19 research outputs found

    Contribution in the study of genetic predisposition of adenic epithelium

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    […] Η παρούσα μελέτη εστιάζει το ενδιαφέρον της στην εκτίμηση της μοριακής έκφρασης δυο γονιδίων, μελών της ομάδας των καλλικρεϊνων, της καλλικρεϊνης 4 και της καλλικρεϊνης 11 στο αδενοκαρκίνωμα του παγκρέατος. Σκοπός της μελέτης είναι η εκτίμηση της μοριακής έκφρασης στον καρκίνο, συγκριτικά με το φυσιολογικό αδενικό επιθήλιο, καθώς και η πιθανή συσχέτιση με το στάδιο και την επιβίωση

    Colonic fibromatosis ‒ a case report and review of the literature

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    Intra-abdominal desmoids tumours are very rare and usually occur in patients with familiar adenomatous polyposis and previous surgery. They represent fibroepithelial growths with varied biologic behavior and therefore different prognosis. We report a case of a 60-year-old patient with a large right colonic mass who underwent right hemicolectomy. Histology proved morphological and immuno-histochemical features indicating fibromatosis. This desmoid tumour appeared growing from the colonic wall rather than the mesocolon, confirming a true colonic wall fibromatosis, a deep isolated form of intra-abdominal fibromatosis. Surgical resection is the treatment of choice in isolated well confirmed lesions. Multidisciplinary team approach is crucial for treatment and prognosis. Resumo: Os tumores desmoides intra-abdominais são muito raros e geralmente ocorrem em pacientes com polipose adenomatosa familiar e cirurgia prévia. Eles representam crescimentos fibroepiteliais com comportamento biológico variado e, portanto, prognóstico diferente. Relatamos o caso de um paciente de 60 anos com grande massa colônica à direita, submetido a hemicolectomia direita. A histologia demonstrou características morfológicas e imuno-histoquímicas que indicavam fibromatose. Este tumor desmoide surgiu crescendo a partir da parede do cólon, e não do mesocólon, confirmando uma verdadeira fibromatose da parede do cólon, uma forma isolada profunda de fibromatose intra-abdominal. A ressecção cirúrgica é o tratamento de escolha em lesões isoladas bem confirmadas. A abordagem multidisciplinar é crucial para o tratamento e prognóstico. Keywords: Desmoid, Tumour, Colon, Palavras-chave: Desmoide, Tumor, Cólo

    The impact of robotic surgery on the treatment of benign esophageal and gastric disease: early experience of a specialized unit

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    Laparoscopic surgery is a well-established approach in the surgical treatment of reflux, hiatal hernia and esophageal motility disorders such as achalasia. Robotic platforms have only recently been incorporated in surgery for esophageal motility disorders and their exact value remains to be determined. In the present study, we present the preliminary results of our early experience with a case series of benign upper gastrointestinal diseases treated using the robotic system in our department. Data on all consecutive patients undergoing surgery for benign upper gastrointestinal tract (UGI) disease during the last 5 years (01/2029–12/2023) was prospectively collected and retrospectively reviewed. All patients attended regular follow-up appointments. Patients with relapse or deterioration of their symptoms were referred for objective testing using high-resolution manometry and/or 24-h impedance pHmetry. A total of 34 patients were included in our series. Fourteen patients with achalasia underwent robotic Heller myotomy and modified Dor fundoplication, sixteen patients underwent hiatal hernia repair with fundoplication and four patients had a Nissen fundoplication for reflux esophagitis. The median postoperative Eckardt score of the patients treated for achalasia was 2 and a median GERD score of 1 was recorded for patients treated for reflux. Two patients with achalasia were evaluated with manometry due to temporary symptom relapse. The manometric findings were unremarkable. The incorporation of the robotic approach in the surgical treatment of benign UGI diseases is safe and feasible with excellent perioperative and postoperative functional results. Further experience and investigation will allow for reliable comparison to the laparoscopic approach. © The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature 2024

    Saliva stress biomarkers in ERCP trainees before and after familiarisation with ERCP on a virtual simulator

