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Seminars in Thrombosis and Hemostasis
Journal Prestige (SJR): 1.159  Citation Impact (citeScore): 3 Number of Followers: 46  Hybrid journal (It can contain Open Access articles)ISSN (Print) 0094-6176 - ISSN (Online) 1098-9064 Published by Thieme Publishing Group  [233 journals]
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- Recent Advances in Thrombosis and Hemostasis—Part VIII
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A 5 star rating indicates the linked pre-print has the exact same content as the published article.Semin Thromb Hemost 2022; 48: 405-406
DOI: 10.1055/s-0042-1748886
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
Artikel in Thieme eJournals:
Semin Thromb Hemost 2022; 48: 405-4062022-06-30T08:34:16+01:00
Inhaltsverzeichnis Volltext
Issue No: Vol. 48, No. 04 (2022)
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- Prophylaxis of Venous Thromboembolism in Children: A Systematic Review
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Authors: Pedersen; Lotte Hejberg, Villadsen, Gitte Bonde, Hellfritzsch, Maja, Hvas, Anne-Mette
Pages: 413 - 421
Abstract: Venous thromboembolism (VTE) in children is a rare but serious event. Current guidance on pharmacological thromboprophylaxis in children is mostly based on adult studies and expert opinions. The aim of this systematic review was to examine under which conditions children (age ≤ 18 years) would benefit from pharmacological thromboprophylaxis with low molecular weight heparin or unfractionated heparin. Eligible studies included children, who did not receive pharmacological thromboprophylaxis as comparator, and VTE events were radiologically verified. MEDLINE and Embase were searched up to October 3, 2021. Ten studies were included presenting data for 976 children receiving pharmacological thromboprophylaxis. We divided the studies into three categories based on the population studied: children in the intensive care unit (n = 2), children with fractures and/or undergoing surgery (n = 5), and children with systemic disease (n = 3). A lower incidence of VTE was found when pharmacological thromboprophylaxis was used compared with no prophylaxis in children in intensive care unit with central venous catheter and mechanical ventilation (7/27 vs. 13/24), children in the intensive care unit admitted after trauma with a very high risk of VTE based on several risk factors (0/21 vs. 13/96), and children with acute lymphoblastic leukemia treated with L-asparaginase concomitant with steroid and presence of central venous catheter (0/82 vs. 8/121). Pharmacological thromboprophylaxis was not associated with an increased bleeding risk. In conclusion, pharmacological thromboprophylaxis in children is sparsely investigated. Only children with several risk factors for VTE are likely to benefit from pharmacological thromboprophylaxis.
Citation: Semin Thromb Hemost 2022; 48: 413-421
PubDate: 2022-06-30T08:34:11+01:00
DOI: 10.1055/s-0042-1748151
Issue No: Vol. 48, No. 04 (2022)
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- Risk Factors for Major Adverse Cardiovascular Events and Major Adverse
Limb Events after Venous Thromboembolism: A Large Prospective Cohort Study
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Authors: Noumegni; Steve Raoul, Didier, Romain, Mansourati, Vincent, Moigne, Emmanuelle Le, Mao, Raphael Le, Hoffmann, Clément, Moreuil, Claire De, Tromeur, Cécile, Roux, Pierre-Yves Le, Nasr, Bahaa, Gentric, Jean-Christophe, Guegan, Marie, Poulhazan, Elise, Lacut, Karine, Bressollette, Luc, Couturaud, Francis
Pages: 465 - 480
Abstract: Background There is an increased risk of arterial events including major adverse cardiovascular events (MACE) and major adverse limb events (MALE) after venous thromboembolism (VTE). However, their risk factors remain little explored. Methods We aimed to determine the risk factors for MACE (acute coronary syndrome/stroke/cardiovascular death) and MALE (limb ischemia/critical limb ischemia/non-traumatic amputation/any limb revascularization) after VTE. Competing risk models (Fine-Gray) were used in a multicenter prospective cohort of 4,940 patients (mean age: 64.6 years and median follow-up: 64 months). Results MACE occurred in 17.3% of participants (2.35% per patient-years) and MALE in 1.7% (0.27% per patient-years). In multivariable analysis, the identified risk factors for MACE were the age of 50 to 65 years (vs. 65 years (vs.
Citation: Semin Thromb Hemost 2022; 48: 465-480
PubDate: 2022-06-30T08:34:24+01:00
DOI: 10.1055/s-0042-1748152
Issue No: Vol. 48, No. 04 (2022)
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- Cancer-Associated Thrombosis: Implications toward Health-Related Quality
of Life-
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A 5 star rating indicates the linked pre-print has the exact same content as the published article.Semin Thromb Hemost 2022; 48: 490-496
DOI: 10.1055/s-0042-1744365
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
Artikel in Thieme eJournals:
Semin Thromb Hemost 2022; 48: 490-4962022-06-30T08:34:22+01:00
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Issue No: Vol. 48, No. 04 (2022)
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- 2021 Eberhard F. Mammen Award Announcements: Part II—Young
Investigator Awards-
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A 5 star rating indicates the linked pre-print has the exact same content as the published article.Semin Thromb Hemost 2022; 48: 265-273
DOI: 10.1055/s-0042-1743175
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
Artikel in Thieme eJournals:
Semin Thromb Hemost 2022; 48: 265-2732022-04-12T00:00:00+01:00
Inhaltsverzeichnis Volltext
Issue No: Vol. 48, No. 03 (2022)
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- Hemostasis and Neuroscience—Hemostasis and Fibrinolysis Involved in
Brain Pathology and Brain Disorders-
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A 5 star rating indicates the linked pre-print has the exact same content as the published article.Semin Thromb Hemost 2022; 48: 274-276
DOI: 10.1055/s-0042-1742737
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
Artikel in Thieme eJournals:
Semin Thromb Hemost 2022; 48: 274-2762022-04-12T00:00:00+01:00
Inhaltsverzeichnis Volltext
Issue No: Vol. 48, No. 03 (2022)
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- Post-Pulmonary Embolism Syndrome and Functional Outcomes after Acute
Pulmonary Embolism-
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Authors: Luijten; Dieuwke, de Jong, Cindy M. M., Ninaber, Maarten K., Spruit, Martijn A., Huisman, Menno V., Klok, Frederikus A.
