Incidence of Cytomegalovirus-associated thrombosis and its risk factors: A case-control study

Atzmony, Lihi; Halutz, Ora; Avidor, Boaz; Finn, Talya; Zimmerman, Ofer; Steinvil, Arie; Zeltser, David; Giladi, Michael; Justo, Dan

doi:10.1016/j.thromres.2010.09.006

Cited by 64 publications

(51 citation statements)

References 9 publications

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“…According to the findings from Atzmony et al, the incidence of thrombosis in a study enrolling 140 patients with acute HCMV infection and 140 consecutive matched patients in whom acute infection had been excluded (control group) was 6.4% [83]. Moreover, acute HCMV infection in this study population was associated with thrombosis independent of other risk factors for thrombosis [83].…”

Section: Hcmv In Thrombosismentioning

confidence: 58%

“…There were also several reports on acute HCMV infection and splenic infarcts in immunocompetent patients [82]. In addition, in an immunocompetent female patient with acute HCMV infection an association with concomitant thrombosis was reported, a syndrome that had previously only been recognized in immunocompromised patients [83]. Similarly, the case of a previously healthy adult with cytomegalovirus infection was complicated by tibiopopliteal deep venous thrombosis and associated with a Factor V Leiden heterozygous mutation [84].…”

Section: Hcmv In Thrombosismentioning

confidence: 97%

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Human cytomegalovirus infection and atherothrombosis

Popović

Smiljanić

Dobutović

et al. 2011

J Thromb Thrombolysis

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Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to intima-media thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the intima of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.

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Section: Hcmv In Thrombosismentioning

confidence: 58%

Section: Hcmv In Thrombosismentioning

confidence: 97%

Human cytomegalovirus infection and atherothrombosis

Popović

Smiljanić

Dobutović

et al. 2011

J Thromb Thrombolysis

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“…A growing bulk of reports link acute CMV infection to thrombotic events [Justo et al, 2011]. The incidence of thrombosis among patients with acute CMV infection as well as the incidence of acute CMV infection among patients with thrombotic events is not low [Atzmony et al, 2010;Tichelaar et al, 2011]. Venous thromboembolism and splanchnic vein thrombosis are the most common thromboses associated with acute CMV infection.…”

Section: Discussionmentioning

confidence: 99%

Transient ischemic attack associated with acute cytomegalovirus infection

Amit

Gadoth

Giladi

et al. 2012

Journal of Medical Virology

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Acute cytomegalovirus (CMV) infection is associated with thromboembolism. However, cerebrovascular ischemic events have not been reported in relation to acute CMV infection. A patient with a transient ischemic attack and acute CMV infection is described. Transient appearance of anti-phospholipid antibodies suggests a causal relationship between the two. Physicians should be alert to symptoms and signs of acute CMV infection in patients with idiopathic cerebrovascular ischemic events.

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“…Binary logistic regression analysis showed that acute CMV infection was independently associated with thrombosis in the whole cohort (p ¼ 0.004), and the use of OCs/hormones or pregnancy were independently associated with thrombosis among patients with acute infection (p ¼ 0.043). 11 In another case-control study, five cases of VTE (three DVT and two PE) and active CMV infection were detected in hospitalized patients, all females, aged below 37 years and showing at least one concomitant VTE acquired risk factor (three during OC treatment, one after surgery, and one in puerperium). 12 In a case-control study that investigated the potential role of CMV in hospitalized immunocompetent patients, a higher frequency of positive CMV-IgM and CMV-IgG was observed in VTE patients than in controls.…”

mentioning

confidence: 96%

“…►Table 1 summarizes the largest studies and reviews reflecting on the association between CMV infection and SVT. Risk factors and clinical characteristics of hospitalized patients with acute CMV infection-associated thrombosis were evaluated in 2010 in a retrospective case-control study 11 including 140 consecutive patients (mean age: 37.3 AE 17.4 years) diagnosed with the acute infection in a tertiary medical center and 140 matched controls without CMV infection. Among the control group, none of the patients had thrombotic events, whereas among the study group, nine (6.4%; p ¼ 0.003) patients had thromboses: five arterial thromboses (four splenic infarcts and one renal infarct) and four venous thromboses (one PE, one lower limb DVT, one upper limb DVT, and one jugular vein thrombosis).…”

mentioning

confidence: 99%