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Aim: This study aimed to predict cases of acute superior mesenteric artery (SMA) occlusion requiring bowel resection using occlusion site and time from symptom onset to diagnosis at five Japanese institutions. Advances in imaging, endovascular treatment, and perioperative management have improved the clinical outcomes of patients with acute SMA occlusion; however, in clinical practice it remains difficult to effectively determine patients requiring bowel resection. Methods: We retrospectively analyzed the data of 48 patients (mean age: 82.5 y; male: 37.5%) diagnosed with acute SMA occlusion between June 2009 and August 2018. Background data of patients who required and did not require bowel resection were compared. A multivariable predictive model was developed using the time from symptom onset to diagnosis and whether SMA occlusion was proximal, including the origin of the middle colic artery. Results: Fifteen patients (31.3%) died during the hospital stay. Atrial fibrillation (83.3%) was the most common comorbidity. The median time from symptom onset to diagnosis was 13.0 (interquartile range, 4.75-24.0) h. Laparotomy, bowel resection, and thrombus embolectomy were performed in 41 (85.4%), 26 (54.2%), and 21 (43.8%) patients, respectively. A logistic regression model achieved 78.6% sensitivity in predicting cases not requiring bowel resection. Proximal occlusion was significantly associated with the requirement for bowel resection (P = .039). Conclusion: The time from symptom onset to diagnosis and occlusion site contributed to high sensitivity in determining the need for bowel resection in patients with acute SMA occlusion. Further prospective studies are warranted to investigate the clinical impact of this model.
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INTRODUCTION: Since its discovery in 2002, presepsin (P-SEP) has been reported to be useful in the early diagnosis of sepsis and has been evaluated in many clinical studies. However, as antibodies that bind to mouse P-SEP were previously unavailable, serum P-SEP levels in mice are limited. This study used a P-SEP enzyme-linked immunosorbent assay kit to evaluate the changes in serum P-SEP levels in mouse sepsis models compared with changes in other inflammatory markers and determine whether P-SEP can function as a biomarker specific to bacterial infections. METHODS: Sepsis was induced in mice via cecal ligation and puncture (CLP), induction with lipopolysaccharide (LPS), and cecal ligation (CL) model was created as a control for the CLP model, following which clinical biomarkers (P-SEP, C-reactive protein, and procalcitonin) were evaluated. RESULTS: The 48-h survival rates in the CLP, CL, and LPS-induced sepsis models were 67%, 89%, and 57%, respectively. Serum C-reactive protein levels did not increase in the CLP and CL models within 24 h but significantly increased in the LPS-induced sepsis model. Serum procalcitonin levels increased in the CLP and CL models and especially increased in the LPS-induced sepsis model. In contrast, an increase in serum P-SEP level was found in the CLP model at 6 h compared with those at baseline, the CL, and LPS-induced sepsis models. CONCLUSIONS: Mouse P-SEP is elevated early in infection and more specific to bacterial infection compared with other biomarkers.