Background: The pathogenesis of duodenal ulcer has never been explained although the first description of this disease in medical literature appeared in 1817. Marshall et al. concluded that Helicobacter pylori was the most important etiological factor for duodenal ulcer in 1988, but the etiology based on this bacterium is controversial and how the bacterial infection leads to ulceration is presently unknown. Objectives: This study aims to identify the cause of duodenal ulcer, address the controversial issues surrounding Helicobacter pylori, elucidate the roles of gastric acid, and describe the pathological process of duodenal ulceration. Methods: First, a comprehensive systematic review on peptic ulcers (including gastric ulcer and duodenal ulcer) was conducted and the results were summarized. Second, a recently published causal relationship was employed to identify the etiology of peptic ulcers. Third, novel concepts and methods were applied to analyze the existing data on duodenal ulcer. Results: The etiology of duodenal ulcer and the roles of Helicobacter pylori and gastric acid in this disease were identified. The controversies surrounding Helicobacter pylori were addressed, and many characteristics and phenomena/observations of duodenal ulcer were elucidated. The pathological process of duodenal ulceration was described. Conclusion: Existing data accumulated over the past 300 years was sufficient, when analyzed using novel concepts, to understand the pathogenesis of duodenal ulcer. Duodenal ulcer is not an infectious disease caused by the infection of Helicobacter pylori, but a psychosomatic disease triggered by psychological stress. Helicobacter pylori plays a secondary role in only the late phase of duodenal ulceration.

Presenting a case report about an occurrence of duodeno-duodenal intussusception in a 17-year-old female patient. Intussusception is typically observed in children. The patient has a history of recurrent pain and vomiting for four days. During the examination tenderness in the epigastric area worsened when the legs were elevated. An initial X-ray of the abdomen was done and the findings were normal. Subsequent ultrasound and abdominal CECT scans of the abdomen revealed intussusception involving the 2^nd, 3^rd, and 4^th part of the duodenum ampulla of Vater and pancreas without any identifiable cause for this condition. There was no abnormal thickening of the wall. This case shows how using radiological imaging and surgical management helps to prevent severe complications in cases like duodeno-duodenal intussusception in adults.

It is currently believed that the cause of superior mesenteric artery syndrome (SMAS) is compression of the duodenum in the angle between the aorta and superior mesenteric artery (SMA). It is recognized that a decrease in aortomesenteric angle (AMA) <25° and intervascular distance < 8 mm, caused by fat loss, is characteristic of SMAS. Based on these statements, surgeons operate on patients with symptoms of dyspepsia only based on a reduction of AMA. This study is devoted to the analysis of the literature, including four own studies on this issue. Results: Measurement of the length of the constriction in the third part of the duodenum on radiograms from available sources showed that its true length ranged from 2.5 to 4.2 (3.30±0.15) cm and began a few centimeters cranial to the AMA. Therefore, it could not have been caused by compression in the AMA. In terms of length (3.20±0.15 cm) and location, this constriction corresponded to Ochsner’s sphincter, which normally short-term contracts to prevent the penetration of an acid bolus into the jejunum. Conscientious studies have shown that AMA is proportional to BMI, i.e., a decrease in AMA is observed in all thin people. An analysis of 211 cases of SMAS made it possible to differentiate two types of diseases. In 101 patients, the disease occurred acutely 1–53 (8.2 ± 1.9) days after stressful situations, accompanied by a catabolic reaction and hypersecretion of hydrochloric acid. In 110 patients, SMAS developed 3-72 (17.2±3.2) months after the diagnosis of acid-dependent diseases. Conclusion: The analysis of the literature led to the conclusion that hypersecretion of hydrochloric acid causes damage to the upper level of the digestive system, including duodenal dyskinesia. One of the manifestations of duodenal dyskinesia is an increase in tone and hypertrophy of the Ochsner’s sphincter. The clinic of the disease depends on the varying degree of Ochsner’s sphincter dyskinesia. In severe cases, partial or complete intestinal obstruction. New ideas about the etiology and pathogenesis of the so-called SMAS have made it possible to propose a tactic for the diagnosis and treatment of Ochsner’s sphincter dyskinesia, where there is no place for surgical treatment.

