The Double Pylorus

Double pylorus is a rare condition consisting of a double communication between the gastric antrum and the duodenal bulb. Double pylorus can occur as a congenital abnormality or as a complication of peptic ulcer disease. Although almost 100 patients with acquired double pylorus have been described (1,2), only a few patients with congenital double pylorus have been described, and, in only one patient, this anomaly was recognized in childhood (3). Herein we describe another child with congenital double pylorus, who presented with gastric outlet obstruction.

INTRODUCTION: A double pylorus channel can be congenital or acquired. Acquired double pylorus is thought to be the result of a gastric or duodenal ulcer forming a fistula between the prepyloric antrum and the duodenal bulb. Although it is a rare endoscopic finding, seen in only 0.001%–0.4% of upper gastrointestinal endoscopies1, when acquired, it signifies peptic ulcer disease (PUD) which needs risk factor modification and treatment. CASE DESCRIPTION/METHODS: A 50-year-old man with alcohol use disorder, newly diagnosed alcoholic cirrhosis and recent NSAID use presented with confusion, melena and dark emesis. His physical exam was notable for hypotension (BP 86/55 mmHg), somnolence, confusion and positive asterixis. Laboratory values were remarkable for hemoglobin of 5 g/dL, BUN of 48 mmol/L, platelets of 271 × 109/L and INR of 2. Management included fluid resuscitation, blood transfusion, proton pump inhibitor and octreotide drip. Once hemodynamically stabilized, an upper endoscopy was performed revealing blood in the gastric body, two antral ulcers with visible vessels, but no endoscopic stigmata of liver disease. Adjacent to the pylorus, a slit-like channel connecting the prepyloric antrum to the duodenal bulb was noted and traversed with the endoscope. Helicobacter pylori work up revealed a positive serum antibody. Patient did well post-procedure and received Helicobacter pylori eradication treatment and counseling on alcohol cessation and NSAID avoidance. DISCUSSION: In contrast to congenital double pylorus which is an incidental finding, patients with acquired double pylorus often present with symptoms of PUD. In this case, likely culprits included NSAIDs and Helicobacter pylori. It should be distinguished from other similar appearing endoscopic findings such as gastric diverticulum, as risk factors for PUD need to be investigated in patients with an acquired double pylorus. While treatment with acid suppression and Helicobacter pylori eradication should be pursued, the fistula tract often persists despite treatment2. Endoscopic recognition and familiarity are key to ensure appropriate risk modification, treatment and prevention of endoscopic complications with side-viewing scopes.

Effects of Helicobacter pylori and Nonsteroidal Anti-Inflammatory Drugs on Peptic Ulcer Disease: A Systematic Review

Non-ulcer Dyspepsia and Duodenal Eosinophilia: An Adult Endoscopic Population-Based Case-Control Study

Double pylorus (DP), or duplication of the pylorus, is an uncommon condition that can be either congenital or acquired. Acquired DP (ADP) occurs when a peptic ulcer erodes and creates a fistula between the duodenal bulb and the distal stomach. The clinical features and endoscopic characteristics of four patients with ADP were reviewed and compared with previously reported cases. An accessory channel connects the lesser curvature of the prepyloric antrum with the duodenal bulb, and in all cases, a peptic ulcer was located in or immediately adjacent to the accessory channel. In one of the patients, the bridge between the double-channel pylorus disappeared, resulting in a single large opening and duodenal kissing ulcer after two years and three months. Finally, nonsteroidal anti-inflammatory drugs, Helicobacter pylori and other risk factors associated with ADP are assessed.