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    Background: Stress during the early ERCP learning curve may interfere with acquisition of skills during training. The purpose of this study was to compare stress biomarkers in the saliva of trainees before and after familiarisation with ERCP exercises on a virtual simulator. Methods: Altogether 26 endoscopists under training, 14 women and 12 men, completed the three phases of this study: Phase 1. Three different ERCP procedures were performed on the simulator. Saliva for α-amylase (sAA), Chromogranin A (sCgA), and Cortisol (sC) were collected before (baseline), halfway through the exercise (ex.), and 10 min after completion of the exercise (comp.); Phase 2. A three-week familiarisation period where at least 30 different cases were performed on the virtual ERCP simulator; and Phase 3. Identical to Phase 1 where saliva samples were once again collected at baseline, during, and after the exercise. Percentage differences in biomarker levels between baseline and exercise (Diffex) and between baseline and completion (Diffcomp) during Phase 1 and Phase 3 were calculated for each stress marker. Results: Mean % changes, Diffex and Diffcomp, were significantly positive (p < 0.05) for all markers in both Phase 1 and Phase 3. Diffex in Phase 1 was significantly greater than Diffex in Phase 3 (p < 0.05) for sAA and sCgA. Diffcomp for sAA in Phase 1 was significantly greater than Diffcomp in Phase 3 (p < 0.05). No significant differences were found in sC concentration between Phases 1 and 3. Conclusion: This study shows that familiarisation with the ERCP simulator greatly reduced stress as measured by the three saliva stress biomarkers used with sAA being the best. It also suggests that familiarisation with an ERCP simulator might reduce stress in the clinical setting

    Saliva stress biomarkers in ERCP trainees before and after familiarisation with ERCP on a virtual simulator

    No full text
    BackgroundStress during the early ERCP learning curve may interfere with acquisition of skills during training. The purpose of this study was to compare stress biomarkers in the saliva of trainees before and after familiarisation with ERCP exercises on a virtual simulator.MethodsAltogether 26 endoscopists under training, 14 women and 12 men, completed the three phases of this study: Phase 1. Three different ERCP procedures were performed on the simulator. Saliva for α-amylase (sAA), Chromogranin A (sCgA), and Cortisol (sC) were collected before (baseline), halfway through the exercise (ex.), and 10 min after completion of the exercise (comp.); Phase 2. A three-week familiarisation period where at least 30 different cases were performed on the virtual ERCP simulator; and Phase 3. Identical to Phase 1 where saliva samples were once again collected at baseline, during, and after the exercise. Percentage differences in biomarker levels between baseline and exercise (Diffex) and between baseline and completion (Diffcomp) during Phase 1 and Phase 3 were calculated for each stress marker.ResultsMean % changes, Diffex and Diffcomp, were significantly positive (p < 0.05) for all markers in both Phase 1 and Phase 3. Diffex in Phase 1 was significantly greater than Diffex in Phase 3 (p < 0.05) for sAA and sCgA. Diffcomp for sAA in Phase 1 was significantly greater than Diffcomp in Phase 3 (p < 0.05). No significant differences were found in sC concentration between Phases 1 and 3.ConclusionThis study shows that familiarisation with the ERCP simulator greatly reduced stress as measured by the three saliva stress biomarkers used with sAA being the best. It also suggests that familiarisation with an ERCP simulator might reduce stress in the clinical setting

    Eugenol Reduced ΜPO, CD45 and HMGB1 Expression and Attenuated the Expression of Leukocyte Infiltration Markers in the Intestinal Tissue in Biliopancreatic Duct Ligation-Induced Pancreatitis in Rats

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    Background and Objectives: Inflammation and dysregulation in the intestinal barrier function in acute pancreatitis (AP) trigger pancreatic lesions, systemic inflammatory response, and multiple organ dysfunction. Eugenol, as the main component of clove (Syzygium aromaticum), is known for its antioxidant and anti-inflammatory properties. We studied the potentially beneficial effect of eugenol in a rodent model of biliopancreatic duct ligation-induced AP. Materials and Methods: Rats were randomly divided into three groups: Sham, AP, and AP + eugenol (15 mg/kg/day). Serum TNFα, IL-6, IL-18, and resistin levels, as well as IL-6, TNFα, MPO, HMGB1, and CD45 tissue expression, were determined at various timepoints after the induction of AP. Results: Eugenol attenuated hyperemia and inflammatory cell infiltration in the intestinal mucosal, submucosal, and muscular layers. IL-6 and resistin serum levels were significantly reduced in the AP + eugenol group, while serum TNFα and IL-18 levels remained unaffected overall. TNFα pancreatic and intestinal expression was attenuated by eugenol at 72 h, while IL-6 expression was affected only in the pancreas. MPO, CD45, and HMGB1 intestinal expression was significantly reduced in eugenol-treated rats. Conclusions: Eugenol managed to attenuate the inflammatory response in the intestine in duct ligation-induced AP in rats

    Gastrointestinal Stromal Tumor (GIST) in Long Standing Crohn’s disease on Anti-TNF Therapy