Abstract: Survivors of acute pulmonary embolism (PE) are at risk of developing persistent, sometimes disabling symptoms of dyspnea and/or functional limitations despite adequate anticoagulant treatment, fulfilling the criteria of the post-PE syndrome (PPES). PPES includes chronic thromboembolic pulmonary hypertension (CTEPH), chronic thromboembolic pulmonary disease, post-PE cardiac impairment (characterized as persistent right ventricle impairment after PE), and post-PE functional impairment. To improve the overall health outcomes of patients with acute PE, adequate measures to diagnose PPES and strategies to prevent and treat PPES are essential. Patient-reported outcome measures are very helpful to identify patients with persistent symptoms and functional impairment. The primary concern is to identify and adequately treat patients with CTEPH as early as possible. After CTEPH is ruled out, additional diagnostic tests including cardiopulmonary exercise tests, echocardiography, and imaging of the pulmonary vasculature may be helpful to rule out non-PE–related comorbidities and confirm the ultimate diagnosis. Most PPES patients will show signs of physical deconditioning as main explanation for their clinical presentation. Therefore, cardiopulmonary rehabilitation provides a good potential treatment option for this patient category, which warrants testing in adequately designed and executed randomized trials. In this review, we describe the definition and characteristics of PPES and its diagnosis and management.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-07-12T08:17:53+01:00
DOI: 10.1055/s-0042-1749659
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- Evaluating Performance of Contemporary and Historical von Willebrand
Factor (VWF) Assays in the Laboratory Identification of von Willebrand
Disease (VWD): The Australasian Experience-
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Authors: Favaloro; Emmanuel J., Dean, Elysse, Arunachalam, Sandya
Abstract: von Willebrand disease (VWD) is a common bleeding disorder that arises from deficiency and/or defects of von Willebrand factor (VWF). Appropriate diagnosis of VWD, including differential identification of qualitative (types 2A, 2B, 2M, 2N VWD) versus quantitative (types 1 and 3 VWD) defects remains problematic but has important management implications, given differential therapy. Complete assessment for VWD in a patient with a bleeding history requires comprehensive test panels, including VWF activity and antigen. We describe the Australasian experience, using data from the Royal College of Pathologists of Australasia (RCPA) Quality Assurance Program (QAP) related to VWF testing in their VWD test module. The RCPAQAP has been providing samples for VWF testing since 1998, representing 25 years of proficiency testing related to VWD diagnosis. A total of 109 samples have been dispatched to participants over these years, with current assessment involving dispatches of two samples (=4 samples) per year. Samples have represented all types of VWD, as well as normal or other samples, including acquired von Willebrand syndrome and plasma VWF concentrates as used in VWD therapy. Different VWF assays and activity/antigen ratios show different utility in VWD and type identification. In the past 9 years of data capture, a total of 166 errors were identified from a total of 1,839 interpretations, representing a base error rate of 9.0%. Identification errors were highest for type 2 VWD samples (15.3%), intermediate for type 1 VWD samples (7.5%), and lowest for normal samples (2.4%). Errors can be linked to assay limitations, including assay variability and low-level VWF detection limits, as well as laboratory issues (including test result misinterpretation, which accounts for approximately 40% of all errors for type 2 VWD). For test-associated errors, VWF:RCo and VWF:GPIbM were associated with the highest variability and error rate, which was up to 10x higher than that using VWF:CB. As a test group, chemiluminescence-based procedures were associated with lowest inter-laboratory variability, best low-level VWF detection (down to
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-07-08T14:49:58+01:00
DOI: 10.1055/s-0042-1753528
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- D-dimers—“Normal” Levels versus Elevated Levels Due to a Range of
Conditions, Including “D-dimeritis,” Inflammation, Thromboembolism,
Disseminated Intravascular Coagulation, and COVID-19-
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Authors: Thachil; Jecko, Favaloro, Emmanuel J., Lippi, Giuseppe
Abstract: D-dimers reflect a breakdown product of fibrin. The current narrative review outlines how D-dimers can arise in normal individuals, as well as in patients suffering from a wide range of disease states. D-dimers in normal individuals without evident thrombosis can arise from background fibrinolytic activity in various tissues, including kidney, mammary and salivary glands, which ensures smooth flow of arising fluids where any blood contamination could be immediately lysed. In addition, healthy individuals can also regularly sustain minor injuries, often unbeknown to them, and wound healing follows clot formation in these situations. D-dimers can also arise in anxiety and following exercise, and are also markers of inflammation. Lung inflammation (triggered by microbes or foreign particles) is perhaps also particularly relevant, since the hemostasis system and fibrinolysis help to trap and remove such debris. Lung inflammation in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may contribute to D-dimer levels additive to thrombosis in patients with COVID-19 (coronavirus disease 2019). Indeed, severe COVID-19 can lead to multiple activation events, including inflammation, primary and secondary hemostasis, and fibrinolysis, all of which may contribute to cumulative D-dimer development. Finally, D-dimer testing has also found a role in the diagnosis and triaging of the so-called (COVID-19) vaccine-induced thrombotic thrombocytopenia.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-07-08T14:47:32+01:00
DOI: 10.1055/s-0042-1748193
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- A Review of Autoimmune Acquired von Willebrand Factor Deficiency in Japan
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Authors: Ichinose; Akitada, Osaki, Tsukasa, Souri, Masayoshi, Favaloro, Emmanuel J.