Metabolic surgery can promote integrated physiologic improvement to ameliorate metabolic illness, particularly type 2 diabetes. Nevertheless, the therapeutic scope has been limited by unexpectedly inconsistent surgical outcomes. Therefore, the purpose of this study is to overcome the obstacles by determining the core mechanism of conflicting results. The surgical anatomy, clinical course, and outcomes of various metabolic surgeries, including modified types of duodenal-jejunal bypass procedures, were compared to comprehend specific surgical patterns from distinctive perspectives. Patients in exclusively nonobese groups are subjected to avoid compounding by weight fluctuations. During intestinal anastomosis, the epithelial identity of the succeeding intestine is replaced by that of the proximal epithelium through altered crosstalk between the epithelium and opposing mesenchymal cells. The rapid turnover rate and compensatory proliferation of the succeeding intestine accelerate the propagation of the replaced epithelium. Propagation of replaced epithelium could provoke inconsistent outcomes of metabolic surgery. The major determinants of the conflicting results of metabolic surgery are inadequate duodenal exclusion and inappropriate length of the biliopancreatic limbs. The replaced enteroendocrine cells during regeneration provoke inconsistent outcomes of metabolic surgery. The critical factors are the type and density of enteroendocrine cells distributed at the terminal end of the preceding proximal intestine.

Background: During esophagogastroduodenoscopy performed with colonoscopy, gastric and duodenal erythema, erosions, and ulcerations are often observed. This investigation was designed to review the prevalence of gastroduodenal lesions in patients who underwent wireless capsule endoscopy using standard bowel cleansing preparations, but no endoscopy or sedation. Methods: A retrospective analysis was conducted on patients referred for capsule endoscopy. Records and capsule reports were reviewed for patient demographics, preparation prescribed, procedural indications, and gastroduodenal findings. Preparations studied included polyethylene glycol lavage (PEG), PEG plus bisacodyl (PEG+bis), bisacodyl (bis), oral sulfate solution (OSS) and no prep. Results: Among the 1236 records, 498 (40.3%) were men and 738 (59.7%) were women. The mean age was 57 years +/- 17.8 years SD. The percentage of patients with lesions after any bowel preparation was 52.7% for gastric lesions and 23.6% for duodenal lesions. The percentage of patients with gastroduodenal lesions was 58.3% with prep, compared to 38.2% without prep. These findings were statistically significant with RR 1.53 [1.19-1.94] (p-value=0.00004). This difference was more pronounced in the OSS group RR 1.65 [1.29-2.1] and bisacodyl groups RR 1.64 [1.25-2.15] compared to the PEG group RR 0.95 [0.7-1.3]. Conclusion: This study showed that patients undergoing wireless capsule endoscopy who received bowel preparations had a significant increase in gastric and duodenal lesions. Of the preparations studied, OSS was associated with the greater number of gastroduodenal lesions, while PEG was the least associated with lesions with an occurrence similar to the non-prep group. The clinical significance of these lesions remains undetermined.

Metabolic surgery can promote comprehensive physiological improvements to alleviate metabolic disorders, particularly for patients with type 2 diabetes. Nevertheless, the therapeutic scope has been limited owing to unexpectedly inconsistent surgical outcomes. Therefore, this study to overcome these obstacles by determining the fundamental mechanism underlying the conflicting outcomes. The surgical anatomy, clinical course, and outcomes of various metabolic surgeries, including modified duodenal-jejunal bypass (DJB) procedures, were compared to understand the specific surgical patterns from different perspectives comprehensively. Patients in the nonobese group were exclusively included to prevent confounding effects from overweight patients with type 2 diabetes. Following intestinal anastomosis, the epithelial identity of the succeeding intestine was replaced by that of the proximal epithelium owing to altered crosstalk between the epithelium and opposing mesenchymal cells. Subsequent intestinal compensatory proliferation and rapid turnover rate accelerate the spread of the replaced epithelium. The main factors contributing to inconsistent outcomes of metabolic surgery are inadequate duodenal exclusion and inappropriate biliopancreatic limb length. Replacement of enteroendocrine cells during regeneration can lead to inconsistent outcomes in metabolic surgery. The type and density of enteroendocrine cells distributed at the terminal end of the proximal intestine play a significant role in diverse outcomes of metabolic surgery.

Celiac disease (CD) is a genetically conditioned autoimmune process that appears in susceptible people. It can affect people of any age, and slightly predominates in females. It has a fairly homogenous global distribution, with an average prevalence of 1-2%, the frequency having increased in recent decades. The only effective treatment is a strict and permanent gluten-free diet (GFD), although the level of compliance with it is poor, at about 50% of cases. To monitor the effectiveness of the GFD, several procedures involving various approaches are employed: a) periodic interviews by nutritionists; b) clinical follow-up; c) serological controls of specific antibodies; d) endoscopies with collection of duodenal biopsies; e) structured questionnaires; f) determination of gluten peptides derived from gluten in feces and/or urine. All of these procedures are useful when applied, alone or in combination, depending on the cases. Some patients will only need to consult to their doctors, while others will require a multidisciplinary approach to assess their compliance with the GFD. In children, normalization of duodenal mucosa was achieved in 95% of cases within 2 years, while it is more delayed in adults, whose mucosa take longer to heal completely.