Page 31 - Postoperative Intra-Abdominal Adhesions- New insights in prevention and consequences
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                                Current status postoperative abdominal adhesions
Fibrinolytic agents as streptokinase, elastase and tissue plasminogen
activator produced by recombinant DNA techniques (rtPA) can contribute
in adhesion prevention directly by reducing the fibrinous mass and
indirectly by stimulating plasminogen activator activity [44]. Although 2 in many studies results were promising, data from clinical and animal
trials suggest that all of these approaches have had only limited success, impeded by lack of safety, efficacy and many adverse effects without eliminating the problem of postoperative adhesion formation [28, 44, 61, 81].
Antibiotics
Antibiotics are commonly used for prophylaxis against postoperative wound infections. Theoretically they also reduce abdominal infections and the subsequent adhesion formation. However, peritoneal irrigation with antibiotic solutions does not reduce adhesion formation, while it has been shown that in some cases it may promote them [44, 61, 82]
Growthfactors
Growthfactors are involved in the pathogenesis of fibrinogenesis and in this context the members of the transforming growthfactor beta (TGF-beta) are of special interest [83]. It was demonstrated that TGF- beta isoforms were expressed after peritoneal damage, suggesting that the pharmacokinetics of interacting agents play a decisive role in their adhesion prevention effectiveness [84]. Further pharmacokinetic as well as pharmacodynamics should be performed to analyze probable side effects [38].
Neurokinin 1-receptor (NK1-R)
Another pharmacological approach is represented by NK1-R. This receptor antagonist is involved in inflammation and wound healing and might be an important signalling molecule in adhesion formation [38, 85]. In different animals NK1-R has resulted in less adhesion formation, although the exact cellular pathway by which the antagonist exerts its effects remains unclear. Cassidy et al found that NK1-R increases peritoneal fibrolysis causing the adhesion reduction [86]. Although these results are promising, at this moment no clinical studies can be found.
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