Thrombosis in inflammatory bowel diseases: what’s the link?

Giannotta, Martina; Tapete, G.; Emmi, Giacomo; Silvestri, Elena; Milla, Mónica

doi:10.1186/s12959-015-0044-2

Cited by 110 publications

(133 citation statements)

References 117 publications

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“…There is evidence that patients with IBD experience the first episode of VTE at a younger age than the general population, with an increased risk of recurrence, and that UC and CD pose an equal thrombotic risk. [12,13] Pregnancy/oral contraceptive use…”

Section: Renal Diseasementioning

confidence: 99%

Thrombotic disorders (part 2)

et al. 2020

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Section: Renal Diseasementioning

confidence: 99%

Thrombotic disorders (part 2)

et al. 2020

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“…Furthermore, endothelial dysfunction and a reduction of fibrinolytic activity may also increase the risk of thrombosis in these patients. 83,84 Given the number of case reports and case series, [85][86][87] the risk of CVT is probably also increased in patients with IBD, although, similar to previously mentioned risk factors, controlled studies are not available. Overall, IBD is reported in 2% of patients with CVT.…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

Risk Factors for Cerebral Venous Thrombosis

Silvis

Middeldorp

Zuurbier

et al. 2016

Semin Thromb Hemost

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Cerebral venous thrombosis (CVT) is a rare thrombotic disorder involving the cerebral veins and dural sinuses. In contrast to more common sites of venous thromboembolism (VTE), such as the legs and lungs, CVT mainly affects young adults and children, and women are affected three times more often than men. Although presenting symptoms are variable, headache is usually the first symptom, often in combination with focal neurologic deficits and epileptic seizures. The primary therapy for CVT consists of heparin followed by oral anticoagulation for at least 3 to 6 months. The mortality in the acute phase is 5 to 10% and a substantial proportion of survivors suffer from long-term disabilities. A large number of risk factors have been linked to CVT, although the scientific evidence for an association varies considerably between risk factors. Some risk factors, such as hereditary thrombophilia, correspond with risk factors for more common sites of VTE, whereas others, such as head trauma, are specific to CVT. In most patients, at least one risk factor can be identified. In this review, we provide an overview of the risk factors for CVT.

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“…9,10 However, the frequency of these risk factors is not different between patients with IBD and coagulation disorders. 11 The JAK2 (Janus kinase 2) V617F (valine to phenylalanine change at position 617 and a gain-of-function mutation) mutation is the most important point mutation that is involved in VTE. In addition, this gene is exists in several Philadelphia-negative myeloproliferative disorders (MDP), such as essential thrombocythemia, polycythemia vera, and idiopathic myelofibrosis, conditions that are complicated with thrombosis.…”

Section: Introductionmentioning

confidence: 99%

V617F‐independent upregulation of JAK2 gene expression in patients with inflammatory bowel disease

Asadzadeh‐Aghdaei

Mashayekhi

Koushki

et al. 2019

J of Cellular Biochemistry

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Background Inflammatory bowel disease (IBD) is one of the most important immune‐mediated disorders of the gastrointestinal tract. Besides, IBD is associated with numerous extraintestinal complications such as venous thromboembolism (VTE), an important risk factor for vascular complications, which results in the increased morbidity and mortality. The JAK2 (Janus kinase 2) V617F mutation is a well‐known point mutation which is involved in the pathogenesis of IBD, and VTE. Therefore, the aims of this study were to evaluate expression of JAK2 and association of V617F mutation in JAK2 of Iranian patients with IBD. Methods Two hundred and forty‐six patients with IBD (209 UC and 37 CD) and 206 healthy controls were enrolled in this study. The genomic DNA and total RNA were extracted from peripheral blood mononuclear cells (PBMCs). Then, the JAK2 V617F mutation detection was performed using the restriction fragment length polymorphism (RFLP) method. In addition, the JAK2 mRNA expression was evaluated using a quantitative polymerase chain reaction (q‐PCR) using the SYBR Green assay. Results There was no association of V61F mutation in patients with IBD with or without thrombosis compared with healthy control. However, the relative mRNA expression of JAK2 was significantly upregulated in patients with IBD in comparison with healthy control (P < 0.0001). In addition, the JAK2 mRNA expression was significantly decreased in patients with IBD having thrombosis compared with those without thrombosis ( P < 0.0001). Conclusions Taken together our findings suggested that JAK2 V61F‐independent upregulation of JAK2 mRNA expression in patients with IBD. Moreover, despite the absence of JAK2 V617F mutation in patients with IBD, the increased gene expression of JAK2 can be explained by another molecular mechanism such as regulation of gene expression at the transcriptional level which may play crucial roles in the pathogenesis of IBD.

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Thrombosis in inflammatory bowel diseases: what’s the link?

Cited by 110 publications

References 117 publications

Thrombotic disorders (part 2)

Thrombotic disorders (part 2)

Risk Factors for Cerebral Venous Thrombosis

V617F‐independent upregulation of JAK2 gene expression in patients with inflammatory bowel disease

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