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Case Studies In Hematology And Coagulation Pdf Viewer

In addition, interpretations that incorporate test results and patient clinical information are provided for a portion of our hemoglobinopathy, coagulation, platelet function, and inherited red blood cell disorder testing. Our goal is to maximize the usefulness of our test results while also providing important knowledge to our colleagues. The Special Hematology and Coagulation Laboratory participates in the education of medical technologists, medical students, residents, and fellows. As a part of our education and clinical mission, we provide seminars for the adult and pediatric hematology clinical services and also participate in case conferences for various specialties.

Case Studies In Hematology And Coagulation Pdf Viewer


About a third of patients with congenital hemophilia A develop inhibitory antibodies when treated with FVIII replacement, but such inhibitors arise very rarely in people without pre-existing hemophilia, at a reported incidence of 1.48 or 1.34 per million/year in two UK studies [9]. The age of presentation is bimodal; a significant portion of disease emerges in the postpartum setting, while most incidence of disease arises in patients over the age of 50. As with many diseases, age portends a worse prognosis. There is no apparent stronger predilection for men or women. This disorder occurs in the postpartum setting, in those with connective tissue disease, as a paraneoplastic syndrome, and after the use of certain medications such as penicillin, sulfamides, and phenytoin [12]. Rare, ambiguous associations have been reported following trauma or even minor surgical procedures. However, in about half of cases, no cause is identified.

At inhibitor titer levels >5 BU, replacement with recombinant factor VIII is generally ineffective. For severe bleeding in these patients, use of bypassing agents, which include activated prothrombin complex concentrate (aPCC; e.g., factor VIII inhibitor bypassing activity [FEIBA]) or recombinant human factor VIIa (rVIIa; e.g., NovoSeven), is recommended. Thus far, in the congenital hemophiliac population, studies have not conclusively shown whether rVIIa or aPCC is more effective than the other [18]. In the largest longitudinal, prospective, observational study to date for acquired hemophiliacs (from the European Acquired Hemophilia Registry, EACH2), both aPCC and rVIIa demonstrated similar efficacy in stopping bleeding (93.0%; P = 1) [2]. Certain patients may respond better to one or the other, and the decision to switch from one to the other is made on a case-by-case basis with close clinical monitoring. Often, multiple, sequential, alternating infusions of both bypassing agents are needed to control a bleeding episode.

Acquired factor VIII deficiency is a bleeding disorder that requires prompt diagnosis and management to avert severe, life-threatening bleeding and death. Despite knowledge of this disorder of coagulation for several decades, relatively little is still known about this disease because of its rare incidence. Its rarity poses challenges in our ability to recognize and diagnose this disease as well as to perform scientific trials to discover better therapies. However, progress has been made in understanding this disease, and, as more case reports accumulate, we will be able to enhance our understanding and refine our therapeutic strategies.

Although disseminated intravascular coagulation (DIC) is a critical disease [1,2,3], there is few gold standard interventions in neonatal medicine. Veldman et al. suggested that DIC in neonates is caused by prenatal risk factors, such as placental abruption (PA), pregnancy-induced hypertension (PIH), and neonatal factors such as sepsis, asphyxia and intravascular hemorrhage (IVH) [4]. Especially at birth, asphyxia was noteworthy in these cases. We previously reported that coagulation parameters, such as prothrombin time-international normalized ratio (PT-INR), activated prothrombin time (aPTT), and D-dimer are all affected by PA, birth asphyxia and IVH. Anticoagulant therapy, such as antithrombin administration and fresh frozen plasma (FFP), has been used to treat neonatal DIC. Since 2008, recombinant human soluble thrombomodulin (rTM) has emerged as a novel anticoagulant for DIC in Japan. Previous studies have reported rTM to be effective for DIC in both pediatric and adult patients [5, 6]. In adults, the efficacy of combined rTM and antithrombin therapy for sepsis-associated DIC has been reported [6]. However, there are few reports about the effects of rTM on premature infants. The Japan Society of Obstetrical, Gynecological & Neonatal Hematology (JSOGNH) recommends rTM administration for the treatment of DIC in neonates, and revised its diagnostic guidelines for neonatal DIC in 2016 [7]. We also reported gestational age (GA) and birth weight (BW) to be related to coagulation parameters [8]. Therefore, it is important to measure coagulation parameters in ill neonates with perinatal risk factors for DIC at birth and diagnose DIC in neonates. The aims of this study were to investigate the underlying conditions affecting DIC at birth and to assess the effectiveness of rTM and FFP therapy.

