Chronic Duodenal Ulcer Disease Research Articles

<I>Helicobacter pylori</I> infection and dermatological diseases

Helicobacter pylori (H. Pylori), microaerophilic spiral-shaped Gram-negative bacteria which colonize the gastric mucosa of human population, is the leading causal factor in the development of a whole range of diseases of the gastroduodenal region (chronic gastritis, gastric and duodenal ulcer disease, MALT lymphoma and gastric adenocarcinoma). Since the discovery of H. pylori infection and the identification of its leading role in the development of a range of gastroenterological diseases, researchers have begun to actively study the potential trigger significance of this pathogen in the development of extragastric pathology. At the epidemiological level, H. pylori infection has been shown to be frequently associated with skin diseases such as rosacea, acne, chronic urticaria and psoriasis, although the clinical significance of these associations remains clouded. In fact, recent meta-analytic studies (2019–2024) demonstrate an increased risk of developing the above diseases in H. pylori-infected individuals with odds ratios ranging from 1.19 to 3.00. On the other hand, not all studies have showed that eradication therapy of this microorganism helps reduce the clinical severity of symptoms of skin diseases, which is hypothetically explained only by the trigger role of infection within the complex pathogenesis. In a modern light, such associations can be viewed in terms of pathogenetic findings through the implementation of the syndrome of increased epithelial permeability (SIEP). The chronic gastritis caused by H. pylori infection is believed to lead to increased permeability of the epithelial lining of the stomach, as well as the walls of the mucosal vessels and a higher exposure of bacterial and nutritional antigens in the systemic circulation, which can induce both local release of inflammatory mediators in tissues and systemic immunological reactions (autoimmune and inflammatory processes, formation of molecular mimicry-induced immune complexes and cross-reactive antibodies).

DNA typing of the gastric mucosa of patients with chronic duodenal ulcer

The work involved a molecular biological technique (ISSR-PCR) using ISSR-primer S-2, with structure (AGC) 6G. Changes in the gastric mucosa in chronic duodenal ulcer disease against the background of severe chronic atrophic gastritis have been analyzed. Noteworthy is the fact that there is a strong correlation between the degree of dysplasia of the epithelium of the gastric mucosa and the mitotic index, the Pearson's correlation coefficient rxy was 0.853, respectively. A strong and very strong correlation relationship between the indicators of the degree of dysplasia of the epithelium of the gastric mucosa by phenotypic characteristics and indicators of DNA typing of samples of the gastric mucosa, the Pearson's correlation coefficient rxy was 0.863, respectively.
 DNA profiles of the gastric mucosa of patients with duodenal ulcer according to the results of typing by the ISSR-PCR method ranging from 520 to 620 bp. had the character of microsatellite expansions and differed from the profile of the norm, which is evidence of precancerous changes.

Abstract OR-5: Helicobacter pylori Surface Structures

Background: Helicobacter pylori, which infects at least half of the human population, is an etiopathogenetic factor in the development of chronic gastritis (CG), gastric and duodenal ulcer disease (UD), and is also considered a risk factor in the occurrence of some forms of stomach cancer. Various surface structures of H. pylori are important pathogenic factors. Methods: Reference (NCTC 11637, NCTC 11639) and freshly isolated H. pylori strains as well as samples of the gastric mucosa were examined using transmission (TEM) and scanning electron microscopy (SEM) by means of “JEM-100 В” (JEOL, Japan) and “Quanta 200 3D” (FEI Company, USA) systems, respectively. Samples for SEM fixed with formalin and not subjected to dehydration were sprayed with an electrically conductive layer of gold. Samples for TEM were prepared using negative contrast (NC) with ammonium molybdate and ultrathin sections (US) contrasted by Reynolds; fixation by Ito-Karnovsky was used in both cases. Accelerating voltage at TEM and SEM was 80 and 10 kV, respectively. Results: Three types of H. pylori surface structures were found: flagella, fimbria, and vesicles. Flagella were found both in the material of cultures maintained in vitro and in each native sample of the gastric mucosa. SEM images suggest the involvement of flagella in biofilm formation. On longitudinal sections of the flagellum, the outer electron-dense layer and the inner content in the form of a filament were visualized; on cross sections, the flagellum looked like an annular structure with a centrally located point accumulation of electron-dense matter. Paradoxically, the H. pylori forms with a defective cell wall also possessed flagella. Freely located flagellar sheaths without central filament were often found in vitro only. Fimbriae were found exclusively in negatively contrasted pure bacterial cultures material. In addition, vesicles detaching from the surface of bacterial cells were found both in the material of aging H. pylori pure cultures and in native samples of the gastric mucosa under CG and UD. A small part of the vesicles retains their connection with the cell wall, while detached vesicles are present in excess in the surrounding space. Massive detachment of vesicles leads to the formation of spheroplasts, devoid of an outer membrane. Conclusion: H. pylori has a representative set of surface structures that play an important role in the onset and development of the infectious process in the gastroduodenal area.