Abstract: von Willebrand factor (VWF) forms high-molecular-weight multimers and plays an essential role in hemostasis, and thus its deficiency leads to bleeding symptoms. Acquired von Willebrand syndrome (AVWS) is rare, but potentially underdiagnosed, and develops in various underlying disorders. AVWS caused by anti-VWF autoantibodies is a rare subcategory of AVWS that can also be referred to as autoimmune VWF deficiency (AiVWFD). We performed a search of patients with autoimmune coagulation factor deficiencies in our nationwide survey in Japan. Among these, suspected cases of AiVWFD were extremely few, with only 11 case consultations in the last 10 years. Of these, three and five were respectively positive for anti-VWF autoantibodies (anti-VWF-Ab) and VWF inhibitor (VWF-inh). We also performed an extensive literature search of other cases from Japan, and in total, 40 cases were finally identified to have AiVWFD, with mean age of 55.0 years. Most underlying disorders were lympho- or myeloproliferative diseases, followed by autoimmune diseases. The major bleeding sites were subcutaneous and mucosal, the bleeding severity was moderate, and there were no hemorrhagic deaths. Bleeding time was prolonged; factor VIII activity, VWF antigen, and VWF activity were decreased, and high-molecular-weight VWF multimers were absent or decreased. These are similar to the common abnormal laboratory findings observed among general AVWS cases. Hemostatic therapy often involved VWF concentrates and vasopressin, and antibody eradication therapy often included corticosteroids and achieved remission. Notably, of all cases, 68% had anti-VWF-Abs, and 83% of anti-VWF-Ab-positive patients were also VWF-inh positive. To accumulate precise clinical information on AiVWFD, it is necessary to verify and improve the measurement methods for both anti-VWF-Ab and anti-VWF-inh. These findings from Japan should be confirmed in other geographic localities.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-07-08T13:54:44+01:00
DOI: 10.1055/s-0042-1749088
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- Arterial Thrombotic Events in Hospitalized COVID-19 Patients: A Short
Review and Meta-Analysis-
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Authors: Candeloro; Matteo, Schulman, Sam
Abstract: It is well established that the risk of venous thromboembolism is high in coronavirus disease 19 (COVID-19). The frequency of arterial thromboembolic events (ATEs) in hospitalized patients with COVID-19 is unclear, as is the magnitude of these events in comparison with other infections. We searched MEDLINE from February 2020 to February 2022 for prospective or retrospective cohort studies and randomized clinical trials that reported the number of acute myocardial infarction (AMI), acute ischemic stroke (AIS), acute limb ischemia (ALI), or other ATE as defined by the original authors in hospitalized patients with COVID-19. The pooled frequencies were calculated through meta-analysis using random effects model with logit transformation and presented with relative 95% prediction intervals (95% PI). We retrieved a total of 4,547 studies, 36 of which (28 retrospective cohorts, five prospective cohorts and three randomized trials) were finally included in our analysis. The resulting cohort counted 100,949 patients, 2,641 (2.6%) of whom experienced ATE. The pooled ATE frequency was 2.0% (95% PI, 0.4–9.6%). The pooled ATE frequency for AMI, AIS, ALI, and other ATE was 0.8% (95% PI, 0.1–8.1%), 0.9% (95% PI, 0.3–2.9%), 0.2% (95% PI, 0.0–4.2%), and 0.5% (95% PI, 0.1–3.0%), respectively. In comparison with the ATE incidence reported in three studies on non-COVID viral pneumonia, we did not detect a significant difference from the results in our analysis. In conclusion, we found a non-negligible proportion of ATE in patients hospitalized for COVID-19. Our results are similar to those found in hospitalized patients with influenza or with non-COVID viral pneumonia.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-07-06T10:37:22+01:00
DOI: 10.1055/s-0042-1749661
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- Thrombotic Thrombocytopenic Purpura: From 1972 to 2022 and Beyond
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Authors: George; James N.
Abstract: This review tells the story of my personal experience with thrombotic thrombocytopenic purpura (TTP). It begins with my first encounter with TTP 50 years ago when 2 sisters presented 2 years apart, both pregnant and both died. At that time, I knew nothing about hereditary TTP (hTTP), the risks of pregnancy, or effective treatments. In 1991, a year after I moved to Oklahoma, therapeutic plasma exchange (TPE) was established as an effective treatment. With the availability of effective treatment, the number of patients presenting with suspected TTP soared. The diagnosis of TTP was imprecise. I worked with the Oklahoma Blood Institute (OBI) to understand the management of TTP. Because the OBI provided all TPE procedures for most of Oklahoma, we saw all consecutive patients within a defined geographic area who were identified at a uniform time early in the course of their TTP, without selection or referral bias. It was an inception cohort; this became the Oklahoma TTP Registry. In 2001, we began a very successful collaboration with the University of Bern, Switzerland, to measure ADAMTS13 activity in all of our patients. From our patients, we learned that acquired, autoimmune TTP (iTTP) is a chronic disease with risks for cognitive impairment and depression. Recognition in 2012 of three sisters with hTTP was reminiscent of the beginning of my story. hTTP has risks for multiple severe morbidities, beginning at birth and especially during pregnancy. Future management of both iTTP and hTTP will be more effective and more convenient.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-07-06T10:34:23+01:00
DOI: 10.1055/s-0042-1749589
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- Right Ventricular Recovery: Early and Late Changes after Acute PE
Diagnosis-
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Authors: Bejjani; Antoine, Khairani, Candrika D., Piazza, Gregory
Abstract: Right ventricular (RV) failure is a critical cause of morbidity and mortality in patients presenting with pulmonary embolism (PE). The presentation of RV failure is based on the combination of clinical findings, laboratory abnormalities, and imaging evidence. An improved understanding of the pathophysiology of RV dysfunction following PE has given rise to more accurate risk stratification and broader therapeutic approaches. A subset of patients with PE develop chronic RV dysfunction with or without pulmonary hypertension. In this review, we focus on the impact of PE on the RV and its implications for risk stratification, prognosis, acute management, and long-term therapy.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-07-01T05:46:20+01:00
DOI: 10.1055/s-0042-1750025
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- Acquired Thrombotic Thrombocytopenic Purpura: A Rare Coincidence after
COVID-19 mRNA Vaccine'-
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DOI: 10.1055/s-0042-1744301
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
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Semin Thromb Hemost ; : -2022-06-27T07:35:53+01:00
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- Platelet Activation and Thrombosis in COVID-19
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Authors: Iba; Toshiaki, Wada, Hideo, Levy, Jerrold H.
