Preoperative C-reactive protein and other inflammatory markers as predictors of postoperative complications in patients with colorectal neoplasia.

BACKGROUND: Inflammatory markers are measured following colorectal surgery to detect postoperative complications. However, the association of these markers preoperatively with subsequent postoperative course has not yet been usefully studied. AIM: The aim of this study is to assess the ability of preoperative C-reactive protein (CRP) and other inflammatory marker measurements in the prediction of postoperative morbidity after elective colorectal surgery. METHODS: This is a retrospective study which catalogs 218 patients undergoing elective, potentially curative surgery for colorectal neoplasia. Preoperative laboratory results of the full blood count (FBC), C-reactive protein (CRP) and carcinoembryonic antigen (CEA) were recorded. Multivariable analysis was performed to examine preoperative variables against 30-day postoperative complications by type and grade (Clavien-Dindo (CD)), adjusting for age, sex, BMI, smoking status, medical history, open versus laparoscopic operation, and tumor characteristics. RESULTS: Elevated preoperative CRP (≥ 5 mg/L) was significantly predictive of all-cause mortality, with an OR of 17.0 (p < 0.001) and was the strongest factor to predict a CD morbidity grade ≥ 3 (OR 41.9, p < 0.001). Other factors predictive of CD morbidity grade ≥ 3 included smoking, elevated preoperative platelet count and elevated preoperative neutrophil-lymphocyte ratio (OR 15.6, 8.6, and 6.3 respectively, all p < 0.05). CRP values above 5.5 mg/L were indicative of all-cause morbidity (AUC = 0.871), and values above 17.5 mg/L predicted severe complications (AUC = 0.934). CONCLUSIONS: Elevated preoperative CRP predicts increased postoperative morbidity in this patient cohort. The results herein aid risk and resource stratification and encourage preoperative assessment of inflammatory propensity besides simple sepsis exclusion.

What the Radiologist Should Know About Treatment of Peritoneal Malignancy.

OBJECTIVE: The purpose of this article is to discuss the role of the radiologist in the treatment of peritoneal cancer, with focus placed on advanced treatment options and selection of patients with resectable disease for whom complete cytoreduction can be achieved. CONCLUSION: Peritoneal cancers traditionally have been associated with significant morbidity and universal mortality; however, the management of such cancers has evolved substantially. Advanced treatment options, including cytoreductive surgery and intraperitoneal chemotherapy, are associated with significantly improved long-term patient survival. To ensure that patients benefit from aggressive multimodality treatments, the radiologist plays a pivotal role in the multidisciplinary team to ensure careful patient selection, identifying individuals with resectable disease for whom complete cytoreduction can be achieved.

Beyond consent--improving understanding in surgical patients.

BACKGROUND: Little is known of the actual understanding that underlies patient choices with regard to their surgical treatment. This review explores current knowledge of patient understanding and techniques that may be used to improve this understanding. METHODS: MEDLINE and PubMed were searched using the terms "patient understanding," "patient comprehension," "consent," "video," "multimedia," "patient information leaflet," "internet," "test-feedback," "extended discussion," "shared decision making," and "decision aid." All retrieved peer-reviewed studies were included in the review. RESULTS: Understanding in surgical patients is poor. There is little evidence to support the use of information leaflets, although multimedia appears to be effective in improving patient understanding. The internet is not used effectively as an aid to consent by health care providers. Patients with lower educational levels may gain most from additional interventions. Improving patient understanding does not impact on their satisfaction with the treatment they have received but may reduce periprocedural anxiety. CONCLUSIONS: There is a need for greater awareness of patients' information needs, and novel approaches that may enhance decision making through improved understanding are required.

Fibrogenesis in Crohn's disease.

INTRODUCTION: Over one-third of patients with Crohn's disease (CD) will develop an intestinal stricture and the great majority of these will require at least one surgical procedure. While the pathogenesis of inflammation in CD has been extensively investigated, knowledge of stricture pathogenesis remains limited. The aim of this review is to discuss the current understanding of fibrogenesis in CD and to outline potential directions in research and therapeutics. METHODS: The electronic literature (January 1966 to May 2006) on CD-associated fibrosis was reviewed. Further references were obtained by cross-referencing from key articles. RESULTS: CD-associated fibrosis results from chronic transmural inflammation and a complex interplay among intestinal mesenchymal cells, cytokines, and local inflammatory cells. The fibroblast is the key cell type mediating stricture formation. The cytoarchitecure of the bowel wall is altered with disruption of the muscularis mucosa, thickening of the muscularis propria, and deposition of collagen throughout. The cytokine TGF-beta appears critical in this process, acting to increase growth factor and extracellular matrix (ECM) production and dysregulate ECM turnover. Potential therapeutic interventions are likely to concentrate on modulating down-stream targets of TGF-beta. CONCLUSIONS: Greater understanding of the biology of fibrostenosis is likely to yield significant advances in our ability to care for patients with stricturing CD. Potential dividends of this approach include identification of novel therapeutic targets and biomarkers useful for prognostication and therapeutic monitoring.

Transforming growth factor-beta promotes pro-fibrotic behavior by serosal fibroblasts via PKC and ERK1/2 mitogen activated protein kinase cell signaling.

OBJECTIVE: To assess the role of fibroblasts, transforming growth factor (TGF)-beta, and cell signal pathways in promoting fibrosis in Crohn's disease (CD). SUMMARY BACKGROUND DATA: Intestinal strictures are a major source of morbidity in CD. Fibroblasts found at sites of stricture promote fibrogenesis. The mechanisms underlying this pro-fibrotic behavior remain elusive. METHODS: Fibroblasts were isolated from strictured and macroscopically normal serosa in patients with CD and from normal serosa in patients with colorectal cancer. Whole cell connective tissue growth factor (CTGF) and fibronectin expression were determined by Western blot analysis. Fibroblast type I collagen expression was evaluated by real-time PCR, while fibroblast contractile activity was measured using fibroblast populated collagen lattices. Cells were stimulated with TGF-beta1 and inhibitors of the protein kinase C (PKC) and ERK 1/2 mitogen activated protein (MAP) kinase cell signaling pathways. RESULTS: Stricture fibroblasts displayed enhanced constitutive expression of fibronectin. TGF-beta promoted fibroblast CTGF, fibronectin, and type I collagen expression and enhanced fibroblast contractile activity. Inhibition of PKC reduced basal collagen expression and contractile activity in Crohn's fibroblasts and attenuated the effect of TGF-beta on fibroblast CTGF, fibronectin, and collagen I expression as well as fibroblast contractility. ERK 1/2 inhibition had a similar effect on TGF-beta-induced CTGF and fibronectin expression. CONCLUSIONS: TGF-beta is a critical pro-fibrotic growth factor in CD, and its effects are mediated via PKC and ERK 1/2 MAP kinase cell signaling. These pathways may represent novel therapeutic targets for patients with CD characterized by recurrent intestinal stricture formation.