Delay in Diagnosis of Adrenal Insufficiency Is a Frequent Cause of Adrenal Crisis

Delay of diagnosis of primary adrenal insufficiency (PAI) leads to adrenal crisis which is potentially lethal complication. The objective of our work was an assessment whether the establishment of diagnosis of adrenocortical insufficiency in Poland is so much delayed as assessed in the past. We have analysed data from 60 patients with diagnosis of PAI established in our department during the past 12 years and who are still under our care. We found that the time to diagnosis of primary adrenal insufficiency in Poland exceeds 3 months in every patient and 6 months in patients admitted with symptoms of adrenal crisis. Forty-four percent of patients were diagnosed only just after the hospitalisation due to crisis, despite the evident signs and symptoms of PAI. Lack of appetite and loss of body weight occurred in all patients and for that reason a diagnosis of chronic gastric and duodenal ulcer disease was the most often incorrect diagnosis. After the proper diagnosis and treatment, in the course of 1–11 years of observation, there was only 6 imminent adrenal crises in 5 patients. Our results indicated that training of primary care physicians in the field of recognising and treatment of adrenal insufficiency is still essential.

Choledochoduodenal fistula (CDF): a compication of chronic peptic ulcer disease. a case report and review of literature

Bilio-enteric fistulas have been reported though not common. They are usually incidental findings during certain investigative procedures. It is mostly associated with gallstones or penetrating abdominal injury. A case of choledochoduodenal fistula (CDF) complicating chronic duodenal ulcer disease picked up on upper gastro-intestinal barium study, is reported. West African Journal of Radiology Vol. 13(1) 2006: 22-24

One hundred patients ten years after parietal cell vagotomy.

One hundred patients with duodenal or pyloric/prepyloric ulcer disease were operated with parietal cell vagotomy (PCV) and followed for a minimum of 10 years. At 6 weeks, 1,5 and 10 years postoperatively gastric secretory tests, haematological work-up and clinical examination or telephone interview were performed. There was no operative mortality and the frequency of postoperative sequelae was minimal. The cumulative ulcer recurrence rate was 18 per cent and another 14 per cent had slight to moderate symptoms of epigastric pain without any signs of ulcer. Upper gastrointestinal endoscopy was used to reveal recurrences but was performed only if the patient had symptoms of recurrence. A rise in basal acid secretion and in pentagastrin-stimulated secretion was observed the first year postoperatively, whereas insulin-stimulated peak acid output increased during the first 5 years. We conclude that PCV has a low rate of per- and postoperative complications and an acceptable recurrence rate. Therefore, it seems that PCV is the method of choice in chronic duodenal ulcer disease.

