scholarly journals Thrombotic Complications in Inflammatory Bowel Disease

Author(s):  
A. V. Borota ◽  
A. A. Borota ◽  
E. V. Onishchenko

The risk of thrombotic complications is known to be 3 times higher in patients with inflammatory bowel disease (IBD) than in healthy individuals, with the relative risk being 15 times higher during the periods of relapses. Aim. To study and generalize literature data available on the prevention and treatment of IBD thrombotic complications.Key findings. In the сonditions under study, the presence of chronic inflammation and increased bleeding of the intestinal wall is shown to activate the coagulation system, impair the fibrinolysis system and reduce the activity of natural anticoagulation mechanisms. The concentration of fibrinogen — a protein of the acute inflammation phase — increases significantly. This results in an imbalance of the blood coagulation system with a tendency to hypercoagulation, which significantly increases the risk of thrombotic complications and the disseminated intravascular coagulation syndrome. In turn, the activation of the coagulation cascade may trigger the inflammatory response, which eventually leads to the formation of a vicious circle between chronic inflammation and thrombosis. The pathogenesis of thrombosis in inflammatory colon diseases is a multifactor process, which remains to be understood.Conclusion.The management of patients with IBD in combination with thromboembolic complications requires an individual multidisciplinary approach. Taking into account the pathogenetic factors, the following options are possible in the prevention and treatment of thrombotic complications in IBD: strengthening the basic therapy of the primary disease; administration of prophylactic doses of anticoagulants under dynamic continuous laboratory control in the acute period using the methods of conservative therapy of thrombotic complications (elastic compression of the lower extremities) in the period of exacerbation of the primary disease.

2004 ◽  
Vol 74 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Liu ◽  
Russell ◽  
Smith ◽  
Bronson ◽  
Milbury ◽  
...  

Because reactive oxygen species have been implicated as mediators of inflammatory bowel disease (IBD), we evaluated the potential preventive and therapeutic effects of two dietary antioxidants, glutathione (GSH) and coenzyme Q10 (CoQ10) on dextran sulfate sodium (DSS)-induced colitis in mice. Fifty female 8-wk old Swiss-Webster mice were randomly assigned to 4 groups for a pre-treatment 'prevention' study: (1) GSH (1% of diet); (2) CoQ10 (200 mg/kg/d); (3) DSS only (3% of drinking water); (4) control (no treatment). The mice in groups 1 and 2 were fed with GSH or CoQ10 for 21 wks, and the mice in groups 1, 2 and 3 were provided DSS from wk 7 for 4 cycles (1 cycle = 1 wk DSS followed by 2-wk water). Another 50 mice were randomly assigned to 4 groups for a 21-wk 'treatment' study where the mice in groups 1, 2, and 3 were administered DSS for 6 cycles (18 wks) to induce colitis. GSH and CoQ10 were added from wk 7 until the completion of the protocol. Loose stools and hemocult positivity were modestly but significantly reduced with GSH or CoQ10 at several periods during the intervention in both the prevention and treatment studies. In contrast, histological evaluation revealed increases in colonic dysplasia and ulceration with GSH or CoQ10. Thus, in this mouse model, GSH and CoQ10 appear to have a beneficial effect on acute signs of IBD, but may have an adverse impact on the chronic pathophysiology of the disease. Further studies using additional animal models are required to determine whether GSH or CoQ10 provide a favorable or unfavorable benefit:risk ratio in the prevention or treatment of IBD.


Author(s):  
Hisham Abdullah Almottowa ◽  
Abdulmohsen Yaseer Alkhars ◽  
Maram Hussam Hassan ◽  
Hamad Adel Alhamad ◽  
Saad Munawwikh Alshammari ◽  
...  

