Kure Guthrie (resthawk3)

Postpartum hemorrhage (PPH) is associated with maternal morbidity and mortality. Accurate diagnosis of the cause of puerperal hemorrhage is as important as treatment strategies for resuscitation. We report a case of coagulation disorder caused by endogenous heparin-like substances in a PPH patient. A 30-year-old woman with no medical history of bleeding disorders suffered intractable hemorrhage following spontaneous delivery in a local hospital. The patient was transferred to the department of obstetrics of a superior hospital. On arrival, the patient was found to have severe hemorrhagic anemia, hemorrhagic shock, and disseminated intravascular coagulation. Active treatments were performed, but the patient continued bleeding. Laboratory testing, performed during early treatment, revealed that all coagulation factors were below normal. The differences between CK-TEG R-time (reaction time in citrated kaolin thromboelastography assay) and CKH-TEG R-time (reaction time in citrated kaolin with heparinase thromboelastography assay) suggested the presence of heparin activity. However, the patient's family denied heparin use prior to presentation. Thus, we deduced that endogenous heparin-like substances were the main cause of the coagulopathy. After receiving treatment with protamine, the patient stopped bleeding. Meanwhile, all coagulation parameters and the TEG assay results improved. In this case report, TEG assay suggested the presence of heparin activity in a PPH patient, and treatment also highlighted the importance of analyzing different parameters in TEG. In this case report, TEG assay suggested the presence of heparin activity in a PPH patient, and treatment also highlighted the importance of analyzing different parameters in TEG.The U antigen (MNS5) is one of 49 antigens belonging to the MNS blood group system (ISBT002) carried on glycophorins A (GPA) and B (GPB). U is present on the red blood cells in almost all Europeans and Asians but absent in approximately 1.0% of Black Africans. U negativity coincides with negativity for S (MNS3) and s (MNS4) on GPB, thus be called S-s-U-, and is thought to arise from homozygous deletion of GYPB. Little is known about the molecular background of these deletions. Bioinformatic analysis of the 1000 Genomes Project data revealed several candidate regions with apparent deletions in GYPB. Highly specific Gap-PCRs, only resulting in positive amplification from DNAs with deletions present, allowed for the exact genetic localization of 3 different breakpoints; 110.24- and 103.26-kb deletions were proven to be the most frequent in Black Americans and Africans. Among 157 CEPH DNAs, deletions in 6 out of 8 African ethnicities were present. Allele frequencies of the deletions within African ethnicities varied greatly and reached a cumulative 23.3% among the Mbuti Pygmy people from the Congo. Similar observations were made for U+ alleles, known to cause strongly reduced GPB expression. The 110- and 103-kb deletional GYPB haplotypes were found to represent the most prevalent hereditary factors causative of the MNS blood group phenotype S-s-U-. Respective GYPB deletions are now accessible by molecular detection of homo- and hemizygous transmission. Platelet concentrates play an important role in transfusion medicine. Their short lifespan and lack of robustness require efforts to ensure adequate product quality. In this study, we compared the in vitro quality of the main concentrate types, pooled platelet concentrate (PPC) from whole blood donations, and platelet concentrate from single-donor apheresis (APC). Twenty PPCs and 20 APCs prepared in plasma were analyzed on days 2, 4, and 7 of storage. Variables related to metabolism, degranulation, platelet aggregation, P-selectin expression, and annexin V binding were analyzed. Morphology was assessed by transmission electron microscopy of ultrathin sections. A microfluidic device was applied to test the ef