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Objectives: Laparoscopic totally extraperitoneal inguinal hernia repair (TEP) surgery technique includes three key steps: reaching the preperitoneal space, reducing hernias, and placement of mesh. However, reaching the preperitoneal space can be complicated in patients with previous lower abdominal surgeries. This study aimed to assess the feasibility of laparoscopic inguinal TEP in patients with previous prostatectomies. Material and Methods: Inguinal hernia patients who underwent laparoscopic TEP between January 2015 and February 2021 at Koç University Faculty of Medicine, Department of General Surgery, were included in this retrospective study. The operations were performed by five senior surgeons experienced in laparoscopy. Patients were divided into two study groups, as the radical prostatectomy (RP) group which included patients with previous prostatectomy non-RP which included patients without previous radical prostatectomy. Operative time (OT), length of hospital stay (LOS), and postoperative complications were compared within two groups. Results: Three hundred and forty-nine patients underwent laparoscopic TEP, and 27 had previous prostatectomies. Among them, 190 patients had unilateral inguinal hernias, and 159 had bilateral inguinal hernias. Mean age of the patients in the non-RP and RP groups was 58.1 ± 14.7 and 73.9 ± 9.6 years, respectively. Only one (3.7%) case was complicated with urinary tract infection in the RP group, and 10 (3.1%) were complicated in the non-RP group. Complications for the non-RP group include hematomas in six cases, urinary tract infection in three cases, and urinary retention in one case. No significant difference in mean operative time was seen between non-RP and RP groups (p= 0.43). There was no significant difference in the means of the length of hospital stay between the two groups (p= 0.7). Conclusion: Laparoscopic TEP in patients with a previous prostatectomy can be performed safely without prolonging the operative time and increasing the length of hospital stay.
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Background: Anastomotic leakage is a major complication in colorectal surgery, resulting in significant morbidity and mortality rates. Despite substantial progress in surgical technique, anastomotic leakage rates remain stable. An early diagnosis of anastomotic leaks was proven to reduce adverse outcomes and improve survival. Objective: This study aims to find a novel scoring system for detecting anastomotic leaks using inflammatory and nutritional indicators after colorectal surgery. Our purpose was to analyze the diagnostic accuracy of leak scores ((CRPPOD3)(CRPPOD1)∗preoperativealbuminlevel) in predicting postoperative complications. Design: The study included colorectal cancer patients who underwent curative surgery at Koc University Hospital between 2014 and 2018. Patients were categorized into two groups depending on the presence of anastomotic leaks and compared in terms of preoperative albumin levels, CRP levels in postoperative days 1 and 3, anastomotic leakage rates, length of hospital stay, and CRP quotient, which was calculated by dividing POD 3 CRP level to POD 1 CRP level. The bedside leak score is calculated by dividing the CRP quotient by the preoperative albumin level. The predictive value of bedside leak score, CRP quotient, and preoperative albumin levels in estimating anastomotic leakage was analyzed, and a cutoff value for the leak score was calculated. Results: A total of 184 patients were included in the study. The leak score, CRP POD 3-1 ratio, and preoperative albumin levels were found to successfully detect anastomotic leakage. The area under the curve for the leak score was calculated as 0.78. The optimal cutoff value was found to be 50.3 for the bedside leak score, which shows 90.9% sensitivity and 59.3% specificity. Conclusion: The leak score may represent a valuable diagnostic tool for detecting patients at risk for anastomotic leakage after colorectal surgery and planning a better strategy to reduce morbidity and mortality rates and associated costs. However, further multicenter studies with large cohorts are necessary to confirm these results.
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BACKGROUND & AIMS: Loss of claudin 18 (CLDN18), a membrane-spanning tight junction protein, occurs during early stages of development of gastric cancer and associates with shorter survival times of patients. We investigated whether loss of CLDN18 occurs in mice that develop intraepithelial neoplasia with invasive glands due to infection with Helicobacter pylori, and whether loss is sufficient to promote the development of similar lesions in mice with or without H pylori infection. METHODS: We performed immunohistochemical analyses in levels of CLDN18 in archived tissues from B6:129 mice infected with H pylori for 6 to 15 months. We analyzed gastric tissues from B6:129S5-Cldn18tm1Lex/Mmucd mice, in which the CLDN18 gene was disrupted in gastric tissues (CLDN18-knockout mice), or from control mice with a full-length CLDN18 gene (CLDN18+/+; B6:129S5/SvEvBrd) or heterozygous disruption of CLDN18 (CLDN18+/-; B6:129S5/SvEvBrd) that were infected with H pylori SS1 or PMSS1 at 6 weeks of age and tissues collected for analysis at 20 and 30 weeks after infection. Tissues from CLDN18-knockout mice and control mice with full-length CLDN18 gene expression were also analyzed without infection at 7 weeks and 2 years after birth. Tissues from control and CLDN18-knockout mice were analyzed by electron microscopy, stained by conventional methods and analyzed for histopathology, prepared by laser capture microdissection and analyzed by RNAseq, and immunostained for lineage markers, proliferation markers, and stem cell markers and analyzed by super-resolution or conventional confocal microscopy. RESULTS: CLDN18 had a basolateral rather than apical tight junction localization in gastric epithelial cells. B6:129 mice infected with H pylori, which developed intraepithelial neoplasia with invasive glands, had increasing levels of CLDN18 loss over time compared with uninfected mice. In B6:129 mice infected with H pylori compared with uninfected mice, CLDN18 was first lost from most gastric glands followed by disrupted and reduced expression in the gastric neck and in surface cells. Gastric tissues from CLDN18-knockout mice had low levels of inflammation but increased cell proliferation, expressed markers of intestinalized proliferative spasmolytic polypeptide-expressing metaplasia, and had defects in signal transduction pathways including p53 and STAT signaling by 7 weeks after birth compared with full-length CLDN18 gene control mice. By 20 to 30 weeks after birth, gastric tissues from uninfected CLDN18-knockout mice developed intraepithelial neoplasia that invaded the submucosa; by 2 years, gastric tissues contained large and focally dysplastic polypoid tumors with invasive glands that invaded the serosa. CONCLUSIONS: H pylori infection of B6:129 mice reduced the expression of CLDN18 early in gastric cancer progression, similar to previous observations from human gastric tissues. CLDN18 regulates cell lineage differentiation and cellular signaling in mouse stomach; CLDN18-knockout mice develop intraepithelial neoplasia and then large and focally dysplastic polypoid tumors in the absence of H pylori infection.