Abstract: Although thrombosis frequently occurs in infectious diseases, the coagulopathy associated with COVID-19 has unique characteristics. Compared with bacterial sepsis, COVID-19-associated coagulopathy presents with minimal changes in platelet counts, normal prothrombin times, and increased D-dimer and fibrinogen levels. These differences can be explained by the distinct pathophysiology of the thromboinflammatory responses. In sepsis-induced coagulopathy, leukocytes are primarily responsible for the coagulopathy by expressing tissue factor, releasing neutrophil extracellular traps, multiple procoagulant substances, and systemic endothelial injury that is often associated with vasoplegia and shock. In COVID-19-associated coagulopathy, platelet activation is a major driver of inflammation/thrombogenesis and von Willebrand factor and platelet factor 4 are deeply involved in the pathogenesis. Although the initial responses are localized to the lung, they can spread systemically if the disease is severe. Since the platelets play major roles, arterial thrombosis is not uncommon in COVID-19. Despite platelet activation, platelet count is usually normal at presentation, but sensitive biomarkers including von Willebrand factor activity, soluble P-selectin, and soluble C-type lectin-like receptor-2 are elevated, and they increase as the disease progresses. Although the role of antiplatelet therapy is still unproven, current studies are ongoing to determine its potential effects.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-06-23T09:40:15+01:00
DOI: 10.1055/s-0042-1749441
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- Proposal for a Simple Algorithmic Approach to Manage Drug–Drug
Interactions of Oral Anticoagulants with Nirmatrelvir/Ritonavir in
COVID-19 Outpatients-
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DOI: 10.1055/s-0042-1750024
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
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Semin Thromb Hemost ; : -2022-06-23T09:37:54+01:00
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- Heparin: The Journey from Parenteral Agent to Nasal Delivery
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Authors: Carpenè; Giovanni, Negrini, Davide, Lippi, Giuseppe, Favaloro, Emmanuel J., Montagnana, Martina
Abstract: Although the worldwide usage of direct oral anticoagulants has continuously increased over the past decade, heparin remains an important weapon in the current arsenal of anticoagulant drugs. Parenteral heparin administration (i.e., either intravenously or subcutaneously) has represented for decades the only possible route for generating a significant anticoagulant effect, although being notoriously associated with some important drawbacks such as discomfort and risk of low compliance, thus paving the way to searching for more amenable means of administration. We provide here an updated analysis of animal and human studies that have explored the feasibility, suitability, and efficiency of heparin administration through the unconventional nasal route, as a possible alternative to the more traditional parenteral injection. The major hurdles that contribute to impair intranasal absorption and systemic delivery of heparin are represented by its relatively high molecular weight and negative charge. Therefore, although pure drug administration would not be associated with efficient nasal adsorption, or by systemic biological activity (i.e., anticoagulant effect), the combination of low molecular weight heparins and absorption enhancers such as surfactants, mucoadhesive, cyclodextrins, polyethylenimines and encapsulation into (nano)carriers seems effective to at least partially improve drug transport through the nasal route and allow systemic delivery in animals. Besides generating anticoagulant effects, intranasal heparin administration can also produce local pleiotropic effects, mostly related to anti-inflammatory properties, such as attenuating airway allergic inflammation or inhibiting the binding of the spike protein of some coronaviruses (including severe acute respiratory syndrome coronavirus 2) to their host cell receptors. This preliminary evidence represents a valuable premise for planning future studies in humans aimed at establishing the pharmacokinetics and biological activity of locally and systemically delivered intranasal heparin formulations.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-06-22T11:37:36+01:00
DOI: 10.1055/s-0042-1749395
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- Molecular Mimicry between hPF4 and SARS-CoV-2 Spike Protein: Response to
Comment-
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DOI: 10.1055/s-0042-1744280
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
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Semin Thromb Hemost ; : -2022-06-21T07:55:24+01:00
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- Antiphospholipid Syndrome in Patients with Venous Thromboembolism
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Authors: Pengo; Vittorio, Denas, Gentian
Abstract: Unprovoked (or provoked by mild risk factors) venous thromboembolism (VTE) in young patients, VTE in uncommon sites, or cases of unexplained VTE recurrence may be positive for antiphospholipid antibodies (aPL) and thus may be diagnosed with antiphospholipid syndrome (APS). The evaluation of aPL is standardized using immunological tests for anticardiolipin and anti-β2-glycoprotein I. The determination of functional antibodies (lupus anticoagulant) is less standardized, especially in patients on anticoagulant treatment. Patients positive for all the three tests are at high risk of recurrence, which, in turn, might lead to chronic obstruction of pulmonary vessels (chronic thromboembolic pulmonary hypertension). Randomized clinical trials have shown that triple-positive patients should be treated with vitamin K antagonists maintaining an international normalized ratio between 2 and 3. Whether patients with VTE and incomplete aPL profile can be treated with direct oral anticoagulants should be further investigated.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-06-21T07:52:53+01:00
DOI: 10.1055/s-0042-1749590
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- 2022 Eberhard F. Mammen Award Announcements: Part I—Most Popular
Articles-
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DOI: 10.1055/s-0042-1748192
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
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Semin Thromb Hemost ; : -2022-06-14T14:04:19+01:00
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- Solid Phase Assays for Antiphospholipid Antibodies
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Authors: Devreese; Katrien M.J.
