Unsuspected Triggers of Venous Thromboembolism—Trivial or Not So Trivial?

Lippi, Giuseppe; Franchini, Massimo; Favaloro, Emmanuel J.

doi:10.1055/s-0029-1242713

Cited by 46 publications

(35 citation statements)

References 52 publications

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“…As such, the pathogenesis of VTE is typically multifactorial, where any single condition, either acquired or congenital, would predispose, but may not be sufficient alone to trigger thrombosis. Plausibly, then, the concomitant presence of one or more additional triggers might be required to precipitate an acute thrombotic episode [19].…”

Section: Introductionmentioning

confidence: 99%

Biochemical markers for the diagnosis of venous thromboembolism: the past, present and future

Lippi

Cervellin

Franchini

et al. 2010

J Thromb Thrombolysis

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106

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Deep venous thrombosis and pulmonary embolism represent two expressions of a similar clinical pathological process traditionally referred to as venous thromboembolism. Several population studies evidence venous thromboembolism as a leading healthcare problem worldwide, highlighting the need for early and reliable diagnosis to enable appropriate triage of affected patients and to optimize outcome. There is still debate, however, on which thrombotic markers to use, as well as their most suitable position within diagnostic algorithms. This article aims to review the pathophysiology and clinical usefulness of past, present and future markers of thrombosis, including soluble fibrin monomers, fibrin/fibrinogen degradation products, thrombin-antithrombin complex, plasmin-antiplasmin complex, fibrinopeptide A and B, prothrombin fragments 1 + 2, thrombus precursor protein, D-dimer, activated protein C-protein C inhibitor complex, myeloperoxidase, thrombin generation assays and proteomic analysis. Several lines of evidence now attest that the global diagnostic performances of some D-dimer assays largely outperform those of any other coagulation or fibrinolytic marker proposed thus far, and a "negative" D-dimer measured with rapid enzyme linked fluorescent immunoassay is now considered the biochemical gold standard for ruling out an acute episode of venous thromboembolism in a patient with a low pretest probability for venous thromboembolism, so that additional testing can be safely omitted. However, to further improve clinical outcomes, the diagnostic efficiency of combining D-dimer testing with other markers covering different pathophysiological aspects of thrombosis such as continuous and progressive thrombin generation (e.g., activated protein C-protein C inhibitor complex) or neutrophil activation (i.e., myeloperoxidase) merits further investigation. Proteomic analysis, which would help to characterize the structure and function of each protein and the complexities of protein-protein interactions in physiological and pathological hemostasis, also holds promise for identifying novel markers and developing effective diagnostic protocols in the future.

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Section: Introductionmentioning

confidence: 99%

Biochemical markers for the diagnosis of venous thromboembolism: the past, present and future

Lippi

Cervellin

Franchini

et al. 2010

J Thromb Thrombolysis

Self Cite

106

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“…In drug users, pulmonary embolism might be the consequence of the oral medications dissolved in water and injected intravenously, such as amphetamines, methylphenidate, methadone, meperidine, pentazocine, hydromorphone, dextropropoxyphene, codeine and temazepam, or of the entrance of residues of talcum, starch, cellulose and cotton [101][102][103][104][105][106].…”

Section: Foreign Materials Pulmonary Embolismmentioning

confidence: 99%

Pathophysiology, clinics and diagnostics of non-thrombotic pulmonary embolism

Montagnana

Cervellin

Franchini

et al. 2010

J Thromb Thrombolysis

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Non-thrombotic pulmonary embolism (NTPE) is commonly defined as the partial or total occlusion of the pulmonary circulation caused by a variety of non-thrombotic embolic agents. Although its prevalence is much lower than that of pulmonary thromboembolism, this life-threatening pathology is often underestimated due to the low specificity of signs and symptoms and because it might be frequently overlooked in the differential diagnosis of the chest pain. The main sources of non-thrombotic pulmonary emboli include cancers, fat, infective agents, amniotic fluid, a variety of foreign materials and gases. The diagnosis is particularly challenging. The spectrum of imaging findings using imaging techniques such as computed tomography is unpredictable and typically heterogeneous, whereas laboratory tests can only be helpful for establishing the cause but not the presence of the disease (i.e., D-dimer testing is frequently negative). As such, the clinical history along with the identification a potential underlying disease are the often the mainstay for the differential diagnosis. The aim of this article is to provide an overview of the pathophysiology, clinics and diagnostic approach to NTPE.

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“…Established VTE triggers include surgery, trauma, immobility, malignancy and chemotherapy, hormonal therapy, and pregnancy and puerperium. 3,4 Infection has been investigated both as a chronic risk factor and acute precipitant or trigger of VTE. A 2012 systematic review by Tichelaar et al summarized previous work on infection and risk of VTE and concluded that infections generally, and HIV, pneumonia, and urinary tract infections specifically, are associated with increased risk of VTE.…”

Section: Introductionmentioning

confidence: 99%