Using platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl3-induced thrombus formation in vivo, and thrombus formation under flow conditions ex vivo.

The COVID-19 pandemic has become a serious public health crisis worldwide since December 2019 [1]. COVID-19 has been linked to a number of critical cardiovascular complications [2, 3], and even individuals without a history of cardiovascular disease are at risk of cardiovascular complications [4]. Patients with severe COVID-19 commonly experience thrombotic disorders, sepsis, and disseminated intravascular coagulation (DIC), and these conditions have been closely linked to higher mortality rates [1, 5, 6]. Large-scale studies have revealed that 18.8% to 36.2% of patients [7, 8] present with thrombocytopenia on admission. In addition, the cumulative incidence of thrombotic complications for COVID-19 patients in the ICU was 31%, while only 1.3% of non-COVID-19 ICU patients experience thrombotic complications [9]. Although the evidence supports a link between COVID-19 and the development of a hypercoagulable state, the underlying mechanisms for this association remain elusive.

Emerging evidence has revealed a high composite incidence of thrombotic events in critically ill COVID-19 patients, including venous and arterial thrombotic events, and thrombocytopenia, all of which have been associated with increased mortality [62,63,64]. Anticoagulation is associated with a reduced risk of mortality without increased bleeding diathesis among patients hospitalized with COVID-19 [65]. However, the underlying mechanism of thrombus formation in COVID-19 is still unclear. We provide evidence that the platelets, key mediators of thrombosis, are hyperactivated in COVID-19 patients. Other recent studies have reported that various platelet activation events, including aggregation, adhesion, infiltration, and inflammatory response, contribute to lung injury and microvascular thrombosis in SARS-CoV-2-associated pneumonia [66,67,68]. These results, together with those from our study, draw attention to the role of platelet activation in the pathogenesis of COVID-19.

Recent studies reported that platelets are hyperactivated in COVID-19 patients [67, 75, 76]. The platelet activity biomarkers are associated with the coagulation dysfunction [67] and the composite outcome of thrombosis or death [75]. These studies emphasized the notion that cytokine storm may trigger hyperinflammation and hypercoagulability. Previous studies have found that fibrinogen level is higher in COVID-19 patients, which may bind and activate platelets to exacerbate thrombotic disorder in capillaries [77]. Our studies are consistent with the recent finding of platelet hyperactivity in COVID-19 patients. We further extend those finding and suggested a possibility that SARS-CoV-2 virus could directly activate platelets via the interaction of Spike protein and platelet ACE2. We cannot rule out the other possibility that virus-containing immune complex or virus-induced immune mediators may also contribute to platelet hyperactivity in COVID-19, which needs further investigation.

Mechanisms perpetuating cardiovascular sequelae in post-acute COVID-19 include direct viral invasion, downregulation of ACE2, inflammation and the immunologic response affecting the structural integrity of the myocardium, pericardium and conduction system. Autopsy studies in 39 cases of COVID-19 detected virus in the heart tissue of 62.5% of patients115. The subsequent inflammatory response may lead to cardiomyocyte death and fibro-fatty displacement of desmosomal proteins important for cell-to-cell adherence116,117.

This paper reports 2 cases of persistent bleeding after tooth extraction under local anesthesia which could not be completely stopped by routine treatments. Both of them denied prior illness and injury, allergies, anticoagulant medication history, systemic and family illness. The APTT and other coagulation screening tests of the two patients before surgery were normal. Finally, they were diagnosed with mild hemophilia A via coagulation factor assays. The patients acquired complete hemostasis by receiving coagulation factor supplement therapy in hematologic department.

Many studies have confirmed that these indicators cannot accurately intimate the coagulation function of patients due to some internal (patient's physical condition and some special coagulation diseases) or external (unregulated collection and processing of the sample) reasons [3, 4]. A patient with coagulation dysfunction might present "normal" laboratory examination results [3]. Similarly, an abnormal APTT result doesn't always indicate abnormal coagulation function because of internal or external influence.


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