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Article ; Online: Reply.

Shi, Hui / Knight, Jason S / Kanthi, Yogendra

Arthritis & rheumatology (Hoboken, N.J.)

2022 Volume 74, Issue 9, Page(s) 1603–1604

Language	English
Publishing date	2022-07-21
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.42141
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Zs.A 24: Show issues

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Article ; Online: Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome.

Knight, Jason S / Kanthi, Yogendra

Seminars in immunopathology

2022 Volume 44, Issue 3, Page(s) 347–362

Abstract: Antiphospholipid syndrome (APS) is an autoimmune thrombophilia propelled by circulating antiphospholipid antibodies that herald vascular thrombosis and obstetrical complications. Antiphospholipid antibodies recognize phospholipids and phospholipid- ... ...

Abstract	Antiphospholipid syndrome (APS) is an autoimmune thrombophilia propelled by circulating antiphospholipid antibodies that herald vascular thrombosis and obstetrical complications. Antiphospholipid antibodies recognize phospholipids and phospholipid-binding proteins and are not only markers of disease but also key drivers of APS pathophysiology. Thrombotic events in APS can be attributed to various conspirators including activated endothelial cells, platelets, and myeloid-lineage cells, as well as derangements in coagulation and fibrinolytic systems. Furthermore, recent work has especially highlighted the role of neutrophil extracellular traps (NETs) and the complement system in APS thrombosis. Beyond acute thrombosis, patients with APS can also develop an occlusive vasculopathy, a long-term consequence of APS characterized by cell proliferation and infiltration that progressively expands the intima and leads to organ damage. This review will highlight known pathogenic factors in APS and will also briefly discuss similarities between APS and the thrombophilic coagulopathy of COVID-19.
MeSH term(s)	Antibodies, Antiphospholipid ; Antiphospholipid Syndrome/complications ; Antiphospholipid Syndrome/diagnosis ; COVID-19/complications ; Endothelial Cells ; Humans ; Thromboinflammation ; Thrombosis/complications ; Vascular Diseases
Chemical Substances	Antibodies, Antiphospholipid
Language	English
Publishing date	2022-02-04
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-022-00916-w
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Zs.A 1425: Show issues

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Article ; Online: VITT(al) insights into vaccine-related clots.

Strich, Jeffrey R / Kanthi, Yogendra

Blood

2021 Volume 138, Issue 22, Page(s) 2159–2160

MeSH term(s)	Humans ; Platelet Factor 4 ; Thrombosis/etiology ; Vaccines/adverse effects
Chemical Substances	Vaccines ; Platelet Factor 4 (37270-94-3)
Language	English
Publishing date	2021-12-02
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.2021014195
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Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 364: Show issues

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Article ; Online: Shining a Light on Venous Thromboembolism.

Kanthi, Yogendra / Sharma, Aditya

JACC. Basic to translational science

2020 Volume 5, Issue 4, Page(s) 357–359

Language	English
Publishing date	2020-04-27
Publishing country	United States
Document type	Editorial
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2020.03.004
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Article ; Online: COVID-19-associated coagulopathy: An exploration of mechanisms.

Colling, Meaghan E / Kanthi, Yogendra

Vascular medicine (London, England)

2020 Volume 25, Issue 5, Page(s) 471–478

Abstract: An ongoing global pandemic of viral pneumonia (coronavirus disease [COVID-19]), due to the virus SARS-CoV-2, has infected millions of people and remains a threat to many more. Most critically ill patients have respiratory failure and there is an ... ...

Abstract	An ongoing global pandemic of viral pneumonia (coronavirus disease [COVID-19]), due to the virus SARS-CoV-2, has infected millions of people and remains a threat to many more. Most critically ill patients have respiratory failure and there is an international effort to understand mechanisms and predictors of disease severity. Coagulopathy, characterized by elevations in D-dimer and fibrin(ogen) degradation products (FDPs), is associated with critical illness and mortality in patients with COVID-19. Furthermore, increasing reports of microvascular and macrovascular thrombi suggest that hemostatic imbalances may contribute to the pathophysiology of SARS-CoV-2 infection. We review the laboratory and clinical findings of patients with COVID-19-associated coagulopathy, and prior studies of hemostasis in other viral infections and acute respiratory distress syndrome. We hypothesize that an imbalance between coagulation and inflammation may result in a hypercoagulable state. Although thrombosis initiated by the innate immune system is hypothesized to limit SARS-CoV-2 dissemination, aberrant activation of this system can cause endothelial injury resulting in loss of thromboprotective mechanisms, excess thrombin generation, and dysregulation of fibrinolysis and thrombosis. The role various components including neutrophils, neutrophil extracellular traps, activated platelets, microparticles, clotting factors, inflammatory cytokines, and complement play in this process remains an area of active investigation and ongoing clinical trials target these different pathways in COVID-19.
MeSH term(s)	Betacoronavirus ; Blood Coagulation Disorders/diagnosis ; Blood Coagulation Disorders/therapy ; Blood Coagulation Disorders/virology ; COVID-19 ; Coronavirus Infections/complications ; Coronavirus Infections/pathology ; Coronavirus Infections/therapy ; Humans ; Pandemics ; Pneumonia, Viral/complications ; Pneumonia, Viral/pathology ; Pneumonia, Viral/therapy ; SARS-CoV-2
Keywords	covid19
Language	English
Publishing date	2020-06-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1311628-9
ISSN	1477-0377 ; 1358-863X
ISSN (online)	1477-0377
ISSN	1358-863X
DOI	10.1177/1358863X20932640
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Zs.A 4409: Show issues

