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  1. Article ; Online: COVID-19 and VITT: same or different?

    Arepally, Gowthami M

    Blood

    2021  Volume 138, Issue 14, Page(s) 1206–1207

    MeSH term(s) COVID-19 ; Humans ; Purpura, Thrombocytopenic, Idiopathic ; SARS-CoV-2 ; Vaccination
    Language English
    Publishing date 2021-10-07
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2021013362
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Vaccine-induced immune thrombotic thrombocytopenia: what we know and do not know.

    Arepally, Gowthami M / Ortel, Thomas L

    Blood

    2021  Volume 138, Issue 4, Page(s) 293–298

    Abstract: The development of vaccines to fight COVID-19 has been a remarkable medical achievement. However, this global immunization effort has been complicated by a rare vaccine-related outcome characterized by thrombocytopenia and thrombosis in association with ... ...

    Abstract The development of vaccines to fight COVID-19 has been a remarkable medical achievement. However, this global immunization effort has been complicated by a rare vaccine-related outcome characterized by thrombocytopenia and thrombosis in association with platelet-activating anti-platelet factor 4 antibodies. In this Spotlight, we will discuss the recently described complication of vaccine-induced immune thrombotic thrombocytopenia (VITT) occurring in response to certain COVID-19 vaccines. Although information about this clinical condition is rapidly evolving, we will summarize our current understanding of VITT.
    MeSH term(s) Anticoagulants/adverse effects ; Anticoagulants/immunology ; COVID-19/immunology ; COVID-19/prevention & control ; COVID-19 Vaccines/adverse effects ; COVID-19 Vaccines/immunology ; COVID-19 Vaccines/therapeutic use ; Disease Management ; Heparin/adverse effects ; Heparin/immunology ; Humans ; Purpura, Thrombocytopenic, Idiopathic/etiology ; Purpura, Thrombocytopenic, Idiopathic/immunology ; Purpura, Thrombocytopenic, Idiopathic/therapy ; SARS-CoV-2/immunology
    Chemical Substances Anticoagulants ; COVID-19 Vaccines ; Heparin (9005-49-6)
    Language English
    Publishing date 2021-06-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2021012152
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Heparin-induced thrombocytopenia.

    Arepally, Gowthami M

    Blood

    2017  Volume 129, Issue 21, Page(s) 2864–2872

    Abstract: Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Pathogenic antibodies to PF4/heparin bind and activate cellular FcγRIIA on platelets and ... ...

    Abstract Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Pathogenic antibodies to PF4/heparin bind and activate cellular FcγRIIA on platelets and monocytes to propagate a hypercoagulable state culminating in life-threatening thrombosis. It is now recognized that anti-PF4/heparin antibodies develop commonly after heparin exposure, but only a subset of sensitized patients progress to life-threatening complications of thrombocytopenia and thrombosis. Recent scientific developments have clarified mechanisms underlying PF4/heparin immunogenicity, disease susceptibility, and clinical manifestations of disease. Insights from clinical and laboratory findings have also been recently harnessed for disease prevention. This review will summarize our current understanding of HIT by reviewing pathogenesis, essential clinical and laboratory features, and management.
    MeSH term(s) Autoantibodies/blood ; Autoantibodies/immunology ; Heparin/adverse effects ; Humans ; Platelet Factor 4/antagonists & inhibitors ; Platelet Factor 4/blood ; Platelet Factor 4/immunology ; Receptors, IgG/blood ; Receptors, IgG/immunology ; Thrombocytopenia/blood ; Thrombocytopenia/chemically induced ; Thrombocytopenia/immunology ; Thrombocytopenia/prevention & control ; Thrombosis/blood ; Thrombosis/etiology ; Thrombosis/immunology ; Thrombosis/prevention & control
    Chemical Substances Autoantibodies ; FCGR2A protein, human ; Receptors, IgG ; Platelet Factor 4 (37270-94-3) ; Heparin (9005-49-6)
    Language English
    Publishing date 2017-04-17
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2016-11-709873
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Pathogenesis of heparin-induced thrombocytopenia.

    Arepally, Gowthami M / Cines, Douglas B

    Translational research : the journal of laboratory and clinical medicine

    2020  Volume 225, Page(s) 131–140

    Abstract: There are currently no effective substitutes for high intensity therapy with unfractionated heparin (UFH) for cardiovascular procedures based on its rapid onset of action, ease of monitoring and reversibility. The continued use of UFH in these and other ... ...