Abstract: The diagnosis of antiphospholipid syndrome (APS) relies on the detection of circulating antiphospholipid antibodies (aPL). Currently, lupus anticoagulant (LA), anticardiolipin (aCL), and anti-β2-glycoprotein I antibodies (aβ2GPI) IgG or IgM are the laboratory criteria if persistently present over time. As aCL and aβ2GPI are two out of the three laboratory criteria, the detection of aPL by solid phase assays is an essential step in the diagnosis of APS. Advancement has been made to resolve some of the methodological challenges of aCL and aβ2GPI assays by providing guidelines how to measure aPL, as well as to gain a better understanding of their diagnostic role. However, solid phase assays for aCL and aβ2GPI still show substantive inter-assay differences, resulting in disagreement concerning positive/negative results, but also differences in titer of antibodies. This hampers the semiquantitative classification into low-medium-high positivity. The non-criteria aPL, such as antibodies against the domain one of β2GPI and anti-phosphatidylserine/prothrombin antibodies (aPS/PT) have roles in confirming the risk in APS, and can be useful, especially in patients with incomplete antibody profiles.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-06-08T08:18:46+01:00
DOI: 10.1055/s-0042-1744364
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- Testing for Lupus Anticoagulants
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Authors: Moore; Gary W.
Abstract: Lupus anticoagulant (LA) is one of the three criteria antiphospholipid antibodies (aPLs) employed in classification, and by default diagnosis, of antiphospholipid syndrome (APS). Detection of LA is not via calibrated assays but is based on functional behavior of the antibodies in a medley of coagulation assays. A prolonged clotting time in a screening test is followed by demonstration of phospholipid dependence and inhibitory properties in confirmatory and mixing tests, respectively, which are modifications of the parent screening test. Complications arise because no single screening test is sensitive to every LA, and no test is specific for LA, because they are prone to interference by other causes of elevated clotting times. Several screening tests are available but the pairing of dilute Russell's viper venom time (dRVVT) with LA-sensitive activated partial thromboplastin time (aPTT) is widely used and recommended because it is proven to have good detection rates. Nonetheless, judicious use of other assays can improve diagnostic performance, such as dilute prothrombin time to find LA unreactive with dRVVT and aPTT, and the recently validated Taipan snake venom time with ecarin time confirmatory test that are unaffected by vitamin K antagonist and direct factor Xa inhibitor anticoagulation. Expert body guidelines and their updates have improved harmonization of laboratory practices, although some issues continue to attract debate, such as the place of mixing tests in the medley hierarchy, and areas of data manipulation such as assay cut-offs and ratio generation. This article reviews current practices and challenges in the laboratory detection of LA.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-06-01T09:24:52+01:00
DOI: 10.1055/s-0042-1744363
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- Tranexamic Acid and Its Potential Anti-Inflammatory Effect: A Systematic
Review-
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Authors: Okholm; Søren Hauge, Krog, Jan, Hvas, Anne-Mette
Abstract: Tranexamic acid (TXA) is an antifibrinolytic drug primarily used for reducing blood loss in patients with major bleedings. Animal and cell studies have shown that TXA might modulate the inflammatory response by either enhancing or inhibiting cytokine levels. Furthermore, recent human studies have found altered inflammatory biomarkers in patients receiving TXA when compared with patients who did not receive TXA. In this systematic review we investigated the effect of TXA on inflammatory biomarkers in different patient groups. A systematic literature search was conducted on the databases PubMed and Embase to identify all original articles that investigated inflammatory biomarkers in patients receiving TXA and compared them to a relevant control group. The review was performed according to the PRISMA guidelines, and the literature search was performed on November 29, 2021. Thirty-three studies were included, among which 14 studies compared patients receiving TXA with patients getting no medication, another 14 studies investigated different dosing regimens of TXA, and finally five studies examined the administration form of TXA. The present review suggests that TXA has an anti-inflammatory effect in patients undergoing orthopaedic surgery illustrated by decreased levels of C-reactive protein and interleukin-6 in patients receiving TXA compared with patients receiving no or lower doses of TXA. However, the anti-inflammatory effect was not found in patients undergoing cardiac surgery, pediatric craniosynostosis patients, or in rheumatoid arthritis patients. The inflammatory response was not affected by administration form of TXA (oral, intravenous, or topical). In conclusion, an anti-inflammatory effect of TXA was consistently found among orthopaedic patients only.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-05-30T00:00:00+01:00
DOI: 10.1055/s-0042-1742741
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- To Anticoagulate or Not to Anticoagulate in COVID-19: Lessons after 2
Years-
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Authors: Rizk; John G., Gupta, Aashish, Lazo, Jose G., Sardar, Partha, Henry, Brandon Michael, Lavie, Carl J., Effron, Mark B.
