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Bleeding Disorders in Pregnancy, Including Thrombocytopenia
Published in Tony Hollingworth, Differential Diagnosis in Obstetrics and Gynaecology: An A-Z, 2015
Thrombocytopenia in pregnancy is relatively common, but it is important to be clear about definitions and terminology (Box 5). The main causes are listed in Box 6. Blood film examination will exclude pseudothrombocytopenia due to consumption, platelet clumps or in vitro aggregation. However, the common differential diagnosis is between the following: gestational thrombocytopenia;immune thrombocytopenia (ITP);associated with pregnancy-induced hypertension (PIH).
Delayed, severe thrombocytemia after abciximab infusion for primary angioplasty in acute coronary syndromes: Moving between systemic bleeding and stent thrombosis
Published in Platelets, 2015
Luca Giupponi, Silvia Cantoni, Nuccia Morici, Alice Sacco, Cristina Giannattasio, Silvio Klugmann, Stefano Savonitto
Abciximab is a platelet glycoprotein (GP) IIb/IIIa receptor blocker used, in association with other antiplatelet and anticoagulant drugs, during high-risk percutaneous coronary intervention (PCI) in the setting of acute coronary syndromes (ACS). Administration of abciximab is associated with development of thrombocytopenia [1]. In approximately one-third of patients, thrombocytopenia is a laboratory artefact (pseudothrombocytopenia) [2]. Immune-mediated thrombocytopenia, either acute (4–96 hours from drug exposure) or delayed (5–8 days) is also well recognised [3–8]. While the acute form is secondary to naturally occurring cross-reacting antibodies, the delayed form reflects an immune response to a neo-antigen resulting from abciximab being bound to the platelet membrane; platelets sensitized by the antibody are cleared from the circulation mainly by splenic macrophages [9]. The immune response is drug-dependent and therefore thrombocytopenia is self-limiting, resolving with clearance of abciximab from the blood stream and bone marrow production of new platelets [7].
Hematological manifestations and complications of Gaucher disease
Published in Expert Review of Hematology, 2021
Shoshana Revel-Vilk, Jeff Szer, Ari Zimran
From the 30 years of experience with ERT, we learned that most signs and symptoms of GD gradually improve with every two weeks intravenous infusion of ERT. Hemoglobin levels usually recover first, followed by a reduction in spleen volume. Platelet counts (mainly, but not only, in patients with massively enlarged spleens who have intrasplenic lesions) may require more extended periods to respond. A small minority of patients have refractory thrombocytopenia, even after high-dose, prolonged ERT; some of these patients may additionally have ITP, as detailed above. Pseudothrombocytopenia should be excluded by examination of the peripheral blood smear.
Acute inhalation toxicity of aerosolized electrochemically generated solution of sodium hypochlorite
Published in Inhalation Toxicology, 2022
Bohdan Murashevych, Dmitry Girenko, Hanna Maslak, Dmytro Stepanskyi, Olha Abraimova, Olha Netronina, Petro Zhminko
As can be seen from Table 5, toxicologically significant changes in the number of erythrocytes, leukocytes, hematocrit, the average volume of red blood cells, average hemoglobin content in erythrocytes, and average hemoglobin concentration in erythrocytes have not been observed, with the exception of a 22.4% decrease in the number of platelets on the 1st day of the study. It is known that compounds capable of forming highly reactive oxygen species affect the platelet aggregation process; however, these data are rather contradictory. On the one hand, hypochlorous acid markedly reduces the rate of clot retraction (Misztal et al. 2019). However, a number of studies confirm, on the contrary, the activation of platelet aggregation under the influence of oxygen-containing free radicals, which are one of the decomposition products of hypochlorous acid (Iuliano et al. 1997). The indirect effect of chlorine-active compounds on platelet processes through the modification of blood plasma components is even more complicated. For example, hypochlorite-modified low-density lipoproteins (LDL), like some other oxidized LDL, have been reported to be potent promoters of platelet aggregation (Volf et al. 2000); at the same time, some studies show, on the contrary, suppression of aggregation in the presence of low concentrations of oxidized LDL, which theoretically can be formed by the interaction of blood components with oxygen-containing radicals (Chou et al. 2004). It is worth noting that most of the mentioned studies were carried out in vitro. An in-depth study of the hematological parameters of experimental animals was out of the purpose of this work, therefore, detailed studies of platelet processes have not been carried out. Pseudothrombocytopenia is also not excluded. This aspect will be the subject of our further study.