Endoscopic appearances and histological changes in ulcer-associated doudenitis

A simple system of grading the endoscopic appearances of duodenitis is described. There was a good association between the degree of duodenitis recorded using this method and that obtained from a histological grading system in a group of duodenal ulcer patients and a group of dyspeptic patients with no endoscopic evidence of duodenitis. Endoscopic assessment is recommended as a reliable guide to the presence of duodenitis. After 1 month of treatment with cimetidine there was a significant improvement in the endoscopic duodenitis scores of a group of 17 duodenal ulcer patients. In 16 of these patients there was complete ulcer healing. Duodenitis can be a manifestation of chronic duodenal ulcer disease. In the absence of ulceration, the endoscopic diagnosis of duodenitis is of value in the recognition of patients with this condition.

The <I>Helicobacter felis</I> Model of Adoptive Transfer Gastritis

The bacterium Helicobacter pylori is a major human pathogen and the principal cause of acute and chronic gastritis, gastric and duodenal ulcer disease, and gastric adenocarcinoma. Infection with gastric Helicobacter results in an early infiltration of neutrophils, monocytes, and natural killer cells, followed by an influx of T cells and plasma cells. Although the critical components of this gastric infiltrate that lead to disease are unclear, the Helicobacter felis-infected mouse and other mouse models of Helicobacter-associated gastritis have demonstrated the critical nature of adaptive immunity in the development of gastric epithelial pathology. To further investigate the role of adaptive immunity in this disease, adoptive transfer models of disease have also been utilized. These models clearly demonstrate that it is the host CD4+ T lymphocyte response that is crucial for the development of Helicobacter-associated gastric epithelial changes.

Helicobacter pylori and gastrointestinal symptoms in school children in Russia.

Helicobacter pylori is considered to be the major cause of chronic gastritis and duodenal ulcer disease recurrence in childhood. However, the association between H. pylori and recurrent abdominal pain (RAP) syndrome is still controversial. Therefore, the spectrum of clinical variants of gastrointestinal symptoms associated with H. pylori-positive status was studied in consecutive symptomatic children who were undergoing diagnostic endoscopy. A consecutive series of 225 school children from the Ural area of Russia (mean age 11.1 + 1.4 years, age range 7-15 years) who presented with RAP were investigated using esophagogastroduodenoscopy, including three antral biopsies for histology and polymerase chain reaction. Helicobacter pylori immunoglobulin G antibodies were found using a second-generation enzyme immunoassay. Information about the clinical symptoms was collected using a special questionnaire. The authors found a high incidence of H. pylori infection (80%) and peptic ulcers (16%) in 225 school children from the Ural area of Russia who were referred for upper gastrointestinal (UGI) endoscopy for chronic abdominal pain. Of the overall 225 symptomatic children who underwent endoscopy, 182 (80,8%) were found to be H. pylori-positive. Duodenal ulcers were detected in 36 H. pylori-positive children. A family history of peptic ulcers was significantly more frequent in the children infected with H. pylori (P < 0.001). Symptom score and duration of symptoms were similar, but night-time pain (P < 0.0001) and fasting pain relieved by food (P < 0.001) were more frequent in the H. pylori-positive children as compared with the H. pylori-negative children. The present results provide further evidence for a significant association between H. pylori and some patterns of gastrointestinal symptoms in children who underwent UGI endoscopy in order to exclude an organic cause of severe chronic gastrointestinal disorders.

Ectopic opening of the common bile duct in the duodenal bulb: clinical implications.

An ectopic opening of the common bile duct in the duodenal bulb is extremely rare, and the clinical significance of this anomaly has not been clarified. This study analyzed the clinical implications and cholangiographic findings of this anomaly. A total of 18 patients (15 men, 3 women; median age, 51 years) with an ectopic opening of the common bile duct in the duodenal bulb were studied. Medical records, endoscopic findings, and cholangiographic and other radiographic findings were reviewed. All 18 patients had biliary pain; 7 had fever and chills. Fifteen (83%) had diffuse dilatation of the extrahepatic bile ducts with or without intrahepatic bile duct dilation. Associated bile duct stones were found in 10 (56%) patients. The papilla in the bulb had an orifice stained with bile at endoscopy, which was associated with duodenal ulcer disease found in 13 (72%) patients. The distal end of the common bile duct was tapered and narrowed and had a hook shape in all patients. An ectopic opening of the common bile duct in the duodenal bulb may be associated with clinical entities such as recurrent or intractable duodenal ulcer, choledocholithiasis, or acute cholangitis. Although these openings are rare, knowledge of the endoscopic and radiographic findings of an ectopic opening of the common bile duct in the duodenal bulb may help to clarify the cause of chronic recurrent duodenal ulcer disease in some patients and prevent damage to the bile duct during surgery.

