Thrombosis Associated with Viral Hepatitis

Galli, Luca; Gerdes, Victor E. A.; Guasti, Luigina; Squizzato, Alessandro

doi:10.14218/jcth.2014.00031

Cited by 29 publications

(28 citation statements)

References 74 publications

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“…Keeping all of the above in mind, the combination of CMV viremia and CMV hepatitis likely contributed to the procoagulant state, leading to PVT. [ 29 , 32 ] These features likely also contributed to the prolonged debilitating fatigue prodrome, which was a unique feature in this case, as it suggested a prolonged failure to clear the virus, despite the patient's immunocompetent status. Although our patient did not require antiviral therapy, further study into the possible benefits of such therapy in cases with immunocompetent patients is warranted.…”

Section: Discussionmentioning

confidence: 91%

Venous thromboembolism related to cytomegalovirus infection

et al. 2017

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Rationale:Herein, we present a case of seemingly unprovoked portal vein thrombosis (PVT) occurring in the context of an acute cytomegalovirus (CMV) infection and prolonged debilitating fatigue.Patient concerns:A 46-year-old male airline pilot presented with a 2 week history of abdominal pain, nausea, vomiting, watery diarrhea, and daily recurrent fevers. This was in the context of progressive, debilitating fatigue for 3 months forcing the patient to leave his job.Diagnoses:Computed tomography of the abdomen revealed PVT, which was managed initially by heparin infusion. Cefepime was ordered for broad-spectrum antibiotic management of sepsis and possible septic thrombosis. Further workup exposed elevated transaminases consistent with mild hepatitis without synthetic dysfunction and colonoscopy revealed colitis. A comprehensive evaluation for liver disease was notable for a markedly elevated ferritin level. Spiking fevers and neutrophilia persisted for several days despite empiric antimicrobial treatment, but eventually resolved. The remainder of the workup was negative except for positive CMV IgM titer and viral load. This raised suspicion for a hypercoagulable state caused by CMV hepatitis with CMV-induced PVT. Heparin was transitioned to warfarin at the time of discharge.Interventions:Given the patient's immunocompetent state and resolution of fevers, antiviral therapy for CMV infection was not initiated.Outcomes:The patient continued to improve with a normalization of the serum ferritin level and anticoagulation therapy was stopped after 6 months.Lessons:There is mounting support for infectious causes of venous thromboembolism (VTE) based on existing molecular biology and clinical research. Meta-analysis of existing data showed that between 1.9% and 9.1% of patients hospitalized with VTE had concurrent acute CMV infection. Theoretical mechanisms for this association include transient formation of antiphospholipid antibodies, transient formation of antibodies targeting CMV capsule phospholipids with procoagulant properties, and direct infection of the endothelial cells. We hope this case will serve as a reminder to consider CMV as a transient cause of PVT and VTE, particularly in light of 2016 guidelines for unprovoked VTE recommending lifelong anticoagulation. We also plan to prospectively study the association of unprovoked VTE and acute CMV infection in our own hospital system.

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Section: Discussionmentioning

confidence: 91%

Venous thromboembolism related to cytomegalovirus infection

et al. 2017

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“…These findings agreed well with previous studies, which demonstrated that viral hepatitis might promote the development of venous thromboembolism. 22 , 23 The imbalance between procoagulant and anticoagulant factors associated with chronic liver disease might have clinical implications. 22 Moreover, RVO described in chronic hepatitis C was usually attributed to the treatment with interferon.…”

Section: Discussionmentioning

confidence: 99%

“… 22 , 23 The imbalance between procoagulant and anticoagulant factors associated with chronic liver disease might have clinical implications. 22 Moreover, RVO described in chronic hepatitis C was usually attributed to the treatment with interferon. 24 It seemed probable that a combination of active hepatitis C virus infection in a genetically susceptible individual receiving interferon accounted for the RVO.…”

Section: Discussionmentioning

confidence: 99%

Systemic abnormalities associated with retinal vein occlusion in young patients

Sinawat

Bunyavee

Ratanapakorn

et al. 2017

OPTH

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ObjectivesTo study the systemic abnormalities associated with retinal vein occlusion in patients aged ≤50 years with a particular emphasis on atherosclerotic diseases and thrombophilic disorders.MethodsMedical charts of patients, aged ≤50 years whose diagnoses were retinal vein occlusions during the period 1995–2015 were retrospectively reviewed. The primary outcome was the number of systemic abnormalities associated with these patients. Secondary outcomes included types of retinal vein occlusion and sites of occlusion.ResultsAtherosclerotic diseases were the most common systemic abnormalities associated with retinal vein occlusion and accounted for 55.1% of the patients in the study. Hypertension in 27.55%, diabetes mellitus in 16.33%, and 5.1% with dyslipidemia were noted. The number of thrombophilic disorders seemed to be less than expected and were noted in only 5.1%. Other systemic abnormalities included viral hepatitis infection, systemic lupus erythematosus, and acquired immunodeficiency syndrome. Oral contraceptives were used by some patients.ConclusionAtherosclerotic diseases remained the most commonly associated systemic diseases in the majority of these patients. Approach to these patients should include a screening for hypertension, diabetes mellitus, and lipid abnormalities. Thrombophilia should also be considered where no obvious atherosclerotic diseases are found or if the patient is <40 years old, a history of thrombosis or a family history of thrombosis is possible.

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“…Viral infections, such as hepatitis B are often associated with vasculitis and subsequently thromboembolic complications 7, 8, 34 . We therefore used immunoprecipitates isolated from a patient with ongoing hepatitis B infection and associated systemic vasculitis, to stimulate primary endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Double-stranded DNA induces a prothrombotic phenotype in the vascular endothelium

Gaitzsch

Czermak

Ribeiro

et al. 2017

Sci Rep

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Double-stranded DNA (dsDNA) constitutes a potent activator of innate immunity, given its ability to bind intracellular pattern recognition receptors during viral infections or sterile tissue damage. While effects of dsDNA in immune cells have been extensively studied, dsDNA signalling and its pathophysiological implications in non-immune cells, such as the vascular endothelium, remain poorly understood. The aim of this study was to characterize prothrombotic effects of dsDNA in vascular endothelial cells. Transfection of cultured human endothelial cells with the synthetic dsDNA poly(dA:dT) induced upregulation of the prothrombotic molecules tissue factor and PAI-1, resulting in accelerated blood clotting in vitro, which was partly dependent on RIG-I signalling. Prothrombotic effects were also observed upon transfection of endothelial cells with hepatitis B virus DNA-containing immunoprecipitates as well human genomic DNA. In addition, dsDNA led to surface expression of von Willebrand factor resulting in increased platelet-endothelium-interactions under flow. Eventually, intrascrotal injection of dsDNA resulted in accelerated thrombus formation upon light/dye-induced endothelial injury in mouse cremaster arterioles and venules in vivo. In conclusion, we show that viral or endogenous dsDNA induces a prothrombotic phenotype in the vascular endothelium. These findings represent a novel link between pathogen- and danger-associated patterns within innate immunity and thrombosis.

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Thrombosis Associated with Viral Hepatitis

Cited by 29 publications

References 74 publications

Venous thromboembolism related to cytomegalovirus infection

Venous thromboembolism related to cytomegalovirus infection

Systemic abnormalities associated with retinal vein occlusion in young patients

Double-stranded DNA induces a prothrombotic phenotype in the vascular endothelium

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