Is proximal demarcation of ulcerative colitis determined by the territory of the inferior meseriteric artery?
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Cited by (32)
The marginal artery of Drummond revisited: A systematic review
2021, Translational Research in AnatomyCitation Excerpt :Billings et al. (1984) found that an inadequate blood supply to the splenic flexure via the MA because of IMA occlusion can lead to ischemic colitis [5]. The MA can also act as a demarcation point for certain pathologies; for example, Hamilton et al. (1995) concluded that the limit of the MA determines the proximal extent of colitis [42]. They contended that the mucosal microvasculature in the area near the IMA as certain characteristics predisposing the dependent colon to ulcerative colitis pathogenesis.
Evidence against a systemic arterial defect in patients with inflammatory bowel disease
2014, Journal of Surgical ResearchCitation Excerpt :These data suggest that an underlying defect in vascular smooth muscle relaxation is not present in the arteries of IBD patients. Evidence of microvascular injury in areas of the gut affected by IBD has been used to suggest that an underlying systemic vascular defect may contribute to the etiology of CD and/or UC [6–8,23]. To explore this possibility, vasoconstrictor and vasodilator responses were examined in mesenteric and omental arteries obtained from patients with CD, UC, and non-IBD pathologies.
Val34Leu factor XIII polymorphism in Italian patients with inflammatory bowel disease
2003, Digestive and Liver DiseaseHemostatic imbalance in active and quiescent ulcerative colitis
2001, American Journal of GastroenterologyCitation Excerpt :This may explain or contribute to UC-related complications, such as thromboembolism, with an incidence between 1% and 7% (5), and in postmortem studies, even 40% (6, 7). In addition, extent and severity of disease (8, 9) and the presumed beneficial therapeutic effect of anticoagulants (10, 11) may be related to hypercoagulability. Moreover, inherited coagulopathies protect against the development of UC (12).
Basic biomedical science and the destruction of the pathophysiologic bridge from bench to bedside
1999, American Journal of Medicine