Duodenal defence mechanisms: role of mucosal bicarbonate secretion

The duodenal epithelium secretes bicarbonate at higher rates than does the stomach (or more distal small intestine) and the duodenal secretion is currently accepted as the most important defence mechanism against acid discharged from the stomach. HCO3- entering the continuous layer of visco-elastic mucus gel on top of the epithelial surface maintains pH in its cell-facing portion at neutrality at acidities encountered in the healthy duodenum. The secretion is decreased in patients with acute and chronic duodenal ulcer disease and is inhibited by non-steroidal anti-inflammatory agents. Studies of the neurohumoral control of the duodenal alkaline secretion and of acid/base transport processes and intracellular signaling in duodenal enterocytes are currently of great research interest.

Gastric metaplasia of the duodenum: identification by an endoscopic selective mucosal staining technique

Background: To understand the pathophysiology of duodenal ulcer disease, it is important to identify and quantitate gastric metaplasia of the duodenum. Methylene blue dye is absorbed well by intestinal mucosa, but not by gastric mucosa. Our aim was to validate a methylene blue staining technique for measurement of gastric metaplasia in the duodenum. Methods: Eight subjects with chronic duodenal ulcer disease and seven subjects with other upper intestinal disorders underwent duodenal methylene blue staining after application of a mucolytic agent. Biopsy specimens were obtained from blue-stained and pale unstained areas and assessed for gastric metaplasia histologically. Results: Pink or pale unstained duodenal areas had more gastric surface cell metaplasia than blue-stained areas. Unstained duodenum was also more likely to have extensive (more than 25% of the biopsy specimens) gastric metaplasia (60%) than blue-stained areas (9%). Subjects with duodenal ulcer disease had more unstained mucosa than controls. Conclusion: Methylene blue staining of the duodenum is useful to identify and quantitate gastric metaplasia. (Gastrointest Endosc 1998;48:32-8.)

Inhibition of Helicobacter pylori sialic acid-specific haemagglutination by human gastrointestinal mucins and milk glycoproteins

Helicobacter pylori, a human gastric pathogen causing chronic gastritis and duodenal ulcer disease, has been found in large amounts in gastric mucous gel layer. Mucin preparations, separated from human gastric juices and isolated from different colon regions, were examined for their ability to inhibit haemagglutination of H. pylori with the emphasis on evaluating the role of sialic acid-dependent haemagglutinins of the bacteria in colonisation of the stomach. The mucins showed high inhibitory activity for H. pylori, which was significantly decreased after the removal of sialic acids from the mucins. The inhibitory potencies using high molecular mass mucin-like components from bovine milk were comparable with those obtained for gastric mucins, suggesting their possible role in the prevention of H. pylori infection.

Serum antibody response against Helicobacter pylori NCTC 11637 smooth- and rough-lipopolysaccharide phenotypes in patients with H. pylori-related gastropathy

