A comparison of observational studies and controlled trials of heparin in ulcerative colitis

Malhotra, Samir; Kondal, A; Shafiq, Nusrat; Sidhu, Shabir; Bhasin, D K; Pandhi, P

doi:10.5414/cpp42690

Cited by 11 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In some cases, this therapeutic approach was successful. 16,17 However, a meta-analysis 18 could not prove efficacy in the treatment of patients with ulcerative colitis.…”

Section: Enoxaparin As a Substitute For Sdc1 Functionmentioning

confidence: 99%

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

Floer

Götte

Wild

et al. 2010

The American Journal of Pathology

View full text Add to dashboard Cite

Syndecan-1 (Sdc1) plays a major role in wound healing and modulates inflammatory responses. Sdc1 expression is reduced in lesions of patients with ulcerative colitis. The aim of this study was to investigate the role of Sdc1 in murine dextran sodium sulfate (DSS)-induced colitis. DSS colitis was induced in Sdc1-deficient (knockout (KO)) and wild-type mice by oral administration of 3% DSS. KO mice exhibited a significantly increased lethality as compared with wild-type controls (61 versus 5% , P < 0.05). Impaired mucosal healing and prolonged recruitment of inflammatory cells in KO mice were accompanied by significant up-regulation of tumor necrosis factor-␣, CC chemokine ligand 3/macrophage inflammatory protein-1␣, and vascular cell adhesion molecule-1 , as determined by histological correlation between 0 and 15 days after colitis induction , TaqMan low-density array analysis , and quantitative real-time PCR. Treatment from days 7 through 14 with enoxaparin , a functional analogue of the Sdc1 heparan sulfate chains , significantly reduced lethality of KO mice due to DSS-induced colitis , which was correlated with improved mucosal healing. In vitro, Sdc1-deficient polymorphonuclear cells displayed increased adhesion to endothelial cells and intercellular adhesion molecule-1, and enoxaparin reverted adhesion to wild-type levels. Small interfering RNA-mediated knockdown of Sdc1 expression resulted in reduced basic fibroblast growth factor-mediated mitogen-activated protein kinase signaling and reduced Caco-2 cell proliferation. We conclude that Sdc1 has a protective effect during experimental colitis. The modification of missing Sdc1 function by heparin analogues may emerge as a promising anti-inflammatory approach. (Am J Pathol

show abstract

“…In some cases, this therapeutic approach was successful. 16,17 However, a meta-analysis 18 could not prove efficacy in the treatment of patients with ulcerative colitis.…”

Section: Enoxaparin As a Substitute For Sdc1 Functionmentioning

confidence: 99%

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

Floer

Götte

Wild

et al. 2010

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…The new results of meta-analysis demonstrated a non-significant effect of heparin in controlled clinical trials differing markedly from observational studies [18]. Mucosal capillary thrombosis and vascular occlusion is either important or not in the pathogenesis of UC.…”

Section: Discussionmentioning

confidence: 93%

“…These results supported that microvascular thrombosis may be still one of important pathogentic factors in some UC. Recent studies indicated that heparin has only little or limited anti-inflammatory activities [18,31]. The effect of heparin or LMWH as adjuvant therapy and when to use in the treatment of UC still needs to be assessed.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Microvacular Thrombi of Colonic Tissue in Ulcerative Colitis

Ouyang

Chen

et al. 2007

Dig Dis Sci

View full text Add to dashboard Cite

Mucosal microvascular thrombi in rectal biopsies were observed in some ulcerative colitis (UC). Heparin may be effective in steroid resistant UC in some studies, however, the new results of meta-analysis demonstrated a non-significant effect of heparin in controlled clinical trials, differing markedly from observational studies. The objective of this study was to identify colonic microvascular thrombi in larger cases with UC, and analyse its possible risk factors: age, gender, histologic score, extent of lesions and operation or biopsy specimens, and assess the significance of microvascular thrombosis in patients with UC. The microvascular thrombi were identified by immunohistochemical staining with anti-CD61 monoclonal antibody and Martius scarlet blue (MSB) staining in 40 colonic tissue samples of UC (31 biopsy specimens and nine operated cases) and 12 cases of normal colon tissue from operated colonic carcinoma. Logistic regression analysis was used to assess the relationship of age, gender, degree of histology, origin of the specimens, extent of lesions and microvascular thrombi examined. Microvascular thrombi were positive in 14 of 40 UC cases, and none in the controls. The presence of microvascular thrombi was related to operation specimens with odds ratio 11.667, P=0.0179, it might be also related to histologic score (OR=1.350) and extent of lesions (OR=1.619). These results suggest that microvascular thrombosis may be one of the important pathogenesis in some UC, and that the effect of anticoagulant treatment still needs to be assessed.

show abstract

“…6,7 On the contrary, in recent articles no beneficial antiinflammatory effect of heparin was seen in cases of IBD. 8 In the absence of well-established guidelines, there is prevailing confusion in the scientific community and most physicians tend to err on the side of safety by withholding anticoagulation to negate the risk of bleeding. In the index case we attribute CVT to underlying ulcerative colitis, as no other prothrombotic state was present.…”

Section: Cerebral Venous Thrombosis In a Patient With Ulcerative Colitismentioning

confidence: 99%

Cerebral venous thrombosis in a patient with ulcerative colitis

Chauhan

Sachdev

D’Cruz

et al. 2007

Inflammatory Bowel Diseases

View full text Add to dashboard Cite

A comparison of observational studies and controlled trials of heparin in ulcerative colitis

Cited by 11 publications

References 0 publications

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

Enoxaparin Improves the Course of Dextran Sodium Sulfate-Induced Colitis in Syndecan-1-Deficient Mice

The Microvacular Thrombi of Colonic Tissue in Ulcerative Colitis

Cerebral venous thrombosis in a patient with ulcerative colitis

Contact Info

Product

Resources

About