    Abstract There are currently no effective substitutes for high intensity therapy with unfractionated heparin (UFH) for cardiovascular procedures based on its rapid onset of action, ease of monitoring and reversibility. The continued use of UFH in these and other settings requires vigilance for its most serious nonhemorrhagic complication, heparin induced thrombocytopenia (HIT). HIT is an immune prothrombotic disorder caused by antibodies that recognize complexes between platelet factor 4 (PF4) and polyanions such as heparin (H).The pathogenicity of anti-PF4/H antibodies is likely due to the formation of immune complexes that initiate intense procoagulant responses by vascular and hematopoietic cells that lead to the generation of platelet microparticles, monocyte and endothelial cell procoagulant activity, and neutrophil extracellular traps, among other outcomes. The development of anti-PF4/H antibodies after exposure to UFH greatly exceeds the incidence of clinical disease, but the biochemical features that distinguish pathogenic from nonpathogenic antibodies have not been identified. Diagnosis relies on pretest clinical probability, screening for anti-PF4/H antibodies and documentation of their platelet activating capacity. However, both clinical algorithms and test modalities have limited predictive values making diagnosis and management challenging. Given the unacceptable rates of recurrent thromboembolism and bleeding associated with current therapies, there is an unmet need for novel rational nonanticoagulant therapeutics based on the pathogenesis of HIT. We will review recent developments in our understanding of the pathogenesis of HIT and its implications for future approaches to diagnosis and management.
    MeSH term(s) Anticoagulants/therapeutic use ; Heparin/adverse effects ; Humans ; Thrombocytopenia/chemically induced ; Thrombocytopenia/drug therapy ; Thrombocytopenia/physiopathology
    Chemical Substances Anticoagulants ; Heparin (9005-49-6)
    Language English
    Publishing date 2020-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2246684-8
    ISSN 1878-1810 ; 1532-6543 ; 1931-5244
    ISSN (online) 1878-1810 ; 1532-6543
    ISSN 1931-5244
    DOI 10.1016/j.trsl.2020.04.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Heparin-Induced Thrombocytopenia: A Focus on Thrombosis.

    Arepally, Gowthami M / Padmanabhan, Anand

    Arteriosclerosis, thrombosis, and vascular biology

    2020  Volume 41, Issue 1, Page(s) 141–152

    Abstract: Heparin-induced thrombocytopenia is an immune-mediated disorder caused by antibodies that recognize complexes of platelet factor 4 and heparin. Thrombosis is a central and unpredictable feature of this syndrome. Despite optimal management, disease ... ...

    Abstract Heparin-induced thrombocytopenia is an immune-mediated disorder caused by antibodies that recognize complexes of platelet factor 4 and heparin. Thrombosis is a central and unpredictable feature of this syndrome. Despite optimal management, disease morbidity and mortality from thrombosis remain high. The hypercoagulable state in heparin-induced thrombocytopenia is biologically distinct from other thrombophilic disorders in that clinical complications are directly attributable to circulating ultra-large immune complexes. In some individuals, ultra-large immune complexes elicit unchecked cellular procoagulant responses that culminate in thrombosis. To date, the clinical and biologic risk factors associated with thrombotic risk in heparin-induced thrombocytopenia remain elusive. This review will summarize our current understanding of thrombosis in heparin-induced thrombocytopenia with attention to its clinical features, cellular mechanisms, and its management.
    MeSH term(s) Animals ; Antibodies/blood ; Anticoagulants/administration & dosage ; Anticoagulants/immunology ; Antithrombins/therapeutic use ; Blood Coagulation/drug effects ; Factor Xa Inhibitors/therapeutic use ; Heparin/adverse effects ; Heparin/immunology ; Humans ; Platelet Factor 4/immunology ; Risk Factors ; Thrombocytopenia/blood ; Thrombocytopenia/chemically induced ; Thrombocytopenia/drug therapy ; Thrombocytopenia/immunology ; Thrombosis/blood ; Thrombosis/chemically induced ; Thrombosis/drug therapy ; Thrombosis/immunology
    Chemical Substances Antibodies ; Anticoagulants ; Antithrombins ; Factor Xa Inhibitors ; PF4 protein, human ; Platelet Factor 4 (37270-94-3) ; Heparin (9005-49-6)
    Language English
    Publishing date 2020-12-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.120.315445
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Clot Imaging Using Photostable Nanodiamond.

    Francis, Samuel J / Torelli, Marco D / Nunn, Nicholas A / Arepally, Gowthami M / Shenderova, Olga A

    Nanomaterials (Basel, Switzerland)

    2023  Volume 13, Issue 6

    Abstract: While thrombosis is the leading cause of morbidity and mortality in the United States, an understanding of its triggers, progression, and response to anticoagulant therapy is lacking. Intravital fluorescence microscopy has advanced the study of thrombus ... ...