The antigenicity of the Helicobacter pylori lipopolysaccharide (LPS) molecule during the course of natural H. pylori infection in humans was investigated. The IgG and IgA responses against smooth (S)- and rough (R)-form LPS were evaluated in H. pylori positive patients with chronic gastritis (CG, n = 30) and duodenal ulcer disease (DU, n = 16), and in 15 H. pylori-negative dyspeptic subjects. The results demonstrated that anti H. pylori LPS IgG and IgA antibody levels were significantly enhanced in both groups of H. pylori-positive patients compared with H. pylori-negative subjects, thus confirming that H. pylori LPS is part of the immunogenic antigen profile of the bacterium. In addition, a marked response against R-LPS, which significantly correlated with that observed against S-LPS, was found for both IgG and IgA, thus indicating that core oligosaccharide plays a powerful immunogenic role. Since the O-side chain of LPS from H. pylori NCTC 11637 contains epitopes which mimic Lewis x (Lex) antigens, the presence of antibodies to monomeric, trimeric, and polymeric Lex was also investigated. Antibodies against polymeric Lex were detected in two patients suffering from chronic atrophic gastritis and active chronic gastritis, respectively.

The vacuolating cytotoxin of Helicobacter pylori.

Helicobacter pylori, the causative agent of chronic superficial gastritis and duodenal ulcer disease in humans, produces a unique cytotoxin (VacA) that induces cytoplasmic vacuolation in eukaryotic cells. The structural organization and processing of the vacuolating cytotoxin are characteristic of a family of proteins exemplified by Neisseria gonorrhoeae IgA protease. Although only 50% of H. pylori isolates produce detectable cytotoxin activity in vitro, vacA homologues are present in virtually all isolates. Several families of vacA alleles have been identified, and there is a strong correlation between presence of specific vacA genotypes, cytotoxin activity, and peptic ulceration. Experiments in a mouse model of H. pylori-induced gastric damage indicate that the cytotoxin plays an important role in inducing gastric epithelial necrosis.

The economic and quality-of-life benefits of Helicobacter pylori eradication in chronic duodenal ulcer disease--a community-based study

A policy of Helicobacter pylori eradication in patients with duodenal ulceration on long-term acid-suppressing therapy was evaluated in a prospective study amongst a general practice population, with particular reference to economic and quality-of-life benefits. One hundred and sixty-eight patients on long-term acid-suppressing therapy had chronic duodenal ulcer disease of whom 88 were eligible for the study; 45 patients attended for review, with 42 testing positive for H pylori (as assessed by 13C-urea breath test). The median duration of acid-suppressing therapy was six years (maximum 15 years); 47.6% of the patients were using additional antacids and 80.9% still experienced epigastric discomfort. Two-thirds (28/42) of the patients eradicated H pylori. Successful eradication was associated with a highly significant reduction in all symptoms. At 12 months follow-up, heartburn had decreased from 28.7% to 7.1%, epigastric discomfort from 75% to 3.6%, nausea from 32.1% to 0% and wind from 50% to 0%. Of the patients that eradicated H pylori 96.4% reported an improvement in their general health compared to none of those that remained H pylori positive. Successful H pylori eradication therapy scored higher on satisfaction ratings than long-term acid-suppressing therapy. Eradication of H pylori resulted in 27/28 patients being able to discontinue acid-suppressing therapy, representing a 5.8% reduction in the use of such drugs per year in the local general practice population. A policy of H pylori eradication in chronic duodenal ulcer disease reduces the use of long-term acid-suppression therapy in general practice. This has important financial implications as well as offering considerable symptomatic benefits to the patients and improving their quality of life.

Helicobacter pylori infection, nutrition and growth of West African infants

Helicobacter pylori is probably the commonest bacterial infection of humankind. In adults, colonization of the stomach is associated with chronic gastritis and duodenal ulcer disease. However, children in the developing world acquire H. pylori soon after birth, and there is evidence that it plays a part, through suppression of the gastric acid barrier, in the pathogenesis of the syndrome of diarrhoea, malnutrition and growth failure. Infants born of mothers who secrete milk with high levels of anti- H. pylori immunoglobulin A (IgA) antibody acquire the infection later than those born of mothers with low specific antibody levels. Enhancement of maternal breast milk anti- H. pylori IgA levels may protect infants from H. pylori infection during the vulnerable weaning period when many are susceptible to enteric infections, leading to recurrent diarrhoea and adverse consequences on nutrition and growth.

