To investigate the effects of bradykinin on reperfusion injury in an experimental intestinal ischemia reperfusion model. We used 32 Wistar-Albino rats. We composed 4 groups each containing 8 rats. Rats in sham group were sacrified at 100 minutes observation after laparotomy. Thirty minutes reperfusion was performed following 50 minutes ischaemia in control group after observing 20 minutes. Ischaemic preconditioning was performed in one group of the study. We performed the other study group pharmacologic preconditioning by infusional administration of 10 μg/kg/minute bradykinin intravenously. We sacrified all of the rats by taking blood samples to evaluate the lactate and lactate dehydrogenase (LDH) after resection of jejunum for detecting tissue myeloperoxidase (MPO) activity. Lactate and LDH levels were significantly higher in control and study groups than the sham group (P0.05). The results were the same for MPO levels. Although definitive cell damage was determinated in the control group by hystopatological evaluation, the damage in the study groups observed was lower in different levels. However, there was no significant difference between the study groups statistically (P>0.05). Either ischeamic preconditioning or pharmacologic preconditioning made by bradykinin reduced the ischemia reperfusion injury at jejunum.
The ectopic stomach mucosa island in the proximal esophagus, which is generally known as the inlet patch or cervical inlet patch, is called as the heterotopic gastric mucosa of the esophagus. Despite its asymptomatic progress, it may cause chest pain, shortness of breath and difficulty in swallowing due to the acid secretion from the ectopic mucosa. The study aimed to present a patient who underwent coronary angiography with an unstable angina pectoris diagnosis by cardiologists for gastric chest pain but found an inlet patch in gastroduodenoscopy.
1 August 2025 in Therapeutics and Clinical Risk Management
Objective: To evaluate the anastomotic leakage (AL) rates in cancerous and non-cancerous intestinal anastomoses and analyze the general risk factors for AL. Methods: The primary endpoint of this study is to investigate whether there is a difference in terms of AL between patients who underwent sigmoid colon resection + colorectal anastomosis due to primary colon cancer (Group 1) and patients with a completely healthy colorectal region who underwent sigmoid colon resection + colorectal anastomosis for use in the orthotopic bladder during radical cystoprostatectomy (Group 2). The secondary endpoint, considering all the patients, is to evaluate and investigate the risk factors affecting the AL rates. Results: A total of 178 patients, including 63 (35.4%) patients in Group 1 and 115 (64.6%) patients in Group 2, were included in the study. The mean age of all patients was 61.7 ± 9.9 years, and there was no statistical difference between the mean ages of the groups (62.8 ± 11.3 vs 60.7 ± 6.1, p = 0.106, respectively). Thirty-six (20.2%) of the patients were female, and 142 (79.8%) were male. There was no significant difference between the groups in terms of AL in the postoperative period. Postoperative AL was seen in three patients (4.8%) and six patients (5.2%) in Group 1 and Group 2, respectively (p = 0.642). According to univariate and multiple logistic regression analysis, the risk of AL increased in patients with comorbidities, in the presence of previous abdominal surgery, in patients with high neutrophil-to-lymphocyte ratio, and patients with postoperative ileus (p values are 0.042, 0.010, 0.029 and 0.048, respectively). Conclusion: Our data suggest that anastomosis due to colon cancer resection does not increase the risk of AL compared with healthy bowel anastomoses. In addition, some clinical factors have been found to compromise anastomotic safety and are risk factors for AL. In addition, some clinical factors have been found to endanger anastomotic safety and are risk factors for AL.