Background
Although self‐expandable metal stent (SEMS) placement as bridge to surgery (BTS) in patients with left‐sided obstructing colonic cancer has shown promising short‐term results, it is used infrequently owing to uncertainty about its oncological safety. This population study compared long‐term oncological outcomes between emergency resection and SEMS placement as BTS.
Methods
Through a national collaborative research project, long‐term outcome data were collected for all patients who underwent resection for left‐sided obstructing colonic cancer between 2009 and 2016 in 75 Dutch hospitals. Patients were identified from the Dutch Colorectal Audit database. SEMS as BTS was compared with emergency resection in the curative setting after 1 : 2 propensity score matching.
Results
Some 222 patients who had a stent placed were matched to 444 who underwent emergency resection. The overall SEMS‐related perforation rate was 7·7 per cent (17 of 222). Three‐year locoregional recurrence rates after SEMS insertion and emergency resection were 11·4 and 13·6 per cent (P = 0·457), disease‐free survival rates were 58·8 and 52·6 per cent (P = 0·175), and overall survival rates were 74·0 and 68·3 per cent (P = 0·231), respectively. SEMS placement resulted in significantly fewer permanent stomas (23·9 versus 45·3 per cent; P < 0·001), especially in elderly patients (29·0 versus 57·9 per cent; P < 0·001). For patients in the SEMS group with or without perforation, 3‐year locoregional recurrence rates were 18 and 11·0 per cent (P = 0·432), disease‐free survival rates were 49 and 59·6 per cent (P = 0·717), and overall survival rates 61 and 75·1 per cent (P = 0·529), respectively.
Conclusion
Overall, SEMS as BTS seems an oncologically safe alternative to emergency resection with fewer permanent stomas. Nevertheless, the risk of SEMS‐related perforation, as well as permanent stoma, might influence shared decision‐making for individual patients.
SummaryActivation of the complement system contributes to the pathogenesis of ischaemia/reperfusion (I/R) injury. We evaluated inhibition of the classical pathway of complement using C1-inhibitor (C1-inh) in a model of 70% partial liver I/R injury in male Wistar rats ( n = = = = 35). C1-inh was administered at 100, 200 or 400 IU/kg bodyweight, 5 min before 60 min ischaemia (pre-I) or 5 min before 24 h reperfusion (end-I). One hundred IU/kg bodyweight significantly reduced the increase of plasma levels of activated C4 as compared to albumin-treated control rats and attenuated the increase of alanine aminotransferase (ALT). These effects were not better with higher doses of C1-inh. Administration of C1-inh pre-I resulted in lower ALT levels and higher bile secretion after 24 h of reperfusion than administration at end-I. Immunohistochemical assessment indicated that activated C3, the membrane attack complex C5b9 and C-reactive protein (CRP) colocalized in hepatocytes within midzonal areas, suggesting CRP is a mediator of I/R-induced, classical complement activation in rats. Pre-ischaemic administration of C1-inh is an effective pharmacological intervention to protect against liver I/R injury.
This study examined the effects of 1 degrees C hypo- or hyperthermia on in vivo liver ischemia and reperfusion (I/R) injury in 15 fasted male Wistar rats. Rats were ventilated, and rectal temperature was maintained at 36, 37 (normothermic), or 38 degrees C. In all rats, 70% liver ischemia was induced by clamping the afferent vessels to the median and left lateral lobes for 60 min, and reperfusion was allowed for 90 min. Changes in plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alpha-glutathione S-transferase (alpha-GST) levels were measured, hemodynamics and bile secretion were monitored, and arterial blood-gas analysis was performed. All ventilated rats showed a normal pH, arterial PCO(2), and arterial PO(2). AST, ALT, and alpha-GST levels were significantly higher in the 38 degrees C group when compared with the 36 and 37 degrees C groups after ischemia. No differences in bile secretion were found between all groups. Histopathological alterations were in agreement with AST, ALT, and alpha-GST levels in plasma. We conclude that a decrease of only 1 degrees C in body temperature significantly attenuates liver I/R injury, whereas an increase of 1 degrees C significantly increases liver I/R injury.
The contribution of acidosis to the development of reperfusion injury is controversial. In this study, we examined the effects of respiratory acidosis and hypoxia in a frequently used in vivo liver ischemia and reperfusion (I/R) injury rat model. Rats were anesthetized with intraperitoneal anesthetics and subjected to partial liver ischemia (70%) for 60 min and subsequent reperfusion for 90 min under the following conditions: 1) no acidosis and normoxia, maintained by controlled ventilation; 2) acidosis and normoxia, maintained by passive supply with oxygen; 3) no acidosis and hypoxia, maintained by bicarbonate administration without respiratory support; and 4) acidosis and hypoxia, i.e., without respiratory support or pH correction. Changes in plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured as parameters of hepatocellular injury, and bile secretion was monitored. AST and ALT levels were lowest in the ventilated rats and highest in the bicarbonate-treated rats. No differences in bile secretion were found between groups. Our results suggest that respiratory acidosis significantly enhanced liver I/R injury under normoxic conditions, whereas respiratory acidosis significantly reduced liver I/R injury under hypoxic conditions.
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