Gastrite à Helicobacter pylori chez l'enfant

Helicobacter pylori associated gastritis in children . Background. - The role of Helicobacter pylori in chronic gastric and duodenal ulcer disease has now been proven in adults as well as in children. Material and methods. - H pylori has been looked for during endoscopy in 130 children suffering from recurrent abdominal pain (78 patients) or other symptoms (52 patients). Biopsy samples were taken from the antrum and the fundus, and were examined for histology and bacteriology (Gram staining, urease test, culture). Results. - H pylori was found in 30 cases ( H pylori+ group, medium age: 12 years) and was absent in the 100 other cases ( H pylori− group, medium age: 6 years). H pylori was present in 27% of children suffering from recurrent abdominal pain and 17% of children with other symptoms. Epigastric location of the pain and vomiting were equally frequent in both groups. Endoscopic gastritis, often nodular, was noted in 60% of the cases in the H pylori+ group and in 46% in the H pylori− group (NS). Chronic gastritis was noted in 90% of the cases in the H pylori+ group, and in 32% of the cases in the H pylori− group ( p < 0.01). Culture was positive in 27 out of 28 cases (97%) in the H pylori+ group, including 3 cases with negative histologic examination. Twenty-two children in the H pylori+ group were treated with amoxicillin and metronidazole. Endoscopy performed about 2 months later showed eradication of H pylori in 63% of the cases, associated with disappearance of histologic lesions in 6 out of 14 cases and of symptoms in 5 out of 7 cases. Conclusions. - H pylori is associated with some pediatric cases of antral gastritis. Further studies are needed to determine the influence of its eradication on symptoms and the interest to search this pathology (by serology) in children suffering from chronic abdominal pain.

Posterior Truncal Vagotomy and Anterior Highly Selective Vagotomy.

Peptic ulcer disease continues to be a major health care problem in the United States. Fortunately, the overall majority of patients can be expected to heal their ulcers with aggressive medical treatment. Nonetheless, a small but discrete group of patients will require surgical treatment for their disease. A minimally invasive approach to the treatment of peptic disease offers numerous advantages to patients including, early discharge from the hospital, early return to normal activity, and minimal postoperative discomfort. Numerous options are available to the surgeon for the treatment of patients presenting with peptic ulcer disease. One of these, posterior truncal vagotomy combined with anterior highly selective vagotomy, seems to provide definitive treatment of chronic duodenal ulcer disease.

Acute perforated duodenal ulcer is not associated with Helicobacter pylori infection.

Most patients with chronic duodenal ulcer disease have Helicobacter pylori infection and eradicating it considerably reduces the relapse rate. The prevalence of H pylori in 80 patients (mean age = 52 years, range 17-85) presenting with acute perforated duodenal ulcer was examined and compared with age and sex matched hospital control patients. H pylori state was assessed by serum anti-H pylori IgG (Helico-G kit, Porton) using a titre of 18 or less as negative with a specificity of 89% and sensitivity of 88%. Only 47% of the perforated duodenal ulcer patients were positive for H pylori and this was similar to the value of 50% in the controls. In 51 of the perforated duodenal ulcer patients 14C-urea breath tests were also performed 4-10 weeks after surgery and this confirmed that only 49% were positive for H pylori. None of these patients had received perioperative drugs that might have eradicated the infection. The H pylori positive and H pylori negative perforated duodenal ulcer patients were similar with respect to age (53, 51), smoking (84%, 83%), and consumption of more than 15 units of alcohol per week (42%, 38%). Duodenal ulcer disease had been diagnosed before acute perforation in only 24% of those with H pylori and also 24% of those without the infection. Regular non-steroidal anti-inflammatory drug (NSAID) use was common in both those with (44%) and without (45%) H pylori. In conclusion, the lack of association of acute perforated duodenal ulcer and H pylori infection suggests that perforated duodenal ulcer has a different pathogenesis from chronic duodenal ulcer disease, and that the first should not be regarded simply as a complication of the second.