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    Introduction Patients suffering from inflammatory bowel disease (IBD) are at increased risk for developing cancer. Adenocarcinomas are the most commonly observed tumors of the gastrointestinal tract whereas data on gastrointestinal stromal tumor (GIST) in IBD patients is limited. GIST is a neoplasm that originates from the interstitial cells of Cajal in the smooth muscle layers of the gastrointestinal tract. [1] The association between GIST and Crohn’s disease (CD) is debated, as the tumor inconsistently present in areas of inflammatory activity. We report an interesting case of CD maintained on Infliximab, who presented with a flare that revealed GIST in the stomach. To our knowledge, this is the first reported occurrence of GIST in stomach in a patient with CD maintained on anti-TNF therapy. Case Report A 40-year-old Caucasian man with a history of small bowel Crohn’s disease on infliximab therapy presented with a two-day history of abdominal pain, hematochezia, and diffuse joint pain. Upon admission, the patient was hemodynamically stable and afebrile, with a blood pressure of 140/70 mmHg, heart rate of 90 beats per minute, and respiratory rate of 14 per minute. Physical exam was remarkable for abdominal distension and diffuse abdominal tenderness. Complete blood count, comprehensive metabolic panel, and C-reactive protein were within normal range. The patient reported no history of alcohol abuse, smoking, recent abdominal procedures, or trauma. The patient had computed tomography (CT) of the abdomen done that revealed a 2.5-centimeter exophytic mass in the stomach with possible liver metastases (Fig. 1). Endoscopic ultrasound (EUS) guided biopsies of the exophytic mass confirmed gastrointestinal stromal tumor (GIST) on fine needle aspiration and flow cytometry results (Fig. 2,3). The patient underwent surgical resection without complication and is back to his usual state of health. Discussion GIST is the most common mesenchymal neoplasm in the gastrointestinal tract [1,2]. The annual incidence of GIST has been reported as 11-19.6 per million [3,4], however a more recent analysis in 2015 estimates the annual incidence to be 6.8 per million with a 53% predominance in males and 73% predominance in Caucasians [5]. Individuals are typically diagnosed with GIST in their seventh decade of life [5]. Immunologically, it is reported that 70-80% of GIST have a mutation in the KIT gene, leading to a continuously active KIT receptor, independent of its activating ligand [1]. KIT activation leads to overexpression of the protein CD117. In KIT-negative GIST, a small number are observed to have a mutation in platelet-derived growth factor receptor-a (PDGFRA). Dysregulated activation of either of these genes results in uncontrolled cell growth and survival. It is estimated that 10-15% of GIST do not have mutations in either KIT or PDGRFA, and while they are considered wild-type, they are shown to express high levels of KIT [1]. More recently, Novelli et al. found that the presence of proteins CD117 and DOG1 had the highest sensitivity and specificity for GIST [6]. The majority of GIST develop in the stomach (60%), with the jejunum and ileum representing the next most common site of involvement (30%) [7]. Several prognostic factors have been researched, most notably tumor location and mitotic index. Emory et al. found that GIST originating from the esophagus had the highest survival rate, followed by those that arose from the stomach, small bowel, colon/rectum, and omentum/mesentery in decreasing order [8]. Additionally, mitotic index, defined as the number of mitotic figures per high-power field (HPF), is reported an independent prognostic factor, with greater than 10 mitotic figures per 50 HPF showing the largest difference in survival in gastric GIST [8]. Small bowel GIST exhibited minimally different survival curves with respect to mitotic index. Age was also found to be an independent prognostic factor of survival in GIST [8]. Later research by Miettinen demonstrated that larger gastric GIST with a diameter of 10cm and 5 mitotic figures per 50 HPF carried a lower metastatic risk in comparison to gastric GIST with