    Abstract While thrombosis is the leading cause of morbidity and mortality in the United States, an understanding of its triggers, progression, and response to anticoagulant therapy is lacking. Intravital fluorescence microscopy has advanced the study of thrombus formation by providing targeted, multi-color contrast. However, photodegradation of fluorophores limits the application in longitudinal studies (e.g., clot progression and/or dissolution). Fluorescent nanodiamond (FND) is a fluorophore which utilizes intrinsic fluorescence of chromogenic centers within and protected by the diamond crystalline lattice. Recent developments in diamond processing have allowed for the controlled production of nanodiamonds emitting in green or red. Here, the use of FND to label blood clots and/or clot lysis is demonstrated and compared to commonly used organic fluorophores. Model ex vivo clots were formed with incorporated labeled fibrinogen to allow imaging. FND was shown to match the morphology of organic fluorophore labels absent of photobleaching over time. The addition of tissue plasminogen activator (tPa) allowed visualization of the clot lysis stage, which is vital to studies of both DVT and pulmonary embolism resolution.
    Language English
    Publishing date 2023-03-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662255-5
    ISSN 2079-4991
    ISSN 2079-4991
    DOI 10.3390/nano13060961
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  7. Article ; Online: Bad weed: synthetic cannabinoid-associated coagulopathy.

    Arepally, Gowthami M / Ortel, Thomas L

    Blood

    2019  Volume 133, Issue 9, Page(s) 902–905

    Abstract: Recent multistate outbreaks of coagulopathy caused by brodifacoum-tainted synthetic cannabinoids or "fake weed" highlight the public health impact of long-acting anticoagulant rodenticides (LAARs). Patients presenting with this syndrome have had recent ... ...

    Abstract Recent multistate outbreaks of coagulopathy caused by brodifacoum-tainted synthetic cannabinoids or "fake weed" highlight the public health impact of long-acting anticoagulant rodenticides (LAARs). Patients presenting with this syndrome have had recent exposure to synthetic cannabinoids, evidence of isolated vitamin K antagonism with or without bleeding, and detectable levels of brodifacoum and other LAARs in circulation. This article will provide information on synthetic cannabinoids, LAARs, and coagulopathic manifestations arising from use of adulterated synthetic cannabinoids and their management.
    MeSH term(s) 4-Hydroxycoumarins/poisoning ; Anticoagulants/poisoning ; Blood Coagulation Disorders/chemically induced ; Blood Coagulation Disorders/drug therapy ; Blood Coagulation Disorders/pathology ; Cannabinoids/poisoning ; Disease Management ; Drug Contamination ; Humans
    Chemical Substances 4-Hydroxycoumarins ; Anticoagulants ; Cannabinoids ; bromfenacoum (A25P3CP5S7)
    Language English
    Publishing date 2019-01-17
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-11-876839
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Clot Imaging Using Photostable Nanodiamond

    Samuel J. Francis / Marco D. Torelli / Nicholas A. Nunn / Gowthami M. Arepally / Olga A. Shenderova

    Nanomaterials, Vol 13, Iss 961, p

    2023  Volume 961

    Abstract: While thrombosis is the leading cause of morbidity and mortality in the United States, an understanding of its triggers, progression, and response to anticoagulant therapy is lacking. Intravital fluorescence microscopy has advanced the study of thrombus ... ...

    Abstract While thrombosis is the leading cause of morbidity and mortality in the United States, an understanding of its triggers, progression, and response to anticoagulant therapy is lacking. Intravital fluorescence microscopy has advanced the study of thrombus formation by providing targeted, multi-color contrast. However, photodegradation of fluorophores limits the application in longitudinal studies (e.g., clot progression and/or dissolution). Fluorescent nanodiamond (FND) is a fluorophore which utilizes intrinsic fluorescence of chromogenic centers within and protected by the diamond crystalline lattice. Recent developments in diamond processing have allowed for the controlled production of nanodiamonds emitting in green or red. Here, the use of FND to label blood clots and/or clot lysis is demonstrated and compared to commonly used organic fluorophores. Model ex vivo clots were formed with incorporated labeled fibrinogen to allow imaging. FND was shown to match the morphology of organic fluorophore labels absent of photobleaching over time. The addition of tissue plasminogen activator (tPa) allowed visualization of the clot lysis stage, which is vital to studies of both DVT and pulmonary embolism resolution.
    Keywords nanodiamond ; nanoparticles ; fluorescence ; imaging ; microscopy ; thrombus ; Chemistry ; QD1-999
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: HIT and run: heparin's unusual immune response.

    Arepally, Gowthami M

    Blood

    2012  Volume 120, Issue 20, Page(s) 4119–4120

    MeSH term(s) Anticoagulants/adverse effects ; Antigens, Human Platelet/immunology ; Autoantibodies/immunology ; Autoantigens/immunology ; Heparin/adverse effects ; Humans ; Immunoglobulin G/immunology ; Platelet Factor 4/immunology ; Postoperative Complications/chemically induced ; Purpura, Thrombocytopenic, Idiopathic/chemically induced
    Chemical Substances Anticoagulants ; Antigens, Human Platelet ; Autoantibodies ; Autoantigens ; Immunoglobulin G ; Platelet Factor 4 (37270-94-3) ; Heparin (9005-49-6)
    Language English
    Publishing date 2012-11-14
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2012-09-455097
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Nothing typical about HIT.

    Arepally, Gowthami M

    Blood

    2009  Volume 113, Issue 20, Page(s) 4825–4826

    Language English
    Publishing date 2009-05-14
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2009-02-198549
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