Abstract: A hypercoagulable state associated with coronavirus disease 2019 (COVID-19) has been well documented and is believed to be strongly supported by a proinflammatory state. The hypercoagulable state in turn results in increased incidence of arterial and venous thromboembolism (VTE) seen in hospitalized COVID-19 when compared with hospitalized non-COVID-19 patient cohorts. Moreover, patients with arterial or VTE and COVID-19 have higher mortality compared with COVID-19 patients without arterial or VTE. Prevention of arterial or VTE thus remains an essential question in the management of COVID-19 patients, especially because of high rates of reported microvascular and macrovascular thrombosis. This has prompted multiple randomized control trials (RCTs) evaluating different anticoagulation strategies in COVID-19 patients at various stages of the disease. Herein, we review findings from RCTs in the past 2 years of antithrombotic therapy in critically ill hospitalized patients, noncritically ill hospitalized patients, patients postdischarge from the hospital, and outpatients. RCTs in critically ill patients demonstrated therapeutic dose anticoagulation does not improve outcomes and has more bleeding than prophylaxis dose anticoagulant in these patients. Trials in noncritically ill hospitalized patients showed a therapeutic dose anticoagulation with a heparin formulation might improve clinical outcomes. Anticoagulation with a direct oral anticoagulant posthospital discharge may improve outcomes, although there is a large RCT in progress. Nonhospitalized COVID-19 patients have an insufficient burden of events to be candidates for antithrombotic therapy. Anticoagulation in pregnant and lactating patients with COVID-19, as well as antiplatelet therapy for COVID-19, is also reviewed.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-04-25T00:00:00+01:00
DOI: 10.1055/s-0042-1744302
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- Molecular Mimicry between hPF4 and SARS-CoV-2 Spike Protein: Comment
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DOI: 10.1055/s-0042-1744279
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Semin Thromb Hemost ; : -2022-04-21T00:00:00+01:00
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- Aspirin use Reduces Platelet Hyperreactivity and Degranulation in COVID-19
Patients-
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DOI: 10.1055/s-0042-1744281
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Semin Thromb Hemost ; : -2022-03-07T00:00:00+0100
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- Systemic Antiangiogenic Therapies for Bleeding in Hereditary Hemorrhagic
Telangiectasia: A Practical, Evidence-Based Guide for Clinicians-
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Authors: Al-Samkari; Hanny
Abstract: Management of bleeding in hereditary hemorrhagic telangiectasia (HHT), the second most common hereditary bleeding disorder in the world, is currently undergoing a paradigm shift. Disease-modifying antiangiogenic therapies capable of achieving durable hemostasis via inducing telangiectasia regression have emerged as a highly effective and safe modality to treat epistaxis and gastrointestinal bleeding in HHT. While evidence to date is incomplete and additional studies are ongoing, patients presently in need are being treated with antiangiogenic agents off-label. Intravenous bevacizumab, oral pazopanib, and oral thalidomide are the three targeted primary angiogenesis inhibitors, with multiple studies describing both reassuring safety and impressive effectiveness in the treatment of moderate-to-severe HHT-associated bleeding. However, at present there is a paucity of guidance in the literature, including the published HHT guidelines, addressing the practical aspects of antiangiogenic therapy for HHT in clinical practice. This review article and practical evidence-based guide aims to fill this unaddressed need, synthesizing published data on the use of antiangiogenic agents in HHT, relevant data for their use outside of HHT, and expert guidance where evidence is lacking. After a brief review of principles of bleeding therapy in HHT, guidance on hematologic support with iron and blood products, and alternatives to antiangiogenic therapy, this article examines each of the aforementioned antiangiogenic agents in detail, including patient selection, initiation, monitoring, toxicity management, and discontinuation. With proper, educated use of antiangiogenic therapies in HHT, patients with even the most severe bleeding manifestations can achieve durable hemostasis with minimal side-effects, dramatically improving health-related quality of life and potentially altering the disease course.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-02-28T00:00:00+0100
DOI: 10.1055/s-0042-1743467
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- Flow Cytometric Assessment of Changes in Platelet Reactivity after Acute
Coronary Syndrome: A Systematic Review-
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Authors: Pedersen; Oliver Buchhave, Pasalic, Leonardo, Nissen, Peter H., Grove, Erik Lerkevang, Kristensen, Steen Dalby, Hvas, Anne-Mette
Abstract: Increased platelet activity is an important predictor for recurrent cardiovascular events in patients with acute coronary syndromes (ACS). Flow cytometry is an advanced method for evaluation of platelet activity. We aimed to summarize the current literature on dynamic changes in platelet activity analyzed by flow cytometry in patients with ACS. Employing the guidelines of Preferred Report Items for Systematic Reviews and Meta-Analyses (PRISMA), we searched PubMed and Embase on October 26, 2021, and identified studies measuring platelet activity with flow cytometry in ACS patients in the acute phase (baseline) and at follow-up in a more stable phase. In the 12 included studies, fibrinogen receptor, α-granule secretion, platelet reactivity index, monocyte-platelet aggregates, neutrophil-platelet aggregates, and reticulated platelets were measured. The fibrinogen receptor and α-granule secretion were either unchanged or lower during follow-up measurements than in the acute phase. Platelet reactivity index showed inconsistent results. Values of monocyte-platelet aggregates and neutrophil-platelet aggregates were lower at follow-up than at baseline (p-values 0.64) or lower at 1 to 2 months follow-up (p-value 0.04), and also lower at 5 months to 1-year follow-up (p-value>0.005) compared with baseline. Overall, flow cytometric analyses of platelet function in ACS patients showed that platelet activity was lower at follow-up than at baseline. However, in some patients, platelet activity remained unchanged from baseline to follow-up, possibly indicating a sustained high platelet activity that may increase the risk of recurrent cardiovascular events.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-02-28T00:00:00+0100
DOI: 10.1055/s-0042-1742742
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- The Benefits of Heparin Use in COVID-19: Pleiotropic Antiviral Activity
beyond Anticoagulant and Anti-Inflammatory Properties-
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DOI: 10.1055/s-0042-1742740
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Semin Thromb Hemost ; : -2022-02-14T00:00:00+0100
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- Trousseau's Syndrome in 19th Century Qing Dynasty Paintings of Breast
Tumors: Early Insights into Cancer and Thrombosis Risk-