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Article ; Online: Inflammation, Infection and Venous Thromboembolism.

Colling, Meaghan E / Tourdot, Benjamin E / Kanthi, Yogendra

Circulation research

2021 Volume 128, Issue 12, Page(s) 2017–2036

Abstract: The association between inflammation, infection, and venous thrombosis has long been recognized; yet, only in the last decades have we begun to understand the mechanisms through which the immune and coagulation systems interact and reciprocally regulate ... ...

Abstract	The association between inflammation, infection, and venous thrombosis has long been recognized; yet, only in the last decades have we begun to understand the mechanisms through which the immune and coagulation systems interact and reciprocally regulate one another. These interconnected networks mount an effective response to injury and pathogen invasion, but if unregulated can result in pathological thrombosis and organ damage. Neutrophils, monocytes, and platelets interact with each other and the endothelium in host defense and also play critical roles in the formation of venous thromboembolism. This knowledge has advanced our understanding of both human physiology and pathophysiology, as well as identified mechanisms of anticoagulant resistance and novel therapeutic targets for the prevention and treatment of thrombosis. In this review, we discuss the contributions of inflammation and infection to venous thromboembolism.
MeSH term(s)	Adaptive Immunity ; Blood Coagulation/physiology ; Blood Platelets/physiology ; Endothelium, Vascular/physiology ; Extracellular Traps ; Extracellular Vesicles/physiology ; Fibrinolysis ; Hematopoiesis ; Hemostasis/physiology ; Humans ; Immune System/physiology ; Infections/complications ; Inflammation/complications ; Leukocytes/physiology ; Monocytes/physiology ; Neutrophils/physiology ; Venous Thromboembolism/etiology ; Venous Thromboembolism/prevention & control ; Venous Thromboembolism/therapy
Language	English
Publishing date	2021-06-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.318225
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Ui IV Zs.70: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Ui IV Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Thrombotic manifestations of VEXAS syndrome.

Groarke, Emma M / Dulau-Florea, Alina E / Kanthi, Yogendra

Seminars in hematology

2021 Volume 58, Issue 4, Page(s) 230–238

Abstract: VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a recently described autoinflammatory syndrome characterized by diffuse inflammatory manifestations, predisposition to hematological malignancy, and an association with a high ... ...

Abstract	VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a recently described autoinflammatory syndrome characterized by diffuse inflammatory manifestations, predisposition to hematological malignancy, and an association with a high rate of thrombosis. VEXAS is attributed to somatic mutations in the UBA1 gene in hematopoietic stem and progenitor cells with myeloid restriction in mature forms. The rate of thrombosis in VEXAS patients is approximately 40% in all reported cases to date. Venous thromboembolism predominates thrombotic events in VEXAS. These are classified as unprovoked in etiology, although systemic and vascular inflammation are implicated. Here, we review the clinical and laboratory characteristics in VEXAS that provide insight into the possible mechanisms leading to thrombosis. We present knowledge gaps in the mechanisms and management of VEXAS-associated thromboinflammation and propose areas for future investigation in the field.
MeSH term(s)	Antiphospholipid Syndrome ; Humans ; Inflammation/complications ; Inflammation/genetics ; Mutation ; Syndrome ; Thrombosis/genetics ; Ubiquitin-Activating Enzymes/genetics
Chemical Substances	Ubiquitin-Activating Enzymes (EC 6.2.1.45)
Language	English
Publishing date	2021-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	206923-4
ISSN	1532-8686 ; 0037-1963
ISSN (online)	1532-8686
ISSN	0037-1963
DOI	10.1053/j.seminhematol.2021.10.006
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Zs.A 328: Show issues

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Article ; Online: At a crossroads: coronavirus disease 2019 recovery and the risk of pulmonary vascular disease.

Cascino, Thomas M / Desai, Ankit A / Kanthi, Yogendra

Current opinion in pulmonary medicine

2021 Volume 27, Issue 5, Page(s) 342–349

Abstract: Purpose of review: The coronavirus disease 2019 (COVID-19) pandemic has led to almost 3,000,000 deaths across 139 million people infected worldwide. Involvement of the pulmonary vasculature is considered a major driving force for morbidity and mortality. ...