Double pylorus, also known as acquired double pylorus, is a rare condition defined as a gastrointestinal fistula connecting stomach antrum and duodenal bulb. The prevalence of double pylorus ranges from 0.001 to 0.4% by esophagogastroduodenoscopy (EGD). Although the etiology is unknown, the formation of double pylorus is related to Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID). The development of the occurrence of double pylorus is still unknown, but many systemic diseases play a role. We present the case of a 59-year-old man who was admitted to Dr. Soetomo General Hospital with hematemesis and melena. The patient had a history of diabetes mellitus since 3 years and consumption of medicinal herbs for myalgia, which was suspected of NSAIDs for the past 5 months. The patient had anemia with hemoglobin at 8.3 g/dL, enterogenous azotemia with blood urea nitrogen 28 mg/dL and serum creatinine 1.14 mg/dL. At EGD, double pylorus was found and accompanied by gastric ulcer, a giant white base ulcer, part of it covered by clotting without any sign of active bleeding. Biopsy revealed chronic inactive gastritis, and no H. pylori was found. Treatment mainly depends on gastrointestinal acid suppression through a proton pump inhibitor (PPI). The patient was given a high-dose PPI and a mucosal protective agent. He was treated for 1 week and had improved complaints.

The Prevalence of Idiopathic Peptic Ulcer and Changing Trend of Peptic Ulcer Disease and Helicobacter Pylori Infection Between 10 Years in Korea

A 62-year old man, who was newly diagnosed as a case of cryptogenic cirrhosis, underwent screening esophago-gastro-duodenum (OGD) scopy for varices; he had no previous history of hepatic decompensation, upper gastrointestinal symptoms, other comorbidities, prolonged drug or alcohol intake. On physical examination, vital signs were stable and moderate ascites was detected. There were two openings noted in the gastric antrum, one of them was true pylorus and the other was a fistula (Figure 1a).The OGD scopy also showed small esophageal varices and mild portal hypertensive gastropathy seen as snake-skin appearance of the gastric mucosa surrounding the two openings (Figure 1b). The OGD scope could be passed into the duodenum through the pylorus but not from the fistulous tract. There was no evidence of peptic ulceration or scarring between the two openings. Double pylorus (DP) is a rare finding reported in 0.06%-0.4% of upper gastrointestinal endoscopies, [1] characterized by the presence of two openings from the gastric antrum to the duodenal bulb, which may be congenital or acquired. The fistula remained open in the majority of patients (60%), converged with the normal pyloric ring in 25% of patients and disappeared in 5% on long term follow-up [2]. The most common cause of acquired DP is a benign gastric ulcer. [1] Other causes of acquired DP are malignant ulcers, systemic diseases such as diabetes mellitus, chronic renal failure, systemic lupus erythematous, etc. Also, prolonged intake of steroids, NSAID’S and alcohol may lead to fistula formation [1,3]. In congenital double pylorus, an error of canalization seems to occur [4]. In our case, possibility of a peptic etiology for the additional opening to the duodenum was more likely. A biopsy was taken from the region between the two openings, which showed normal mucosa and a muscularis mucosae layer. Apart from a mild gastritis, no other pathology (chronic peptic ulcer, ulcerated malignancy) suggesting an acquired origin of the double pylorus was observed. Therefore, the case was considered to be congenital in origin. To our knowledge, only a few cases of DP in patients with liver diseases have been reported in the literature [5-7]. We report a unique case of congenital DP in a cirrhotic patient which is first of its kind to be reported.

To evaluate the accuracy of several methods aimed to detect Helicobacter pylori stool antigens in patients with upper gastrointestinal bleeding. Thirty-four patients with upper gastrointestinal bleeding because of peptic ulcer were included. The first stool sample during hospitalization was collected, and stool antigens were determined with: polyclonal enzyme-linked immunosorbent assay (Premier-Platinum-HpSA); monoclonal enzyme-linked immunosorbent assay (Amplified-IDEIA-HpStAR); and rapid monoclonal immunochromatographic test (ImmunoCard-STAT HpSA). A patient was considered infected when H. pylori was diagnosed with invasive tests (rapid urease test or histology) or with (13)C-urea breath test. When all tests were negative, a new breath test was repeated after stopping proton pump inhibitors. All patients were infected and, therefore, only sensitivity of the tests could be calculated: polyclonal enzyme-linked immunosorbent assay (74%), monoclonal enzyme-linked immunosorbent assay (94%), and rapid monoclonal immunochromatographic test (60%; concordance between the two observers was high, kappa = 0.9). Neither the presence of maelena nor the delay in obtaining stool samples explained false negatives. Neither the polyclonal enzyme-linked immunosorbent assay stool antigen test nor the rapid immunochromatographic stool antigen test can be recommended to diagnose H. pylori infection in patients with upper gastrointestinal bleeding. However, the monoclonal enzyme-linked immunosorbent assay stool antigen test is highly sensitive for detecting the infection in patients with this complication, although more studies are necessary to evaluate the specificity of the method.

