fibrin and Intestinal-Diseases

This paper reviews the evidence that glove powder plays an important role in adhesion formation and has adverse effects on the healing of abdominal incisional wounds. The underlying mechanisms leading to these adverse effects are beginning to be revealed. By affecting the mesothelial cell function, powder contamination disrupts the delicate balance of fibrin deposition and degradation, provoking adhesion formation, and interfering with wound healing. Studies are described showing that starch impairs incisional wound healing by its effect on the T cell-mediated immune system. Furthermore starch powder may act as a vector for endotoxin. This paper concludes that starch powder is harmful and its use in a hospital setting can no longer be supported.

Topics: Abdomen; Animals; Endotoxins; Epithelium; Fibrin; Gloves, Surgical; Humans; Intestinal Diseases; Powders; Starch; T-Lymphocytes; Tissue Adhesions; Wound Healing

Data regarding biomarkers to understand disease pathogenesis and to assess disease activity of intestinal Behçet's disease (BD) are limited. Therefore, we aimed to investigate the differentially expressed proteins in sera from patients with intestinal BD and to search for biomarkers using mass spectrometry-based proteomic analysis.. Serum samples were pooled for the screening study, and two-dimensional electrophoresis (2-DE) was performed to characterize the proteins present in intestinal BD patients. Candidate protein spots were identified using matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry (MALDI-TOF/TOF MS) and bioinformatic analysis. To validate the proteomic results, serum samples from an independent cohort were assessed by enzyme-linked immunosorbent assay.. Pooled serum samples were used for 2-DE, and approximately 400 protein spots were detected in the sera of intestinal BD patients. Of the 22 differentially expressed proteins, 3 were successfully identified using MALDI-TOF/TOF MS. The three up-regulated proteins identified in the intestinal BD group included fibrin, apolipoprotein A-IV, and serum amyloid A (SAA). Serum SAA in intestinal BD patients (2.76 ± 2.50 ng/ml) was significantly higher than that in controls (1.68 ± 0.90 ng/ml, p = 0.007), which is consistent with the proteomic results. In addition, the level of IL-1β in patients with intestinal BD (8.96 ± 1.23 pg/ml) was higher than that in controls (5.40 ± 0.15 pg/ml, p = 0.009). SAA released by HT-29 cells was markedly increased by tumor necrosis factor-α (TNF-α) and lipopolysaccharides stimulation.. Our proteomic analysis revealed that SAA was up-regulated in intestinal BD patients.

Topics: Adult; Apolipoproteins A; Behcet Syndrome; Biomarkers; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Fibrin; HT29 Cells; Humans; Interleukin-1beta; Intestinal Diseases; Male; Mass Spectrometry; Middle Aged; Proteomics; Serum Amyloid A Protein

The small bowel is a dose-limiting normal tissue in radiation therapy of malignancies in the abdomen and pelvis, as well as an important determinant of survival after non-therapeutic radiation exposure. Irradiation of normal tissues, including intestine, causes loss of vascular thromboresistance and upregulation of thrombin receptors. Radiation-induced endothelial dysfunction is thought to be involved in both early and delayed radiation responses. Hence, thrombin may be a potential target for ameliorating normal tissue radiation toxicity.. To assess direct thrombin inhibition as a protective strategy against small bowel radiation toxicity.. Rat small intestine was exposed to localized orthovoltage X-radiation. Recombinant hirudin, a direct thrombin inhibitor, or vehicle was infused from 2 days before irradiation to 14 days after irradiation. Structural, cellular, and molecular aspects of intestinal radiation injury were assessed at 2 weeks (early toxicity) and 26 weeks (chronic toxicity) after irradiation.. Compared with unirradiated intestine, irradiated intestine showed increased expression of tissue factor, increased immunoreactivity for enzymatically active thrombin, and increased extravascular fibrin(ogen) deposition. Hirudin treatment significantly attenuated radiation-induced mucosal damage (P = 0.04), reactive intestinal wall thickening (P = 0.02), transforming growth factor-beta immunoreactivity levels (P = 0.0002), and collagen III deposition (P = 0.003). The differences between hirudin-treated and control rats were more pronounced at 2 weeks than at 26 weeks after irradiation. Hirudin treatment did not affect postradiation granulocyte infiltration.. Short-term thrombin inhibition attenuates important aspects of intestinal radiation toxicity. Thrombin is a promising target for minimizing normal tissue injury after radiation therapy of cancer, as well as for protecting normal tissues from the adverse effects of non-therapeutic radiation exposure.

Topics: Animals; Fibrin; Gamma Rays; Hirudins; Intestinal Diseases; Intestines; Male; Radiation Injuries; Radiation Tolerance; Radiation-Protective Agents; Rats; Rats, Sprague-Dawley; RNA, Messenger; Thrombin; Thromboplastin

Topics: Aged; Female; Fibrin; Humans; Intestinal Diseases; Male; Peritoneal Diseases; Surgical Wound Dehiscence; Sutures; Tissue Adhesives

Twenty cases of ischemic bowel disease were analysed to determine the frequency and significance of fibrin thrombi in this condition. Fibrin thrombi were present in all 10 patients with occlusive ischemic bowel disease and in 7 of the 10 patients with nonocclusive ischemic bowel disease. In addition, fibrin thrombi were noted in a wide variety of specific and nonspecific inflammatory bowel diseases and in acute appendicitis. We conclude that fibrin thrombi are a nonspecific feature of tissue necrosis and that their mere presence in the bowel should not be regarded as an expression of disseminated intravascular coagulation.

Topics: Appendicitis; Colitis, Ulcerative; Crohn Disease; Fibrin; Humans; Intestinal Diseases; Intestinal Obstruction; Intestines; Ischemia; Necrosis; Thrombosis

The significance and frequency of fibrin thrombi (FT), the pathological hallmark of disseminated intravascular coagulation (DIC), in ischemic intestine were analyzed in a retrospective study of the infarcted bowel of patients with occlusive mesenteric ischemia (OMI) and nonocclusive mesenteric ischemia (NOMI). Representative intestinal sections were studied from 10 patients with NOMI of the small and/or large bowel and 12 patients, with OMI of varied etiology. Three patients with inflammatory bowel disease and 1 patient with DIC and bowel necrosis were also studied. Routine hematoxylin and eosin stains for fibrin were prepared for each specimen. The number of FT was quantitated. FT were identified in each of the 10 cases of NOMI; however in only 2 were they prominent. FT were identified in 6 of the 12 cases of OMI and in 4 of these 6 they were a prominent feature. Rare FT were present in the cases of inflammatory bowel disease and did not correlate with the inflammatory process. No FT were present in the intestinal sections of the DIC case. FT are a nonspecific feature of necrosis and can be identified in both occlusive and nonocclusive ischemic bowel disease. Their presence in the intestine of NOMI therefore cannot be used to implicate DIC as the primary cause of this entity.

Topics: Blood Platelets; Disseminated Intravascular Coagulation; Enteritis; Fibrin; Humans; Infarction; Intestinal Diseases; Intestines; Ischemia; Mesenteric Vascular Occlusion; Mesentery; Necrosis; Retrospective Studies; Thrombosis