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Non-Metastatic Esophageal Cancer with Enlarged Carinal Lymph Nodes with Previous Sleeve Gastrectomy
Published in Savio George Barreto, Shailesh V. Shrikhande, Dilemmas in Abdominal Surgery, 2020
Apurva Ashok, Devayani Niyogi, Sabita Jiwnani, George Karimundackal, C.S. Pramesh
A 55-year-old man had a body mass index (BMI) of 42 kg/m2 (weight = 120 kg; height = 1.70 m) and associated comorbidities of type 2 diabetes mellitus, dyslipidemia, and hypertension. He also had a 20 pack-year history of smoking and no previous gastroesophageal reflux disease symptoms. Preoperative upper gastrointestinal endoscopy did not reveal a hiatus hernia, esophagitis, or Helicobacter pylori infection. He underwent an uneventful laparoscopic sleeve gastrectomy followed by an uneventful recovery. In the follow-up period, he lost 70% of his excess weight. Two years after surgery, he complained of new onset reflux symptoms. On evaluation with upper gastrointestinal endoscopy, intestinal metaplasia without atypia was seen at the gastroesophageal junction. He was started on proton pump inhibitors and surveillance endoscopy was advised. However, the patient failed to follow-up. Four years later, he presented with dysphagia and weight loss. An upper gastrointestinal endoscopy revealed an ulcero-proliferative growth in the lower esophagus and gastroesophageal junction, the biopsy of which revealed moderately differentiated adenocarcinoma. A staging positron emission tomography computed tomography (CT) scan confirmed a bulky lower third esophageal malignancy involving the gastroesophageal junction with evidence of gastrohepatic and subcarinal lymphadenopathy.
The Stomach
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
Mucosa changes include dysplasia and metaplasia. Severe dysplasia and intestinal metaplasia are precancerous lesions. Severe dysplasias of the mucosa (grades III and IV) are usually found near benign gastric ulcers as well as cancers. Patients with nonspecific chronic gastritis may have mild to moderate dysplasia with no evidence of cancer, and these are not considered precancerous lesions. However, patients with severe dysplasia without gastric lesions should be closely monitored by frequent gastroscopy, as they have tenfold increase in risk of developing gastric carcinoma. However, in such cases, surgical resections are not warranted. On the other hand, atrophic gastritis (acquired or hereditary) may lead to intestinal metaplasia, which may result in severe dysplasia, then neoplasia. In some cases of gastric carcinoma, such dysplastic changes are not present. These carcinomas are usually of the diffuse type with genetic predisposition.
The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
Helicobacter pylori is a spiral bacterium that has become remarkably well adapted to life at the interface between the surface epithelium of the stomach and the covering layer of secreted mucus. The organism causes direct epithelial cell injury, and also excites a vigorous immune response – two mechanisms for developing a chronic inflammatory reaction. Histologically, the mucosa shows a mixed inflammatory cell response with neutrophil infiltration of the epithelium, and a lymphocyte and plasma cell infiltrate in the stroma (this mixed pattern is often referred to as ‘active chronic gastritis’; Figure 10.23). Severe, long-standing epithelial injury may lead to glandular atrophy. The epithelium may also show an adaptive response termed ‘intestinal metaplasia’, in which a partial or almost complete change in epithelial cell differentiation towards small intestinal type occurs. This benefits the host insofar as the intestinal mucosa is resistant to H. pylori infection.
Characteristic analysis of early gastric cancer after Helicobacter pylori eradication: a multicenter retrospective propensity score-matched study
Published in Annals of Medicine, 2023
Xinyuan Liu, Xinyu Wang, Tao Mao, Xiaoyan Yin, Zhi Wei, Jindong Fu, Jie Wu, Xiaoyu Li
The endoscopic and histopathological characteristics of H. pylori infection-related well-differentiated adenocarcinoma are shown in Figure 3. There was a slightly reddish, transverse, patchy mucosa with a rough surface and slight depression in the center, approximately 28 × 18 mm in size on the side of the lesser curvature in the middle of the gastric body (Figure 3(A)). Under NBI, the boundary was clear, and most of the microstructures were caviar-like with dilated microvessels (Figure 3(B)). The glands in the adenocarcinoma area were mainly thick papillary structures covered with atypical epithelium (Figure 3(C)). Tumor cell atypia was remarkable and the nucleocytoplasmic ratio was significantly increased (Figure 3(D)). In the comparison of the two cases, the map-like redness and depressed features of GC after H. pylori eradication were more obvious, which was in line with the endoscopic characteristics. Intestinal metaplasia was observed in both cases and cell atypia was obvious.
Potential utility of nano-based treatment approaches to address the risk of Helicobacter pylori
Published in Expert Review of Anti-infective Therapy, 2022
Sohaib Khan, Mohamed Sharaf, Ishfaq Ahmed, Tehsin Ullah Khan, Samah Shabana, Muhammad Arif, Syed Shabi Ul Hassan Kazmi, Chenguang Liu
The transmission of H. pylori from person to person can occur through saliva, and it might be spread out through the excrement of food or water, untreated water, poor hygiene, and crowded conditions that largely contribute to the prevalence of H. pylori infection [49]. In brief, it is more likely to be transmitted within the household conditions as it enters the body through the oral cavity and travels to the digestive system, where it infects the stomach or the first part of the small intestine, thereby causing inflammation at the targeted area. The most peculiar characteristic of H. pylori is to survive in the harsh acidic environment of the stomach. It produces urease upon entering the stomach, which then reacts with urea to form ammonia and neutralizes the surrounding environment, consequently leads to the overproduction of the stomach acid (Figure 1) illustrates the invasion of H. pylori infection in the stomach that comprises of six steps; 1) movement of the pathogen through normal stomach lining (mucosa), 2) causing inflammation of the stomach lining (chronic gastritis), 3) loss of stomach cells and weakening of digestive system (atrophic gastritis), 4) transformation of the stomach lining (intestinal metaplasia), 5) initial stages of stomach cancer (dysplasia), and finally cause stomach cancer (gastric adenocarcinoma) [49].
Effectiveness of esophagogastroduodenoscopy in changing treatment outcome in refractory gastro-esophageal reflux disease
Published in Scandinavian Journal of Gastroenterology, 2022
Ye Eun Kwak, Ahmed Saleh, Ahmed Abdelwahed, Mayra Sanchez, Amir Masoud
Our study found that about a half of the patients who underwent EGD solely for refractory GERD symptoms had completely normal EGD findings, and about one-third of the patients had benign or incidental findings. Although 16.3% of the patients had salmon-colored mucosa into the tubular esophagus or irregular z-line which raised suspicion for intestinal metaplasia, only 4% of the patients had biopsy-proven intestinal metaplasia, and none had dysplasia or esophageal adenocarcinoma. Due to the lack of consistent endoscopic report regarding length or extent of columnar mucosa and irregular Z line, gross EGD findings suspicious for intestinal metaplasia may have been over-estimated. Clinicians should accurately describe and document the endoscopic intestinal metaplasia suspected lesions in the reports. Most gastroenterologists perform EGD in patients with persistent GERD symptoms refractory to PPI therapy, due to the prevalent belief that refractory GERD increases the chance of intestinal metaplasia or esophageal adenocarcinoma. However, our study revealed that the prevalence of intestinal metaplasia in patients with refractory reflux symptoms without alarm features is similar to that of intestinal metaplasia in the general population with or without GERD symptoms [9].