Quantitative Platelet Abnormalities Research Articles

Immune-Mediated Platelet Activation in COVID-19 and Vaccine-Induced Immune Thrombotic Thrombocytopenia.

Both qualitative and quantitative platelet abnormalities are common in patients with coronavirus disease 2019 (COVID-19) and they correlate with clinical severity and mortality. Activated platelets contribute to the prothrombotic state in COVID-19 patients. Several groups have shown immune-mediated activation of platelets in critically ill COVID-19 patients. Vaccine-induced immune thrombotic thrombocytopenia is an autoimmune condition characterized by thrombocytopenia and life-threatening thrombotic events in the arterial and venous circulation. Although the initial trigger has yet to be determined, activation of platelets by immune complexes through Fc gamma RIIA results in platelet consumption and thrombosis. A better understanding of platelet activation in COVID-19 as well as in vaccine-induced thrombotic complications will have therapeutic implications. In this review, we focused on the role of immune-mediated platelet activation in thrombotic complications during COVID-19 infection and vaccine-induced immune thrombotic thrombocytopenia.

Unusual Manifestations of Paraprotein-Associated Hematological Diseases: Report of 2 Cases and Literature Review

With this review we firstly describe uncommon manifestations of paraprotein-associated hematological diseases in 2 patients presenting with hemoptysis. The differential diagnosis in both cases included qualitative and quantitative platelet abnormalities, infectious diseases, malignancies, vasculitis, collagen diseases and blood disorders. Among other interventions undertaken, bone marrow biopsy provided evidence of a primary hematological disease while serum protein electrophoresis and immunofixation indicated the presence of a paraprotein. As a “take-away” lesson from the literature review performed on the basis of these cases the bleeding diathesis that is occasionally associated with paraproteinemia should be pointed out, irrespectively of the primary hematological condition. Thus, while investigating a patient with bleeding diathesis, at least a serum protein electrophoresis should be among the requested laboratory tests. Moreover, clinical vigilance is required in order to recognize other unusual manifestations of not so unusual hematological abnormalities.

Spontaneous Soft Tissue Haematomas- A Rare Presentation of Chronic Myeloid Leukemic (CML)

Spontaneous soft tissue haematomas are rarely found in haematological malignancies. Chronic myeloid leukemia (CML) is a myeloproliferative disorder which rarely present with thrombo-haemorrhagic phenomenon. It is a malignant clonal disorder of pleuripotent stem cells that results in increase in myeloid, erythroid and platelets cells in peripheral blood and marked myeloid hyperplasia in bone marrow. It is characterized by the presence of Philadelphia chromosome (Ph) with BCR - ABL 1 fusion gene. This gene is responsible for the formation of 210 KDa chimeric proteins with enhanced tyrosine kinase activity which leads to the abnormal bone marrow cell proliferation and to the clinical and morphologic manifestations of leukemia. Cutaneous and mucous membrane bleeding is common in CML whereas bleeding in deep soft tissue is rarely found because of qualitative and quantitative platelet abnormalities. Here, we report a case of CML (BCR-ABL rearrangement positive) who presented with large haematoma in the anterior as well as posterior compartment of left thigh and treated successfully with hydroxyurea and imatinib.

Thrombocytopenia in ESRD Patients: Epidemiology, Mechanisms and Interventional Nephrology Perspective

A well-functioning vascular access is essential for provision of life-sustaining dialysis treatment in patients with end-stage renal disease. Arteriovenous accesses are preferred form of vascular access. Although significant advances have been made in the field of dialysis access, arteriovenous access dysfunction remains the single most important cause of morbidity in ESRD patients. While thrombosis and stenosis of AV access are more frequently seen, hemorrhage from AV access can be life threatening with or without risk of permanent access loss. Aside from anticoagulation for comorbidities, qualitative and/or quantitative platelet abnormalities are often the predisposing factors. We describe an ESRD patient who developed new onset but severe thrombocytopenia due to metastatic small cell neuroendocrine carcinoma of lung. Given her persistent thrombocytopenia and presence of prolonged bleeding from the cannulation sites, a right internal jugular tunneled dialysis catheter was placed for continuation of maintenance dialysis. This review discusses the definition of thrombocytopenia, mechanisms of thrombocytopenia in patients with ESRD and with a special focus on implications of thrombocytopenia on dialysis access interventions. The review underscores the need for consensus with regard to cannulating AV access as well as guidelines specific to dialysis access-related endovascular intervention in the setting of thrombocytopenia and other coagulation abnormalities.

Polycythemia Vera and Acute Coronary Syndromes: Pathogenesis, Risk Factors and Treatment

Polycythemia vera is a chronic myeloproliferative disorder marked by significant thrombotic complications. Myocardial infarction and heart failure is the most common cause of death. Mechanisms involved in the pathogenesis of these complications are not yet well elucidate; erythrocytosis and quantitative platelet abnormalities may play a major role in the development of thrombosis and ischemia. Age older than 60 years and prior history of thrombosis are the two main risk factors. Evidence for the prevention and treatment of specific cardiovascular complications in PV is too scarce. However, current evidence supports the use of hydroxyurea as the initial choice of cytoreductive agent in PV patients with acute coronary syndrome.

