations.

IgM antibodies against apoptotic cells and phosphorylcholine in patients with acute myocardial infarction in relation to infarct size and inflammatory response.

BACKGROUND: Natural IgM antibodies, and anti-phosphorylcholine IgM (anti-PC IgM) in particular, may modulate the pathogenesis of acute myocardial infarction (AMI). OBJECTIVES: An exploratory study was conducted to evaluate the hypothesis that circulating anti-PC IgM and IgM binding to damaged cells increases the infarct size and post-infarct inflammatory response in patients with AMI. MATERIAL AND METHODS: Plasma IgM binding to apoptotic cells (anti-apop IgM) and anti-PC IgM levels were compared in plasma samples from 50 patients with AMI and 46 healthy controls after correction for hemodilution. The cumulative release of cardiac markers LDH (lactate dehydrogenase), CK or CK-MB in human myocardium at 48 hours was used as an indication of infarct size. The circulating levels of mediators such as activated complement, C-reactive protein (CRP), interleukin-6 (IL6), interleukin-8 (IL8) and secretory phospholipase A2 (sPLA2) were used to assess the post-infarct inflammatory response. Patients with low (< median) and high (> median) levels of anti-apop IgM or anti-PC IgM were compared regarding infarct size and post-infarct inflammatory response. An electrocardiographical scoring system (Selvester score) was used to asses myocardial infarct size in patients with a first AMI (n = 24). RESULTS: AMI patients demonstrated lower levels of anti-PC IgM on admission (p < 0.01) and at 48 hours (p < 0.001) when compared to the healthy controls, whereas anti-apop IgM levels were comparable to control levels. In patients with a first infarct, patients with levels of anti-PC IgM above the median demonstrated larger electrocardiographic infarct sizes (p = 0.04) and a more pronounced response of the acute phase protein sPLA2 (p = 0.06), with a similar post-infarct course of LDH, CK and CK-MB. CONCLUSIONS: These findings suggest that anti-PC IgM plasma levels may participatie in amplifying the inflammatory response of the ischemic heart and contribute to infarct size. However, the levels of anti-PC IgM in patients with AMI in this study do not show a significant effect on cardiac markers LDH, CK and CK-MB. Hence, conclusive evidence is not provided by this limited cohort.

Rat C-reactive protein activates the autologous complement system.

Activation of complement is a biological function of human C-reactive protein (hCRP), whereas rat CRP (rCRP) has been claimed to be unable to activate complement. As important biological functions of proteins are probably conserved among species, we re-evaluated, using various ligands, the capability of rCRP to activate complement. The activation of complement by hCRP and rCRP was investigated in solid- and fluid-phase systems. In the solid-phase system, purified CRP was fixed to enzyme-linked immunosorbent assay (ELISA) plates and incubated with human or rat recalcified plasma. Dose-dependent binding of human and rat C3 and C4 was observed to human and rat CRP, respectively. In the fluid-phase system, recalcified rat plasma, which contains about 500 mg/l of CRP, or human plasma supplemented with hCRP, were incubated with lyso-phosphatidylcholine. A dose-dependent activation of complement was observed upon incubation with this ligand, as reflected by the generation of activated C4 as well as of CRP-complement complexes. This activation was, in both cases, inhibited by preincubation of plasma with p-aminophosphorylcholine, a specific inhibitor of the interaction of CRP with its ligands, or by chelation of calcium ions. We conclude that rat CRP, similarly to human CRP, can activate autologous complement. These results support the notion that opsonization of ligands with complement is an important biological function of CRP.