Free Protein S Deficiency in Patients with Chronic Inflammatory Bowel Disease

Aadland, E; Ødegaard, O.R.; Røseth, Arne; Try, K.

doi:10.3109/00365529209000170

Cited by 53 publications

(26 citation statements)

References 13 publications

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“…Deficiency of the proteins C and S in IBD patients was proposed by the studies of Jorens et al [38] gree of inflammatory activity and prothrombotic abnormalities has been found [19]. Studies using sensitive and Aadland et al [39,40]. Other studies did not confirm these data [19,[42][43][44].…”

Section: Hypercoagulability In Inflammatory Bowel Diseasementioning

confidence: 42%

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Koutroubakis

2000

Dig Dis

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Thromboembolic disease is a significant cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). It is recognized that a hypercoagulable state exists in IBD which involves all components of the clotting system. It has been suggested that this hypercoagulable state is closely linked to the disease pathogenesis. Recent studies have shown that genetic defects such as factor V Leiden mutation and C677T methylenetetrahydrofolate reductase polymorphism associated with hyperhomocysteinemia seem to interfere in the thrombotic manifestations of IBD. Acquired factors such as antiphospholipid antibodies could also participate in the development of the thrombotic process. Deficiencies of other anticoagulant factors play a less important role in the thrombosis, and therefore it is not surprising that the results on these factors in IBD are contradictory. In conclusion the resultant gene–gene and gene–environment interactions between risk factors are the key to the understanding of why an IBD patient develops thrombosis at a specific point in time.

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Section: Hypercoagulability In Inflammatory Bowel Diseasementioning

confidence: 42%

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Koutroubakis

2000

Dig Dis

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“…80,81 Of note, proteins C and/or S may be deficient secondary to acute thrombosis and cannot be interpreted while on warfarin pharmacotherapy. Dysfibrinogenemias and plasminogen deficiency are associated with venous and, less often, arterial thrombi; however, to date the prevalence of these very rare disorders has not been studied in IBD.…”

Section: Anticoagulant Deficiencies and Other Rare Thrombotic Disordersmentioning

confidence: 99%

Thrombosis and inflammatory bowel disease: A call for improved awareness and prevention

Zitomersky

Verhave

Trenor

2011

Inflammatory Bowel Diseases

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Thrombotic complications in patients with inflammatory bowel disease (IBD) are common and require improved awareness and prevention. In this review the interface between IBD and thrombosis is discussed, with emphasis on risk assessment and data to aid clinical decision making. Thromboembolic complications are 3-fold more likely in IBD patients than controls and the relative risk exceeds 15 during disease flares. Improved assessment of thrombosis risk for an individual patient includes thorough personal and family history and awareness of prothrombotic medications and lifestyle choices. Patients with the highest risk of thrombosis are those with active colonic disease, personal or strong family history of thrombosis, and those with significant acquired risk factors. Combined risk factors or hospitalization should prompt mechanical thromboprophylaxis. Indications for prophylactic anticoagulation are not defined currently by clinical studies, especially in pediatric patients, although some groups now advocate prophylactic anticoagulation for all hospitalized IBD patients and even some outpatients with disease flares. Thrombosis management requires a multidisciplinary therapeutic approach to balance anticoagulation and bleeding risk. While bleeding may occur with anticoagulation in IBD, data and experience indicate that therapeutic heparin is safe and bleeding manifestations can be managed supportively in most patients. Until prospective trials of prophylactic anticoagulation are published, management of thrombotic risk and prophylaxis in IBD will remain a clinical challenge.

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“…This hypercoagulable state may be related to an increased tendency for thromboembolic events and may be linked to the disease pathogenesis through promoting microthrombi formation in intestinal microcirculation [7,8] . The etiology and pathogenesis of the hypercoagulable state in IBD have not been fully elucidated but may be induced through a procoagulant effect of proinflammatory cytokines [9][10][11][12][13] in combination with acquired or genetic defects of clotting factors (protein S, protein C, antithrombin, factor V Leiden, prothrombin mutation 20210A, and antiphospholipid antibodies) [14][15][16] . Recently, the factor V Leiden has been implicated in the increased risk of venous thrombosis in IBD patients [17][18][19] .…”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

Hyperhomocysteinemia in ulcerative colitis is related to folate levels

Zezos

Papaioannou²,

Nikolaidis³

et al. 2005

WJG

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Abstract Abstract Abstract AIM:To study the prevalence and clinical significance of hyperhomocysteinemia (hHcys), an independent factor for arterial and venous thrombosis, in a group of patients with ulcerative colitis (UC). METHODS:Fasting homocysteine (Hcys), folate, and vitamin B 12 serum levels were measured in 40 UC patients and 50 healthy controls. Clinical data regarding UC were gathered. RESULTS:Median serum Hcys levels in UC patients were similar to those in controls (12.26 μmol/L vs 12.32 μmol/ L), but the prevalence of hHcys was higher in UC patients than in controls (30% vs 10%, P = 0.028). UC significantly increased the risk of hHcys (adjusted odds ratio: 4.125; 95%CI: 1.26-13.44). Multivariate regression analysis showed that male sex, folate and vitamin B 12 deficiency or lower serum values were significant independent predictors of higher Hcys levels in UC patients (r 2 = 0.4; P<0.001).CONCLUSION: hHcys is common in UC patients and it is related to folate and vitamin B 12 deficiency or lower serum values. It would be reasonable for patients with UC to receive folate and vitamin B complex supplements as a prophylactic measure.

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Free Protein S Deficiency in Patients with Chronic Inflammatory Bowel Disease

Cited by 53 publications

References 13 publications

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Thrombosis and inflammatory bowel disease: A call for improved awareness and prevention

Hyperhomocysteinemia in ulcerative colitis is related to folate levels

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