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DOI: 10.1055/s-0042-1742437
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Semin Thromb Hemost ; : -2022-02-09T00:00:00+0100
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- Response to “Parathyroid Adenoma in a Young Girl with Type 3 von
Willebrand Disease”-
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DOI: 10.1055/s-0042-1742436
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
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Semin Thromb Hemost ; : -2022-02-09T00:00:00+0100
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- Effects of Inflammation on Hemostasis in Acutely Ill Patients with Liver
Disease-
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Authors: Driever; Ellen G., Lisman, Ton
Abstract: Patients with liver diseases are in a rebalanced state of hemostasis, due to simultaneous decline in pro- and anticoagulant factors. This balance seems to remain even in the sickest patients, but is less stable and might destabilize when patients develop disease complications. Patients with acute decompensation of cirrhosis, acute-on-chronic liver failure, or acute liver failure often develop complications associated with changes in the hemostatic system, such as systemic inflammation. Systemic inflammation causes hemostatic alterations by adhesion and aggregation of platelets, release of von Willebrand factor (VWF), enhanced expression of tissue factor, inhibition of natural anticoagulant pathways, and inhibition of fibrinolysis. Laboratory tests of hemostasis in acutely-ill liver patients may indicate a hypocoagulable state (decreased platelet count, prolongations in prothrombin time and activated partial thromboplastin time, decreased fibrinogen levels) due to decreased synthetic liver capacity or consumption, or a hypercoagulable state (increased VWF levels, hypofibrinolysis in global tests). Whether these changes are clinically relevant and should be corrected with antithrombotic drugs or blood products is incompletely understood. Inflammation and activation of coagulation may cause local ischemia, progression of liver disease, and multiorgan failure. Anti-inflammatory treatment in acutely-ill liver patients may be of potential interest to prevent thrombotic or bleeding complications and halt progression of liver disease.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-02-08T00:00:00+0100
DOI: 10.1055/s-0042-1742438
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- Parathyroid Adenoma in a Young Girl with Type 3 von Willebrand Disease:
Comment on “Cancers in Patients with von Willebrand Disease”-
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DOI: 10.1055/s-0042-1742435
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
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Semin Thromb Hemost ; : -2022-02-02T00:00:00+0100
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- Mutations Accounting for Congenital Fibrinogen Disorders: An Update
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Authors: Richard; Maxime, Celeny, David, Neerman-Arbez, Marguerite
Abstract: Fibrinogen is a complex protein that plays a key role in the blood clotting process. It is a hexamer composed of two copies of three distinct chains: Aα, Bβ, and γ encoded by three genes, FGA, FGB, and FGG, clustered on the long arm of chromosome 4. Congenital fibrinogen disorders (CFDs) are divided into qualitative deficiencies (dysfibrinogenemia, hypodysfibrinogenemia) in which the mutant fibrinogen molecule is present in the circulation and quantitative deficiencies (afibrinogenemia, hypofibrinogenemia) with no mutant molecule present in the bloodstream. Phenotypic manifestations are variable, patients may be asymptomatic, or suffer from bleeding or thrombosis. Causative mutations can occur in any of the three fibrinogen genes and can affect one or both alleles. Given the large number of studies reporting on novel causative mutations for CFDs since the review on the same topic published in 2016, we performed an extensive search of the literature and list here 120 additional mutations described in both quantitative and qualitative disorders. The visualization of causative single nucleotide variations placed on the coding sequences of FGA, FGB, and FGG reveals important structure function insight for several domains of the fibrinogen molecule.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-01-24T00:00:00+0100
DOI: 10.1055/s-0041-1742170
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- Is Molecular Mimicry between hPF4 and SARS-CoV-2 Spike Protein a Potential
Basis for Autoimmune Responses in Vaccinated and Naturally Infected
Patients'-
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DOI: 10.1055/s-0041-1742092
Thieme Medical Publishers, Inc. 333 Seventh Avenue, 18th Floor, New York, NY 10001, USA
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Semin Thromb Hemost ; : -2022-01-12T00:00:00+0100
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- The Role of Plasminogen Activator Inhibitor Type 1 (PAI-1) in
Placenta-Mediated Pregnancy Complications: A Systematic Review-
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Authors: Agersnap; Ida, Nissen, Peter H., Hvas, Anne-Mette
Abstract: Plasminogen activator inhibitor type 1 (PAI-1) is a main inhibitor of fibrinolysis. The PAI-1 gene (SERPINE1) harbors genetic variants with the potential of modifying plasma levels of PAI-1. A delicate balance exists between the coagulation and fibrinolytic system, and changes in PAI-1 have been suggested to compromise establishment of a successful pregnancy. Therefore, this systematic review investigated the association between genetic variants and/or plasma levels of PAI-1 and placenta-mediated pregnancy complications. An extensive literature search was conducted in PubMed, Embase, and Web of Science on the 29th of April 2021. All studies underwent quality rating according to The Study Quality Assessment Tools checklist provided by National Heart, Lung and Blood Institute. A total of 71 studies were included, among which 60 studies investigated PAI-1 genotypes and 11 studies measured PAI-1 plasma levels. In 32 out of 59 studies, no association was found between the PAI-1 4G/5G polymorphism (rs1799768) and placenta-mediated pregnancy complications, which was stated as no significant difference in the genotype distribution comparing women with and without placenta-mediated pregnancy complications or no significantly increased odds of placenta-mediated pregnancy complications carrying the 4G/4G or 4G/5G genotype. Eight out of 11 studies reported significantly higher PAI-1 plasma levels in preeclamptic women than in women without preeclampsia. In conclusion, no clear evidence indicates that PAI-1 polymorphisms are associated with placenta-mediated pregnancy complications, and the possible association between high PAI-1 plasma levels and preeclampsia needs further investigations. Thus, investigation of PAI-1 genotypes and PAI-1 plasma levels does not currently seem to have a place in daily clinical practice managing placenta-mediated pregnancy complications.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-01-12T00:00:00+0100
DOI: 10.1055/s-0041-1742082
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- What We Know (and Do not Know) Regarding the Pathogenesis of Pulmonary
Thrombosis in COVID-19-
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Authors: Lippi; Giuseppe, Favaloro, Emmanuel J.