Ulcerative colitis (UC) and Crohn’s disease (CD) are two major inflammatory disorders of the intestinal wall collectively known as inflammatory bowel disease (IBD). Colorectal carcinoma (CRC) is the most significant and grave consequence of IBD and is preceded by dysplasia in majority of the cases. In this review we aim to discuss the various types of dysplasia found in patients with CRC due to IBD. A thorough literature search was conducted in online databases such as PubMed, Google Scholar, from which all studies published in the last ten years were included in this review. The major development in diagnostic procedures and visualization modalities have aided our understanding of dysplasia, which is now known to be the strongest predictor and marker for CRC development. However, the unpredictable behavior and progression of dysplasia still warrants vigilant surveillance. Dysplasia has been classified on histological characteristics using grades of dysplasia from ‘negative for dysplasia’ to ‘high grade dysplasia’. On visibility via an endoscope from ‘visible dysplasia’ to ‘invisible dysplasia’ and macroscopic features of ‘conventional dysplasia’ and ‘non-conventional dysplasia’. No single classification can be utilized to define the stage of dysplasia and more importantly predict its progression and outcome of CRC. Using evidence-based medicine an integrated classification expanding on a management algorithm must be formulated by a panel of experts to steer management of the disease. A multidisciplinary, tailored approach with a strong emphasis on regular and timely surveillance to ensure early detection of CRC can enhance quality of life and patient outcomes.


2001 ◽  
Vol 96 (4) ◽  
pp. 1301-1302 ◽  
Author(s):  
Alfredo Papa ◽  
Valerio De Stefano ◽  
Silvio Danese ◽  
Antonio Gasbarrini ◽  
Giovanni Gasbarrini

2018 ◽  
Vol 9 (8) ◽  
pp. 4143-4152 ◽  
Author(s):  
Shuai Chen ◽  
Meiwei Wang ◽  
Lanmei Yin ◽  
Wenkai Ren ◽  
Peng Bin ◽  
...  

Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is strongly associated with intestinal immunity and the microbiome.


2017 ◽  
Vol 35 (1-2) ◽  
pp. 25-31 ◽  
Author(s):  
Dominik Bettenworth ◽  
Florian Rieder

Background: Intestinal fibrosis with stricture formation is a common feature of inflammatory bowel disease (IBD) and leads to a significantly impaired quality of life in affected patients, intestinal obstruction as well as to the need for surgical intervention. This constitutes a major treatment challenge. Key Messages: Fibrosis results from the response of gut tissue to the insult inflicted by chronic inflammation. Similarly to what occurs in other organs, the underlying fibrogenic mechanisms are complex and dynamic, involving multiple cell types, interrelated cellular events, and a large number of soluble factors. Owing to a breakdown of the epithelial barrier in IBD, luminal bacterial products leak into the interstitium and induce an innate immune response mediated by the activation of both immune and non-immune cells. Other environmental factors as well as chronic inflammation will certainly impact the quality and quantity of intestinal fibrosis. Finally, the composition of the intestinal extracellular matrix is dramatically altered in chronic gut inflammation and actively promotes fibrosis through its mechanical properties. The conventional view that intestinal fibrosis is an inevitable and irreversible process is gradually changing in light of an improved understanding of the cellular and molecular mechanisms that underline its pathogenesis. In addition, clinical observations in patients who undergo strictureplasty have shown that stricture formation is reversible. Conclusions: Identification of the unique mechanisms of intestinal fibrogenesis should create a practical framework to target and block specific fibrogenic pathways, estimate the risk of fibrotic complications, permit the detection of early fibrotic changes and, eventually, allow the development of treatment methods customized to each patient's type and degree of intestinal fibrosis.


2012 ◽  
Vol 6 ◽  
pp. S189
Author(s):  
T. Lobaton Ortega ◽  
D. Azuara ◽  
F. Rodriguez-Moranta ◽  
J. de Oca ◽  
J. Guardiola ◽  
...  

2002 ◽  
Vol 29 (4) ◽  
pp. 120-123 ◽  
Author(s):  
A. Kirchgatterer ◽  
H. H. Wenzl ◽  
G. Aschl ◽  
M. Hinterreiter ◽  
B. Stadler ◽  
...  

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