diameter of \u3e 5cm but with \u3e 5 mitotic figures per 50 HPF [9]. This may suggest that in gastric GIST, mitotic index carries the most prognostic value. Miettinen found that in intestinal GIST, a diameter of \u3e 5cm and \u3e 5 mitotic figures per HPF each independently carried a moderate or high risk of metastasis, respectively. Intestinal GIST carried a 39% tumor-related mortality rate, compared to 17% for gastric GIST [10,11]. Currently, surgery is the primary treatment modality for nonmetastatic GIST that is technically amenable to resection. Imatinib, a tyrosine kinase inhibitor (TKI), may be used as neoadjuvant therapy or as initial therapy for nonresectable disease [12]. Imatinib directly binds to the KIT protein and prevents further signaling [1]. This medication first demonstrated favorable treatment effects in 2002, with over 50% of the 147 patients showing at least a partial response to therapy [13]. Some patients develop resistance to Imatinib, prompting the development of alternative TKI therapy. Currently, Sunitinib is FDA approved for Imatinib-resistant GIST [14], with a host of other TKI’s and alternative therapies under investigation [1]. In 2012, Körner examined glucagon-like peptide-2 receptor (GLP-2) expression in a variety of neoplasm and found that 68% of the GISTs expressed this receptor in the intestinal myenteric plexus [15]. Additionally, this receptor was expressed in high density in patients with Crohn’s disease. Interestingly, this expression was absent in active or inactive ulcerative colitis as well as Hirschsprung’s disease [15]. Table 1: GIST with concurrent IBD. Author (ref) Age, Sex IBD Symptoms Location of GIST Imaging or operative findings Pfeffela, 1999 [16] 51, M CD Weight loss, Abdominal pain, Fever, Fatigue Ileum Large tumorous lesions in the right lower abdomen (terminal ileum) measuring 8 × 5 × 6 cm Grieco, 2002 [17] 57, F UC Melena, progressive anemia Ileum Solid mass in the left pelvic cavity with a diameter of 7 cm Mijandrusić Sincić, 2005 [18] 81, M CD Ileus Meckel’s diverticulum Dilated loops of intestine with large packets of gas and anti-peristalsis Kaiser, 2006 [19] 64, M UC Severe bleeding, abdominal distension Omentum 8 cm mass attached to greater omentum Ruffolo, 2010 [20] 59, M UC Rectal bleeding Rectum 0.5 cm GIST located 20 cm from anal adenocarcinoma Theodoropoulos, 2009 [21] 45, M CD Abdominal pain, vomiting, constipation, bloating Jejunum and Ileum 6 mm GIST within jejunoileal intussusception Bocker U, 2008 [22] 26, F CD Abdominal cramping, gastrointestinal bleeding Duodenum Ulcerated lesion noted 140 cm past proximal duodenum on enteroscopy Gianluca, 2016 [7] 38, M CD Asymptomatic Small bowel A mass found along the small bowel Gianluca, 2016 [7] 53, M UC Abrupt postoperative bleeding Stomach No evidences of masses at surgery. Gastric bleeding at endoscopy Present paper 40, M CD Abdominal pain, hematochezia Stomach 2.5 cm exophytic mass in the stomach with possible liver metastases CONCLUSION Our case of Crohn’s disease diagnosed with gastric GIST sheds light on a rare link between two separate disease entities native to the gastrointestinal system. While there exists a well-known association between inflammatory bowel disease and colon cancer, other malignancies are described much less frequently in the literature. The development of gastric GIST with underlying Crohn’s disease is a rare occurrence, but is one that should be kept in mind when evaluating patients with inflammatory bowel disease found to have new masses on imaging. References: 1. Corless CL, Barnett CM, Heinrich MC. Gastrointestinal stromal tumours: Origin and molecular oncology. Nat Rev Cancer. 2011;11(12):865-878. doi:10.1038/nrc3143 2. Katzka DA, Loftus E V., Camilleri M. Evolving molecular targets in the treatment of nonmalignant gastrointestinal diseases. Clin Pharmacol Ther. 2012;92(3):306-320. doi:10.1038/clpt.2012.77 3. Nilsson B, Bümming P, Meis-Kindblom JM, et al. Gastrointestinal stromal tumors: The incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era - A population-based study in western Sweden. Cancer. 