Gastric diverticulum causing gastric outlet obstruction in the setting of duodenal atresia

INTRODUCTION: Peptic ulcer disease (PUD) develops in approximately 25% of chronic users of non-steroidal anti-inflammatory drugs (NSAIDs). The incidence of uncomplicated PUD has been declining over the past 3 decades unlike that of complicated PUD especially in the elderly. We aimed to evaluate physician compliance with the American College of Gastroenterology (ACG) guidelines on the prevention of NSAID-related PUD complications in a tertiary academic setting. METHODS: We examined the Saint Louis University Hospital medical record database for a 9-month period extending from April 2018 until December 2018. Using this database, we identified 2,064 adult elderly patients (>64 years old) who were chronic (>3 months) users of low dose aspirin (81 mg once daily). We performed a retrospective analysis of patients who were at least on aspirin and had an indication for PUD prophylaxis as per ACG guidelines. Data collected from patient charts included age, gender, relevant medications (including proton pump inhibitors (PPI), aspirin, P2Y12 inhibitors, direct oral anticoagulants (DOACs), warfarin, or oral steroids), and whether prophylaxis was provided as per the ACG guidelines. RESULTS: A total of 301 adult elderly patients who were at least on aspirin and had an indication for PUD prophylaxis were identified in this study. The mean age was 75 years old. Six percent of included patients had a history of peptic ulcer disease. In addition to aspirin, patients were using P2Y12 inhibitors (clopidogrel or ticagrelor, 50%), DOACs (24%), warfarin (11%), or steroids (9%). DOAC users were prescribed apixaban (16%), rivaroxaban (7%), or dabigatran (1%) (Table 1). All antiplatelets, anticoagulants, and steroids were prescribed by non-gastroenterologists. Only 35% of patients with an indication for PUD prophylaxis received a PPI. The prophylaxis rates were highest for patients with a history of peptic ulcer disease (62%) and were lowest for users of P2Y12 inhibitors (29%). There were no statistically significant age or gender related differences in the rates of compliance when independent sample t and chi square tests were performed (Table 1). CONCLUSION: Peptic ulcer disease prophylaxis with proton pump inhibitors may be underutilized in elderly patients. This finding, along with increasing rates of NSAID use and aging population, may help explain the increased incidence of complicated PUD in the elderly. Efforts are needed to raise physician awareness of PUD prophylaxis guidelines.

The main aim of the present study was to identify the patient with rheumatoid arthritis (RA) taking non-steroidal anti-inflammatory drugs (NSAIDs) at risk for peptic ulcer disease (PUD) and its life-threatening complications. During a retrospective study in which more than 1000 patients were interviewed, current gastrointestinal (GI) complaints were of no use in detecting current PUD. A history of PUD was an important predictor of current PUD, while the predictive value of serologic parameters, such as serum values of pepsinogen and antibodies to Helicobacter pylori, was disappointingly low. A prospective study in which 81 consecutive RA patients underwent a gastroscopy revealed 16% PUD; again a history of PUD was the most important predictive parameter. Since no study had been undertaken into the effects of a NSAID on intragastric pH we performed such a study, the main conclusion being that indomethacin does not influence the intragastric pH of RA patients. A placebo-controlled study of ranitidine 300 mg b.i.d. for the prevention of recurrent PUD in RA patients on NSAIDs is underway.