Qualitative and quantitative platelet abnormalities in hepatitis C virus associated chronic liver disease

Qualitative and quantitative platelet abnormalities in hepatitis C virus associated chronic liver disease

Bilateral carotid artery thrombosis in a young man

Carotid artery thrombosis in young patients without evidence of premature atherosclerosis prompts investigation of unusual forms of carotid disease in addition to a workup for cardiac and arch vessel sources for emboli. Noninvasive imaging and conventional angiographic techniques play an important part in the diagnostic evaluation looking for potential vascular sources. Physicians should also be aware that, in addition, hypercoagulable conditions may predispose to carotid thrombosis. One such patient is presented with bilateral carotid thrombosis and stroke. The management of the problem is reviewed, as well as the investigation of potential hypercoagulable conditions, with a primary focus on qualitative and quantitative platelet abnormalities.

Quantitative and qualitative platelet abnormalities during pregnancy

In a 1-year period, 15 of 4048 pregnant women were found to have thrombocytopenia during their first prenatal visit. Their qualitative and quantitative platelet abnormalities were followed up prospectively for 1 to 6 months post partum. Platelet counts returned to normal in 14 of 15 patients 4 to 6 weeks post partum, von Willebrand factor antigen and ristocetin cofactor activity were low in three of 15 patients 4 to 6 weeks post partum, but had been normal during the antepartum period. Two of these three patients had prolonged bleeding times ante partum and post partum. All three patients subsequently were found to have mild type I von Willebrand disease. Six patients had detectable platelet antibodies. Neonatal thrombocytopenia was found in one term infant of a patient with mild thrombocytopenia and negative platelet antibodies. This study suggests that mild, transient, isolated thrombocytopenia can occur in an otherwise normal pregnancy and its incidence may be lower than previously reported. Extensive testing is not indicated unless there is an associated prolonged bleeding time. The possibility of von Willebrand disease or a qualitative platelet disorder should be considered.

Quantitative and qualitative platelet abnormalities during pregnancy

In a 1-year period, 15 of 4048 pregnant women were found to have thrombocytopenia during their first prenatal visit. Their qualitative and quantitative platelet abnormalities were followed up prospectively for 1 to 6 months post partum. Platelet counts returned to normal in 14 of 15 patients 4 to 6 weeks post partum. von Willebrand factor antigen and ristocetin cofactor activity were low in three of 15 patients 4 to 6 weeks post partum, but had been normal during the antepartum period. Two of these three patients had prolonged bleeding times ante partum and post partum. All three patients subsequently were found to have mild type I von Willebrand disease. Six patients had detectable platelet antibodies. Neonatal thrombocytopenia was found in one term infant of a patient with mild thrombocytopenia and negative platelet antibodies. This study suggests that mild, transient, isolated thrombocytopenia can occur in an otherwise normal pregnancy and its incidence may be lower than previously reported. Extensive testing is not indicated unless there is an associated prolonged bleeding time. The possibility of von Willebrand disease or a qualitative platelet disorder should be considered.

Hereditary and Acquired Thrombopathias

Normal platelet function is essential for hemostasis. The pathophysiologic processes that result in acquired quantitative platelet abnormalities are detailed. Platelet pathophysiology associated with acquired qualitative disorders, either drug-induced or secondary to disease, is discussed. Numerous hereditary platelet defects also exist. Their functional and biochemical features are presented.

Platelet volume and intraplatelet adenine nucleotides in various hematologic disorders.

By recent advanced techniques, blood platelets have proved to be varied in size and metabolism in various hematologic disorders. We examined platelet volume and intraplatelet adenine nucleotides in 36 patients with various hematologic disorders in order to clarify the quantitative platelet abnormalities. Platelet volumes were smaller in patients with acute leukemia and aplastic anemia, and larger in patients with immune thrombocytopenic purpura (ITP). The amount of intraplatelet ADP was decreased and ATP/ADP ratio was increased in acute leukemia, aplastic anemia and myeloproliferative disorders (MPD), which strongly suggested the presence of storage pool deficiency in these patients. Intraplatelet ADP per volume was decreased in acute leukemia, aplastic anemia and MPD, and ATP per volume was decreased in aplastic anemia. ATP content was increased in ITP in proportion to the increased platelet volume. These parameters were examined in 36 patients with the following hematologic disorders: 7 acute leukemia treated with cytotoxic chemotherapy, 5 aplastic anemia, 3 paroxysmal nocturnal hemoglobinuria (PNH), 9 immune thrombocytopenic purpura (ITP), 5 hypersplenism and 7 myeloproliferative disorders (MPD).

Platelet survival studies in man with diisopropylphosphorofluoridate (DF32P). Some observations in patients with hypocoagulability, 'hypercoagulability' and platelet disorders.

Diisopropylphosphorofluoridate (DF32P) acts as a cell label by combining irreversibly with esterases in the cell membrane. It was first used in man for tagging red cells (Cohen and Warringa, 1954) and later for platelets (Leeksma and Cohen, 1956) and leucocytes (Athens, Mauer, Ashenbrucker, Cartwright and Wintrobe, 1959). Since DF32P allows platelets to be labelled directly in vivo it has obvious advantages over the 51Cr method (Aas and Gardner, 1958) which necessitates removal of platelets from the body for labelling and subsequent re‐injection.The precise form of the normal platelet survival curve in man and the relative importance of intrinsic factors such as cell age, and extrinsic factors such as variations in the concentration of plasma coagulation factors, remains to be established. As part of an investigation into some of these factors, DF32P has been used in a small comparative study of platelet survival in some hypocoagulable and some ‘hypercoagulable’ states. During the course of this study the opportunity arose to apply the method to patients with qualitative and quantitative platelet abnormalities. These studies are presented and discussed in this paper.