2005;103(4):821-829. doi:10.1002/cncr.20862 4. Goettsch WG, Bos SD, Breekveldt-Postma N, Casparie M, Herings RMC, Hogendoorn PCW. Incidence of gastrointestinal stromal tumours is underestimated: Results of a nation-wide study. Eur J Cancer. 2005;41(18):2868-2872. doi:10.1016/j.ejca.2005.09.009 5. Ma GL, Murphy JD, Martinez ME, Sicklick JK. Epidemiology of gastrointestinal stromal tumors in the era of histology codes: Results of a population-based study. Cancer Epidemiol Biomarkers Prev. 2015;24(1):298-302. doi:10.1158/1055-9965.EPI-14-1002 6. Novelli M, Rossi S, Rodriguez-Justo M, et al. DOG1 and CD117 are the antibodies of choice in the diagnosis of gastrointestinal stromal tumours. Histopathology. 2010;57(2):259-270. doi:10.1111/j.1365-2559.2010.03624.x 7. Pellino G, Marcellinaro R, Candilio G, et al. The experience of a referral centre and literature overview of GIST and carcinoid tumours in inflammatory bowel diseases. Int J Surg. 2016;28:S133-S141. doi:10.1016/j.ijsu.2015.12.051 8. Emory TS, Sobin LH, Lukes L, Lee DH, O’Leary TJ. Prognosis of gastrointestinal smooth-muscle (stromal) tumors: Dependence on anatomic site. Am J Surg Pathol. 1999;23(1):82-87. doi:10.1097/00000478-199901000-00009 9. Miettinen M, Lasota J. Gastrointestinal stromal tumors: Pathology and prognosis at different sites. Semin Diagn Pathol. 2006. doi:10.1053/j.semdp.2006.09.001 10. Miettinen M, Sobin LH, Lasota J. Gastrointestinal stromal tumors of the stomach: A clinicopathologic, immunohistochemical, and molecular genetic study of 1765 cases with long-term follow-up. Am J Surg Pathol. 2005;29(1):52-68. doi:10.1097/01.pas.0000146010.92933.de 11. Miettinen M, Makhlouf H, Sobin LH, Lasota J. Gastrointestinal stromal tumors of the jejunum and ileum: A clinicopathologic, immunohistochemical, and molecular genetic study of 906 cases before imatinib with long-term follow-up. Am J Surg Pathol. 2006;30(4):477-489. doi:10.1097/00000478-200604000-00008 12. Demetri GD, Benjamin R, Blanke CD, et al. NCCN Task Force Report: Optimal Management of Patients with Gastrointestinal Stromal Tumor (GIST)--Expansion and Update of NCCN Clinical Practice Guidelines. Vol 2 Suppl 1.; 2004. 13. Eorge D Emetri GD, Argaret Von Ehren MM, Harles B Lanke CD, et al. The New Eng Land Jour Nal of Medicine EFFICACY AND SAFETY OF IMATINIB MESYLATE IN ADVANCED GASTROINTESTINAL STROMAL TUMORS A BSTRACT Background Constitutive Activation of KIT Receptor. Vol 347.; 2002. www.nejm.org. Accessed January 29, 2020. 14. Demetri GD, van Oosterom AT, Garrett CR, et al. Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial. Lancet. 2006;368(9544):1329-1338. doi:10.1016/S0140-6736(06)69446-4 15. Körner M, Rehmann R, Reubi JC. GLP-2 receptors in human disease: High expression in gastrointestinal stromal tumors and Crohn’s disease. Mol Cell Endocrinol. 2012;364(1-2):46-53. doi:10.1016/j.mce.2012.08.008 16. Pfeffel F, Stiglbauer W, Depisch D, Oberhuber G, Raderer M, Scheithauer W. Coincidence of Crohn’s disease and a high-risk gastrointestinal stromal tumor of the terminal ileum. Digestion. 1999. doi:10.1159/000007684 17. Grieco A, Cavallaro A, Potenza AE, et al. Gastrointestinal stromal tumor (GIST) and ulcerative colitis. J Exp Clin Cancer Res. 2002. 18. Mijandrusic Sincic BM, Kovać D, Jašić M, Grbas H, Uravić M, Depolo A. Crohn’s disease and a gastrointestinal stromal tumor in an 81-year-old man - A rare coincidence. Zentralbl Chir. 2005. doi:10.1055/s-2005-918206 19. Kaiser AM, Kang JC, Tolazzi AR, Sherrod AE, Beart RW. Primary solitary extragastrointestinal stromal tumor of the greater omentum coexisting with ulcerative colitis. Dig Dis Sci. 2006;51(10):1850-1852. doi:10.1007/s10620-006-9217-y 20. Ruffolo C, Massani M, Rossi S, Caratozzolo E, Antoniutti M, Bassi N. Adenocarcinoma and GIST in ulcerative colitis. Int J Colorectal Dis. 2010;25(8):1027-1028. doi:10.1007/s00384-010-0905-x 21. Theodoropoulos GE, Linardoutsos D, Tsamis D, et al. Gastrointestinal stromal tumor causing small bowel intussusception in a patient with Crohn’s disease. World J Gastroenterol. 2009;15(41):5224-5227. doi:10.3748/wjg.15.5224 22. Böcker U, Löhr JM, Marx A. Twenty-six-year-old female with assumed Crohn’s disease and a gastrointestinal stromal tumor: Response. Inflamm Bowel Dis. 2009;15(4):489-490. doi:10.1002/ibd.2065
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