A number of studies have shown an association of gastritis symptoms with the levels of specific cytokines. However, some data observed are quite contradictory. Meanwhile, the peptic ulcer disease is known to be associated with unfavorable course of inflammatory processes in gastric mucosa, Moreover, the potential relationships between gastritis and blood cytokine levels in cases of familial predisposal to gastric ulcer have not been studied in children’s age. The aim of our study was to evaluate associations of cytokines in blood serum (IL-2, IL-4, IL-8, IL-18, IL-1β, IFNα, TNFα) with gastritis in the age groups of schoolchildren with a family predisposal to peptic ulcer disease. To this purpose, sophagogastroduodenoscopy with biopsies of gastric mucosa was performed in the children and adolescents (7 to 17 years old) with gastroenterological complaints. A total of 143 children, who had morphologically confirmed gastritis (Sydney classification), were under study, The presence of H. pylori was also determined by morphological technique. The levels of serum cytokines were measured by ELISA technique. The inter-group differences in laboratory parameters were assessed using the Mann–Whitney test. The study has shown that in schoolchildren with gastritis and reported family predisposal for peptic ulcer, the disease is associated with increased content of IFNα in blood, both in the older age group (p = 0.001) and among younger children (p = 0.023). Meanwhile, there were no differences in IFNα content between children with hereditary burden in different age groups. In addition, in older patients with familial burden, in contrast to younger children, an increased level of IL-2 (p = 0.001) and IL-4 (p = 0.015) was noted. Among children with family predisposal to peptic ulcer and H. pylori infection, no age-dependent differences in cytokine levels were found. No differences in the cytokine contents were revealed between schoolchildren of younger and older age with highly active gastritis (grade 2-3). IL-4 contents was the only exception which was higher in older schoolchildren with grade 1 gastritis (p = 0.049). The differences in blood cytokine profile in the schoolchildren may depend on family history of peptic ulcer disease, with some age-dependent characteristics, in particular, concerning IFNα and IL-4 levels.

Aim: To evaluate the cytokine profile of blood serum in children with erosive gastritis depending on the activity of the inflammatory process, bacterial invasion of H. pylori and family predisposition to peptic ulcer disease. Gastroscopy was performed with the collection of biopsy material from the gastric mucosa in 168 children aged 7-17 years with gastroenterological complaints. Subsequently, a morphological examination of biopsy specimens confirmed the diagnosis of gastritis in all examined patients and determined H. pylori invasion. The content of cytokines in the blood serum (IL-2, IL-4, IL-6, IL-8, IL-10, IL-18, IL-1β, IFNα, TNFα) was determined using the enzyme immunoassay method. When analyzing cytokine levels in schoolchildren infected with H. pylori, there were no differences in cytokine concentrations (p 0.05). While in uninfected children in the presence of erosive changes, a decrease in IL-2 content was noted (p = 0.026). In individuals with a family history of peptic ulcer disease with erosive gastritis, an increase in the content of IL-8 was observed (p = 0.006), which is known to play an important role in maintaining innate immunity. Whereas, in the absence of a family predisposition, schoolchildren with erosive gastritis showed a decrease in IL-2 (p = 0.027), which is similar to the level of IL-2 in schoolchildren with erosive gastritis without H. pylori infection. IL-2 is considered an activator of the antitumor response and this property is being actively studied in patients with gastric cancer. In the context of these data, it can be assumed that in individuals with erosive gastritis, even without a family predisposition and H. pylori infection, inhibition of IL-2 synthesis is observed. What causes this influence is an open question. Thus, the variety of components of the cytokine profile involved in the regulation of the inflammatory process and the influencing negative factors create difficulties in assessing and, even more so, predicting the role and significance of changes in the content of a particular cytokine in the blood serum in children with erosive gastritis.

A study of 11 patients with "double pylorus" revealed that a second channel between the gastric antrum and the duodenal bulb is the result of ulcer penetration. The fistula can be a sign of spontaneous recovery from ulcerative disease; the fistula occurred in conjunction with clinical improvement in the majority of the patients. The advantages of radiological vs. endoscopic diagnostic procedures are discussed.