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Therapeutic apheresis
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
The presentation of TTP is classically described by a clinical pentad of (i) microangiopathic hemolytic anemia (MAHA), (ii) thrombocytopenia; (iii) renal failure, (iv) fever, and (v) mental status changes. In practice, the presence of thrombocytopenia (<100 × 109/l) and an elevated lactate dehydrogenase (LDH > 1000 units/l, a manifestation of systemic ischemia and hemolysis) in the absence of another likely cause is sufficient to make the diagnosis.45,46 Although this disease was once associated with a mortality rate in excess of 80%, following the introduction of daily plasma exchange the mortality rate has been reduced to 10–20%.
Thrombotic Microangiopathy
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
Three major events occur in this condition: hemolysis, thrombocytopenia, and altered functions of various visceral organs. Their occurrence may be explained on the basis of the microthrombotic lesions. The partial occlusion of the arterioles and capillaries allows the passage of blood through altered hemodynamic conditions. Red blood cells flowing through the involved vessels with fibrin covering the thrombi are traumatized and fragmented, forming schistocytes and resulting in hemolysis (Figure 2). This alteration was first demonstrated by Brain et al.34 who termed the process microangiopathic hemolytic anemia. The thrombocytopenia follows excessive platelet consumption due to aggregation and platelet thrombi formation.
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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Microangiopathic Hemolytic Anemia [Greek: micro, small + angeion, vessel + pathos, disease] Term coined by William St Claire Symmers (1863–1937) in 1932 to denote the mechanical damage to red blood cells resulting in poikilocytosis or abnormally shaped red cells.
Beneficial effect of fresh frozen plasma in reducing renal complications in Hemiscorpius lepturus scorpion envenomated children with severe hemoglobinuria: an open label randomized clinical trial
Published in Toxin Reviews, 2023
Ehsan Valavi, Parisa Amoori, Neda Mohtasham, Tahereh Ziaei Kajbaf, Mehri Taheri, Bahman Cheraghian, Soodeh Hooshmandi
In our previous study, acquired ADAMT13 deficiency was highly prevalent in patients with significant hemoglobinuria due to HL envenomation and was effective in the development of HUS (Valavi et al. 2011, 2014). ADAMTS13 deficiency is one of the major causes of atypical HUS. Without ADAMTS13, von Willebrand factor (VWF) multimers can grow to pathologically high molecular weights. This contributes to the unlimited growth of microvascular thrombi, leading to clinical manifestations of microangiopathic hemolytic anemia (Tersteeg et al. 2015). However, it has been recently reported that ADAMTS13 activity decreases in conditions, such as snake bite, liver cirrhosis, idiopathic thrombocytopenic purpura, leukemia, chronic uremia, HUS, DIC, systemic lupus erythematosus, pregnancy, postoperative state, neonatal period, and advancing age (Levy et al. 2005, Isbister et al. 2007, Malbranque et al. 2008).
Cobalamin and folic acid deficiencies presenting with features of a thrombotic microangiopathy: a case series
Published in Acta Clinica Belgica, 2022
Britt Ceuleers, Sofie Stappers, Jan Lemmens, Lynn Rutsaert
‘Microangiopathic hemolytic anemia’ is a term used to describe any Coombs-negative hemolytic anemia resulting from red cell fragmentation in the small vessels, identified as schistocytes and fragmentocytes on peripheral blood smears. When these abnormalities are accompanied by thrombocytopenia, one should be aware of thrombotic microangiopathies. This group of related disorders, including thrombotic thrombocytopenia and hemolytic-uremic syndrome, is characterized by thrombosis in the microvasculature due to an endothelial injury, resulting in the aforementioned nonimmune hemolytic anemia and associated end-organ damage [1–3]. Here, we introduce three cases of vitamin B12 and/or folic acid deficiencies, presenting with features of a thrombotic microangiopathy. In this manner, we aim to make the reader aware of this notorious but rare manifestation of these nutritional deficiencies, hopefully leading to an earlier recognition of these pseudo-thrombotic microangiopathies (pseudo-TMA). Hence, unnecessary and expensive treatment, such as plasmapheresis, should be avoided or at least shortened in duration.
A New Zealand White rabbit model of thrombocytopenia and coagulopathy following total body irradiation across the dose range to induce the hematopoietic-subsyndrome of acute radiation syndrome
Published in International Journal of Radiation Biology, 2021
Isabel L. Jackson, Ganga Gurung, Yannick Poirier, Mathangi Gopalakrishnan, Eric P. Cohen, Terez-Shea Donohue, Diana Newman, Zeljko Vujaskovic
Four of the five surviving animals presented with nucleated red blood cells between days 7 and 20-post-TBI, which was supportive of a regenerative response by the bone marrow. Only one decedent (e.g. euthanized prior to the 45-day study endpoint) presented with very rare nucleated red blood cells (e.g. 1 per 100 cells). This was observed on day 1 post-TBI and was considered an unreliable finding unlikely to be of significance. Polychromatophilic erythrocytes, a sign of bone marrow stress, were noted on peripheral blood smears between days 1 and 10, but did not appear to be correlated with outcomes. Fibrin clots were observed on the blood films between days 3–7 post TBI in seven of twenty-animals, which was not associated with survival outcomes. These features did not appear to correlate with outcomes. Features of microangiopathic hemolytic anemia (e.g. schistocytes) were notably absent.