Abstract: The clinical course of coronavirus disease 2019 (COVID-19) is often complicated by the onset of venous thrombosis and thromboembolism (VTE), encompassing also pulmonary thrombosis. Recent statistics attests that the cumulative frequency of VTE can be as high as 30% in COVID-19 hospitalized patients, increasing to nearly 40 to 70% (depending on systematic screening) in those with severe illness, mechanical ventilation, or intensive care unit admission. The risk of venous thrombosis seems mostly limited to the active phase of disease, and is directly associated with some genetic (i.e., inherited prothrombotic predisposition) and demographical factors (male sex, overweight/obesity), disease severity (risk increasing progressively from hospitalization to development of severe illness, being the highest in patients needing mechanical ventilation and/or intensive care), presence and extent of pulmonary disease, coexistence of multiple risk factors (immobilization, mechanical ventilation, co- or superinfections), along with increased values of inflammatory and thrombotic biomarkers. At least three different phenotypes of pulmonary thrombosis may develop in COVID-19 patients, one caused by typical embolization from peripheral venous thrombosis (e.g., deep vein thrombosis), a second type triggered by local inflammation of nearby pulmonary tissue, and a third one mostly attributable to the prothrombotic state consequent to the pronounced systemic inflammatory response (i.e., the so-called cytokine storm) that is frequently observed in COVID-19. Although the pathogenesis of these three conditions has different features, their discrimination is essential for diagnostic and therapeutic purposes. The prognosis of COVID-19 patients who develop pulmonary thrombosis is also considerably worse than those who do not, thus probably needing frequent monitoring and more aggressive therapeutic management.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-01-12T00:00:00+0100
DOI: 10.1055/s-0041-1742091
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- Interaction between Antiphospholipid Antibodies and Protein C
Anticoagulant Pathway: A Narrative Review-
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Authors: Pengo; Vittorio
Abstract: Thrombotic antiphospholipid syndrome (APS) is a condition in which thrombosis in venous, arterial, and/or small vessels is ascribed to the presence of antiphospholipid antibodies (aPL). Among the various proposed pathogenic theories to explain thrombotic APS, those involving the interaction between aPL and the protein C system have gained much consensus. Indeed, robust data show an acquired activated protein C resistance (APC-R) in these patients. The role of aPL in this impairment is clear, but the mechanism of action is uncertain, as the type of aPL and to what extent aPL are involved remains a gray area. Lupus anticoagulant (LA) is often associated with APC-R, but antibodies generating LA comprise those directed to β2-glycoprotein I and antiphosphatidylserine/prothrombin. Moreover, the induction of APC-R by aPL requires the presence of phospholipids and is suppressed by the presence of an excess of phospholipids. How phospholipids exposed on the cell membranes work in the system in vivo is unknown. Interestingly, acquired APC-R due to aPL might explain the clinical phenotypes of thrombotic APS. Indeed, the literature reports cases of both venous and arterial thromboembolism as well as skin necrosis, the latter observed in the severe form of protein C deficiency and in catastrophic APS.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-01-12T00:00:00+0100
DOI: 10.1055/s-0041-1742083
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- Gastrointestinal Bleeding in Congenital Bleeding Disorders
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Authors: Samii; Amir, Norouzi, Mahshaad, Ahmadi, Abbas, Dorgalaleh, Akbar
Abstract: Gastrointestinal bleeding (GIB) is serious, intractable, and potentially life-threatening condition. There is considerable heterogeneity in GIB phenotypes among congenital bleeding disorders (CBDs), making GIB difficult to manage. Although GIB is rarely encountered in CBDs, its severity in some patients makes the need for a comprehensive and precise assessment of underlying factors and management approaches imperative. Initial evaluation of GIB begins with assessment of hematological status; GIB should be ruled out in patients with chronic anemia, and in presentations that include hematemesis, hematochezia, or melena. High-risk patients with recurrent GIB require urgent interventions such as replacement therapy for treatment of coagulation factor deficiency (CFD). However, the best management strategy for CFD-related bleeding remains controversial. While several investigations have identified CBDs as potential risk factors for GIB, research has focused on assessing the risks for individual factor deficiencies and other CBDs. This review highlights recent findings on the prevalence, management strategies, and alternative therapies of GIB related to CFDs, and platelet disorders.
Citation: Semin Thromb Hemost ; : -
PubDate: 2022-01-12T00:00:00+0100
DOI: 10.1055/s-0041-1741571
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