Pseudothrombocytopenia in a neonate due to mother?

UNLABELLED: Ethylenediaminetetraacetic acid (EDTA)-dependent pseudothrombocytopenia (PTCP) is the phenomenon of a false low platelet count reported by an automated haematology analyzer due to in vitro aggregation of platelets. This aggregation is due to the interaction between antibodies and EDTA-dependent crypt antigens on platelets. We observed a new born child whose mother was diagnosed with transient PTCP due to transplacental transmission of maternal immunoglobulin G antibodies during pregnancy. CONCLUSION: Although maternal-neonatal PTCP is rare, it is important to consider this phenomenon as a cause of trombocytopenia, as it can result in unnecessary diagnostic workup and treatment.

Temporary impairment of reticulocyte haemoglobin content in subjects with community-acquired pneumonia.

INTRODUCTION: In the case of inflammation, imbalance of iron homoeostasis is caused by increased retention of iron within cells of the reticuloendothelial system. Iron-restricted erythropoiesis occurs because of decreased availability of iron for haemoglobin (Hb) synthesis in erythroid progenitor cells. Deviations in reticulocyte haemoglobin (Ret-He) content are investigated together with inflammation markers in subjects with community-acquired pneumonia (CAP). Short-term alterations with regard to Ret-He during and after completing antibiotic treatment are investigated. METHODS: A total of 75 patients, classified into three subgroups with CURB-65 scores of ≤1, 2 and ≥3, participated in the study. RESULTS: Within the three subgroups, Hb results demonstrate a decline from the day of admission until day 4. From day 4, an increase towards higher values is observed at day 14. Within 24 h after admission, Ret-He results are situated within the lower quartile region of the reference range interval. Until day 4 of hospital admission, a steady trend towards a decline of 3-8% is established. During antibiotic treatment, an increase in reticulocyte count occurs from 0.039 ± 0.014 × 10(12) /L at day 4 to 0.057 ± 0.020 × 10(12) /L at day 14 (mean ± SD). Recovery of Hb and Ret-He occurs towards values within the reference range. CONCLUSION: In subjects with CAP, acute inflammation results in impairment of Ret-He at an early stage. After onset of pneumonia, decreased results of Ret-He and Ret-He/RBC-He ratio are demonstrated, reflecting acute erythropoietic dysfunction, which are amongst others caused by functional iron depletion.

Changes in platelet volume, morphology and RNA content in subjects treated with haemodialysis.

During haemodialysis treatment, blood flows from the body to the extracorporeal circuit and vice versa. In this study, pathophysiological defects in platelets indicated by alterations in RNA content and aberrations in platelet volume and morphology are detected before and during haemodialysis treatment. In subjects receiving haemodialysis treatment, qualitative interpretation of platelet characteristics with application of light microscopic evaluation reveals only 19+/-11 % of platelets with appropriate staining density of the granule-containing cytoplasm. On the contrary, a reference group of apparently healthy subjects shows 70+/-12 % platelets with appropriate staining density of the granule-containing cytoplasm. During haemodialysis treatment, mean values for platelet volume, platelet distribution width and platelet large cell ratio demonstrate a tendency to decrease by 10 %, 11 % and 6 %, respectively, from the mean initial value to the value at t = 150 min. Reduction of the platelet volume parameters just mentioned is hypothesized to be due to platelet degranulation as a result of platelet activation.

Deviations in coagulation activation due to treatment with different haemodialysis membranes.

Despite systemic heparinization, extracorporeal circulation will induce activation of blood coagulation. Thrombogenicity is associated with biocompatibility of dialysis membranes. Investigation of procoagulatory and fibrinolytic activity is performed prior to and during treatment with haemodialysis. In this study fluctuations of plasma coagulation factor XII, thrombin antithrombin complexes, prothrombin fragment 1 + 2 and thrombus precursor protein were monitored in 10 subjects during treatment with haemodialysis. Subjects were treated with both polysulphone high-flux dialyser membranes (F-60) and low-flux poly-methyl-methacrylate (PMMA) membranes. Immediately after start of treatment, blood in contact with artificial membrane surfaces resulted in a marked decrease in factor XII activity amounting to a mean reduction of 80% in the case of PMMA and a reduction of 40% in the case of F-60. In due course, a steady, on-going generation of thrombin antithrombin complexes was observed in several subjects, especially after treatment with F-60 membranes, amounting to increases exceeding 100% of initial values. Establishment of fibrinogen, prothrombin fragment 1 + 2 and thrombus precursor protein plasma concentrations yielded enhanced results for PMMA compared with the results for treatment with F-60 dialysis membranes. In order to prevent activation of clotting during several stages of haemodialysis, supplementation of anticoagulant can be established on the basis of analytical results of coagulation parameters.

Subjects with a shortened activated partial thromboplastin time show increased in-hospital mortality associated with elevated D-dimer, C-reactive protein and glucose levels.

BACKGROUND: Shortened activated partial thromboplastin time (aPTT) values are associated with enhanced coagulation activation. However, the clinical relevance of shortened aPTTs is not well defined. The aim of this study was to determine the in-hospital mortality rate in subjects with shortened aPTTs and the effects of polymorphism in plasminogen activator inhibitor (PAI)-, t-PA- and factor XIII gene on the coagulation status. D-dimer, C-reactive protein (CRP) and glucose, markers that have been related with increased mortality, were tested. RESULTS: We found that a shortened aPTT on admission was associated with an increased risk of in-hospital mortality (OR=2.6, 95% CI: 2.1-3.5). Non-survivors with short aPTTs had significantly higher plasma D-dimer, CRP and glucose levels compared with survivors. Subjects homozygous for PAI-1 5G and t-PA I alleles showed higher plasma D-dimer levels compared with 4G/4G PAI-1 (p=0.02) and D/D t-PA (p=0.001) homozygotes, respectively. CONCLUSIONS: These results suggest that PAI-1 4G/5G and t-PA I/D polymorphisms determine plasma D-dimer levels in patients with shortened aPTT values. Preliminary results show that, among patients with short aPTTs, homozygosity for the hyperfibrinolytic PAI-1 5G or tPA I alleles are at increased risk of in-hospital mortality compared with 4G/4G PAI-1 and D/D tPA homozygotes (OR=2.6, 95% CI: 1.3-5.5 and OR=5.5, 95% CI: 1.3-24.5, respectively).