Background Despite advances in surgery and intensive perioperative care, fecal peritonitis secondary to colonic perforation is associated with high rates of morbidity and mortality. This study was performed to review the outcomes of patients who underwent colonic perforation surgery and to evaluate the prognostic factors associated with mortality.
Methods A retrospective analysis was performed on 224 consecutive patients who underwent emergency colonic perforation surgery between January 2008 and May 2019. We divided the patients into survivor and non-survivor groups and compared their surgical outcomes.
Results The most common cause of colon perforation was malignancy in 54 patients (24.1%), followed by iatrogenic perforation in 41 (18.3%), stercoral perforation in 39 (17.4%), and diverticulitis in 37 (16.5%). The sigmoid colon (n=124, 55.4%) was the most common location of perforation, followed by the ascending colon, rectum, and cecum. Forty-five patients (20.1%) died within 1 month after surgery. Comparing the 179 survivors with the 45 non-survivors, the patient characteristics associated with mortality were advanced age, low systolic blood pressure, tachycardia, organ failure, high C-reactive protein, high creatinine, prolonged prothrombin time, and high lactate level. The presence of free or feculent fluid, diffuse peritonitis, and right-sided perforation were associated with mortality. In multivariate analysis, advanced age, organ failure, right-sided perforation, and diffuse peritonitis independently predicted mortality within 1 month after surgery.
Conclusion Age and organ failure were prognostic factors for mortality associated with colon perforation. Furthermore, right-sided perforation and diffuse peritonitis demonstrated a significant association with patient mortality.
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Cancer incidence has been increasing steadily and is the leading cause of mortality worldwide. Gastric cancer is still most common malignancy in Korea. Cancer initiation and progression are multistep processes involving various growth factors and their ligands. Among these growth factors, we have studied hepatocyte growth factor (HGF), which is associated with cell proliferation and invasion, leading to cancer and metastasis, especially in gastric cancer. We explored the intercellular communication between HGF and other surface membrane receptors in gastric cancer cell lines. Using complimentary deoxyribonucleic acid microarray technology, we found new genes associated with HGF in the stomach cancer cell lines, NUGC-3 and MKN-28, and identified their function within the HGF pathway. The HGF/N-methyl-N’-nitroso-guanidine human osteosarcoma transforming gene (c-MET) axis interacts with several molecules including E-cadherin, urokinase plasminogen activator, KiSS-1, Jun B, and lipocalin-2. This pathway may affect cell invasion and metastasis or cell apoptosis and is therefore associated with tumorigenesis and metastasis in gastric cancer.
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