Abstract	Purpose of review: The coronavirus disease 2019 (COVID-19) pandemic has led to almost 3,000,000 deaths across 139 million people infected worldwide. Involvement of the pulmonary vasculature is considered a major driving force for morbidity and mortality. We set out to summarize current knowledge on the acute manifestations of pulmonary vascular disease (PVD) resulting from COVID-19 and prioritize long-term complications that may result in pulmonary hypertension (PH). Recent findings: Acute COVID-19 infection can result in widespread involvement of the pulmonary vasculature, myocardial injury, evidence of persistent lung disease, and venous thromboembolism. Post COVID-19 survivors frequently report ongoing symptoms and may be at risk for the spectrum of PH, including group 1 pulmonary arterial hypertension, group 2 PH due to left heart disease, group 3 PH due to lung disease and/or hypoxia, and group 4 chronic thromboembolic PH. Summary: The impact of COVID-19 on the pulmonary vasculature is central to determining disease severity. Although the long-term PVD manifestations of COVID-19 are currently uncertain, optimizing the care of risk factors for PH and monitoring for the development of PVD will be critical to reducing long-term morbidity and improving the health of survivors.
MeSH term(s)	COVID-19 ; Humans ; Lung Diseases ; Pandemics ; Pulmonary Circulation ; SARS-CoV-2 ; Vascular Diseases
Language	English
Publishing date	2021-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1285505-4
ISSN	1531-6971 ; 1070-5287 ; 1078-1641
ISSN (online)	1531-6971
ISSN	1070-5287 ; 1078-1641
DOI	10.1097/MCP.0000000000000792
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Article ; Online: Great Debates in Vascular Medicine: Extended duration anticoagulation for unprovoked venous thromboembolism - Coming to consensus when the debate rages on.

Kanthi, Yogendra / Piazza, Gregory

Vascular medicine (London, England)

2018 Volume 23, Issue 4, Page(s) 384–387

MeSH term(s)	Adult ; Anticoagulants/administration & dosage ; Anticoagulants/adverse effects ; Attitude of Health Personnel ; Blood Coagulation/drug effects ; Consensus ; Drug Administration Schedule ; Female ; Health Knowledge, Attitudes, Practice ; Hemorrhage/chemically induced ; Humans ; Patient Preference ; Recurrence ; Risk Factors ; Time Factors ; Treatment Outcome ; Venous Thromboembolism/blood ; Venous Thromboembolism/diagnostic imaging ; Venous Thromboembolism/drug therapy
Chemical Substances	Anticoagulants
Language	English
Publishing date	2018-05-08
Publishing country	England
Document type	Case Reports ; Editorial
ZDB-ID	1311628-9
ISSN	1477-0377 ; 1358-863X
ISSN (online)	1477-0377
ISSN	1358-863X
DOI	10.1177/1358863X18770529
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Article ; Online: Inflammasome Signaling, Thromboinflammation, and Venous Thromboembolism.

Potere, Nicola / Abbate, Antonio / Kanthi, Yogendra / Carrier, Marc / Toldo, Stefano / Porreca, Ettore / Di Nisio, Marcello

JACC. Basic to translational science

2023 Volume 8, Issue 9, Page(s) 1245–1261

Abstract: Venous thromboembolism (VTE) remains a major health burden despite anticoagulation advances, suggesting incomplete management of pathogenic mechanisms. The NLRP3 (NACHT-, LRR- and pyrin domain-containing protein 3) inflammasome, interleukin (IL)-1, and ... ...

Abstract	Venous thromboembolism (VTE) remains a major health burden despite anticoagulation advances, suggesting incomplete management of pathogenic mechanisms. The NLRP3 (NACHT-, LRR- and pyrin domain-containing protein 3) inflammasome, interleukin (IL)-1, and pyroptosis are emerging contributors to the inflammatory pathogenesis of VTE. Inflammasome pathway activation occurs in patients with VTE. In preclinical models, inflammasome signaling blockade reduces venous thrombogenesis and vascular injury, suggesting that this therapeutic approach may potentially maximize anticoagulation benefits, protecting from VTE occurrence, recurrence, and ensuing post-thrombotic syndrome. The nonselective NLRP3 inhibitor colchicine and the anti-IL-1β agent canakinumab reduce atherothrombosis without increasing bleeding. Rosuvastatin reduces primary venous thrombotic events at least in part through lipid-lowering independent mechanisms, paving the way to targeted anti-inflammatory strategies in VTE. This review outlines recent preclinical and clinical evidence supporting a role for inflammasome pathway activation in venous thrombosis, and discusses the, yet unexplored, therapeutic potential of modulating inflammasome signaling to prevent and manage VTE.
Language	English
Publishing date	2023-06-07
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2023.03.017
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