Hemostatic abnormalities in inflammatory bowel disease

Chiarantini, E; Valanzano, Rosa; Liotta, Agatina Alessandrello; Cellai, Anna Paola; Fedi, Sandra; Ilari, I.; Prisco, Domenico; Tonelli, Francesco; Abbate, Rosanna

doi:10.1016/0049-3848(96)00060-6

Cited by 93 publications

(75 citation statements)

References 37 publications

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“…It is characterized by in vitro resistance to the anticoagulant effects of activated protein Recent studies have shown an increased frequency of aCL antibodies in IBD patients [21,[53][54][55][56]. The prevalence C and its cause was proved to be the replacement of arginine by glutamine at residue 506 in the factor V moleof positive aCL in IBD patients in these studies is shown in table 1.…”

Section: Antiphospholipidic Antibodies and Inflammatory Bowel Diseasementioning

confidence: 93%

“…Recent studies have shown that 11-20% of acute venous thrombotic events alence of positive aCL in IBD patients [43,57], in the majority of the studies a significantly higher prevalence of are caused by APCR [62,63]. APCR caused by a factor V Leiden mutation is now recognized as the most prevalent aCL in UC and CD patients compared to controls was found [21,[53][54][55][56]. The differences between the results inherited cause of thrombophilia.…”

Section: Antiphospholipidic Antibodies and Inflammatory Bowel Diseasementioning

confidence: 99%

“…A possible explanation bocytosis is a marker of any chronic inflammation with iron deficiency and it lacks specificity for IBD. Studies for the discrepancy in these results could be measurement of the total and not the free protein S in some of these on platelets activity in IBD have shown enhanced platelet aggregation in vivo and in vitro [20,21], and increased studies. The main physiological thrombin inhibitor, antithrombin-III (AT-III) was also found to be signifiplatelet activation as measured by increased release of intracellular proteins into plasma and expression of plate-cantly reduced in IBD patients in some studies [19,41,44], but this was not confirmed by others [43].…”

Section: Hypercoagulability In Inflammatory Bowel Diseasementioning

confidence: 99%

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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: Antiphospholipidic Antibodies and Inflammatory Bowel Diseasementioning

confidence: 93%

Section: Antiphospholipidic Antibodies and Inflammatory Bowel Diseasementioning

confidence: 99%

Section: Hypercoagulability In Inflammatory Bowel Diseasementioning

confidence: 99%

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Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Koutroubakis

2000

Dig Dis

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“…In addition to that thrombocytosis and increased platelet aggregation have also been documented [5][6][7]. However, there is no substantial evidence to correlate hematological and coagulation abnormalities with cerebral sinus thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Sinus Thrombosis: A Rare but Fatal Complication of Inflammatory Bowel Disease

Hashim¹

2016

JNSK

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Inflammatory bowel disease (IBD) is an idiopathic autoimmune disease. Extra intestinal manifestation of IBD has been reported to be 25 to 35%. There is a well-known risk of thrombosis in patients with IBD. It rarely involves cerebral vasculature in the form of arterial stroke or venous sinus thrombosis. This case is about 35 yrs old male who was a known case of ulcerative colitis for the last 10 years. He presented with history of severe thunderclap headache for the last few hours along with vomiting. He also had three episodes of seizure, generalized tonic clonic in nature. The examination does not show any focal asymmetry except mild drowsiness. His CT brain showed Focal cortical and subcortical area in the left posterior parietal region displaying multiple foci of hyper density with perifocal edema. CT venogram showed an intraluminal filling defect in the superior sagittal sinus suggestive of venous sinus thrombosis. Conclusion: Cerebral venous sinus thrombosis are considered as one of the rare but fatal complication of inflammatory bowel disease. It must be considered in all those with inflammatory bowel disease wherein absence of any other vascular risk factor patient presents with acute severe headache and focal or diffuse neurological symptoms including seizure

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“…Talbot et al zeigten ein signifikant erhöhtes Thromboserisiko bei CED-Patienten [172]. Die Fibrinogenkonzentration im Serum ist bei Crohnpatienten erhöht, häufig findet sich eine Thrombophilie [27]. Durch die Einnahme von oralen Kontrazeptiva -die auch den Fibrinogenspiegel erhöhen -steigt das relative Risiko, an CED zu erkranken um den Faktor vier bis acht [91].…”

Section: Mikrovaskuläres Endothel Und Gewebsischämie Bei Chronisch Enunclassified

Genexpressionsprofile humaner intestinaler mikrovaskulärer Endothelzellen (HIMEC)

Kebschull¹,

Heidemann²,

Klimmek³

et al. 2004

Z Gastroenterol

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Bei der Pathogenese chronisch entzündlicher Darmerkrankungen (CED) kommt den Endothelzellen der intestinalen Mikrovaskulatur eine besondere Bedeutung zu. Da Endothelzellen verschiedener Organe und Gefäße sehr heterogen sind, ist ein valides Modell für die Funktion des mikrovaskulären Endothels des Darmes nur durch Isolation und Kultur humaner intestinaler Endothelzellen (HIMEC) untersuchbar. In dieser Arbeit wurde das Genexpressionsprofil von HIMEC sowie seine Modulation durch das proinflammatorische Zytokin Tumor-NekroseFaktor α (TNF-α) -einem wesentlichen Zytokin in der Pathogenese der CED -qualitativ und quantitativ charakterisiert.Aus chirurgischen Darmresektaten isolierte HIMEC-Primärkulturen wurden nach Verifizierung ihrer endothelialen Herkunft für 4 sowie 24 Stunden mit TNF-α stimuliert, als Kontrolle dienten unstimulierte HIMEC. Nach Isolierung der Gesamt-RNA erfolgte die Expressionsanalyse mittels Gene Arrays. Die Bestätigung ausgewählter Ergebnisse erfolgte mittels quantitativer Realtime RT-PCR. Zur Analyse der speziellen Reaktion intestinaler Endothelzellen auf Stimulation mit TNF-α wurden die ermittelten spezifischen Expressionsprofile mit denen der entsprechend stimulierten mikrovaskulären Referenz-Endothelzellinie HMEC-1 verglichen.Von den nach vier-bzw. 24-stündiger Stimulation hochregulierten bzw. angeschalteten Genen sind nur 93 Gene bei beiden Zellarten gleichermaßen anzutreffen, 148 Gene werden nur in HIMEC, 199 Gene nur in der Referenzzellinie gefunden.Die meisten der in HIMEC regulierten Gene kodieren für Chemokine/Cytokine, Oberflä-chenmarker oder Zellproliferationsgene. Es zeigen sich in HIMEC mehrere bisher unbekannte Genexpressionsmuster sowie einige bislang für Endothelzellen bzw. intestinales Gewebe unbeschriebene hochregulierte Gene.Die in HIMEC durch den proinflammatorischen Mediator TNF-α differenziell regulierten neuen Kandidatengene spielen möglicherweise im Rahmen der mukosalen Entzündung eine bislang unbekannte Rolle.Tag der mündlichen Prüfung: 16. Dezember 2004

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Hemostatic abnormalities in inflammatory bowel disease

Cited by 93 publications

References 37 publications

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Role of Thrombotic Vascular Risk Factors in Inflammatory Bowel Disease

Cerebral Sinus Thrombosis: A Rare but Fatal Complication of Inflammatory Bowel Disease

Genexpressionsprofile humaner intestinaler mikrovaskulärer Endothelzellen (HIMEC)

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