X-ray diagnosis of peptic ulcers of the jejunum

The paper is devoted to a study of the results of clinicoroentgenological and endoscopic investigation of 188 patients aged 23 to 60 who developed jejunal peptic ulcer. It was done to specify the features of an x-ray picture of jejunal peptic ulcers with relation to the cause of ulcer development and optimum methods of x-ray investigation. The predominant localization of peptic ulcer in the jejunal efferent loop and its typical ulcero-cicatricial deformity were established. Jejunal peptic ulcers developing as a result of an insufficient area of resection, are characterized by a relatively benign course of the disease. In case ulcer development was determined by the residual antral stomach mucosa at the duodenal stump or by the Zollinger-Ellison syndrome, considerable pathological changes (gigantic ulcer sizes greater than 2.5 cm and a sharp deformity of the jejunal efferent loop) were noted.     

Is herpes simplex virus associated with peptic ulcer disease?

To test the hypothesis that herpes simplex virus type 1 (HSV-1) may be associated with peptic ulcer disease, we examined ulcerative lesions of the distal stomach and proximal duodenum for the presence of nucleic acids and antibodies specific for HSV-1. Utilizing in situ hybridization, immunocytochemistry, and polymerase chain reaction with sequencing, gastric or duodenal tissues from 4 of 22 patients (18%) with documented peptic ulcer disease demonstrated the presence of both specific HSV-1 nucleic acid sequences and proteins. HSV-1 was found restricted in clusters of cells near the margin of the ulcer but was absent at sites distal to the lesion. Several of such HSV-1-infected cells also contained cholecystokinin. These cholecystokinin-containing cells are of neuroendocrine origin and receive contact from the vagal nerve. Campylobacter pylori bacteria were not found in three of the four peptic ulcer tissues that harbored HSV-1. Further, none of the stomach or duodenal tissue samples from 33 patients undergoing clinical evaluation, but having no evidence of peptic ulcer disease, had HSV-1 materials. Thus, our data suggest that a subset of peptic ulcer disease may be associated with HSV-1 and raise the possibility that some peptic ulcers may be caused by this virus.     

Changes in the intensity of protein synthesis in the gastric mucosa following the laser irradiation of a duodenal ulcer]

The intensity of protein synthesis (incorporation/pool) is usually low in normal stomach mucosa and enhanced in exacerbation of peptic ulcer; following the effective laser therapy it decreases only in one third of cases. Therefore the scarring of ulcer not always coincides with the normalization of protein synthesis. The results characterize also the community of reactions in stomach and duodenal mucose membranes. The changes in protein synthesis intensity following the laser irradiation depended neither on the initial size of ulcer nor on the age of patient and the total duration of disease.     

Cytodiagnosis of gastric ulcer penetration of the liver by examination of endoscopic brushings

The penetration of a gastric peptic ulcer into the liver was initially diagnosed by the cytologic examination of endoscopic brushings and later confirmed by an endoscopic biopsy of the stomach. One of the smears of the gastric brushing contained sparse groups of liver cells with mild atypia. The endoscopic biopsy specimen included liver parenchyma with signs of peptic hepatitis. The differential diagnostic considerations for a gastric brushing containing hepatoid cells are discussed.     

SLC26A9 is expressed in gastric surface epithelial cells, mediates Cl-/HCO3- exchange, and is inhibited by NH4+

HCO3- secretion by gastric mucous cells is essential for protection against acidic injury and peptic ulcer. Herein we report the identification of an apical HCO3- transporter in gastric surface epithelial cells. Northern hybridization and RT-PCR demonstrate the expression of this transporter, also known as SLC26A9, in mouse and rat stomach and trachea (but not kidney). In situ hybridization in mouse stomach showed abundant expression of SLC26A9 in surface epithelial cells with apical localization on immunofluorescence labeling. Functional studies in HEK-293 cells demonstrated that SLC26A9 mediates Cl-/HCO3- exchange and is also capable of Cl--independent HCO3- extrusion. Unlike other anion exchangers or transport proteins reported to date, SLC26A9 activity is inhibited by ammonium (NH4+). The inhibitory effect of NH4+ on gastric HCO3- secretion was also indicated by reduced gastric juxtamucosal pH (pHjm) in rat stomach in vivo. This report is the first to describe the inhibition of HCO3- transport in vitro and the reduction of pHjm in stomach in vivo by NH4+. Given its critical localization on the apical membrane of surface epithelial cells, its ability to transport HCO3-, and its inhibition by NH4+, we propose that SLC26A9 mediates HCO3- secretion in surface epithelial cells and is essential for protection against acidic injury in the stomach. Disease states that are associated with increased ammonia (NH3)/NH4+ generation (e.g., Helicobacter pylori) may impair gastric HCO3- secretion and therefore predispose patients to peptic ulcer by inhibiting SLC26A9.     

幽门螺杆菌与 2005 年诺贝尔医学奖

今年的诺贝尔医学或生理学奖授予 Robin Warren 和 Barry Marshall 两位坚韧不拔且敢于挑战传统观念的科学家 . 奖励他们所做出的非凡的和出人意料的发现：慢性胃炎、胃溃疡以及十二指肠溃疡主要是由幽门螺杆菌感染所导致的 .     

Echography of the stomach and duodenum in children in health and disease

The paper is concerned with the results of echography of the stomach and duodenum in 100 healthy children aged 1 month to 15 years and in 141 children with different types of gastritis, duodenitis and peptic ulcer. Echographic investigation of these hollow organs was made possible after their acoustic filling with 5% glucose solution. Echography permitted fast and reliable differentiation of the type and site of stomach and duodenal lesions, determining the presence of a gastroduodenal reflux and sizes of an ulcerative defect of the duodenal wall.     

Genetic and evolutionary implications in peptic ulcer disease

The evidence for a genetic component in peptic ulcer disease has been based on twin, family, and blood group studies. A polygenic model for the inheritance of peptic ulcers has been displaced by a genetic heterogeneity model based on several lines of evidence, some of the most powerful being recent work using subclinical markers. One marker in particular, an elevated level of serum pepsinogen I (PG I), a pepsin precursor produced by the gastric mucosa, secreted into the stomach lumen and also appearing in the bloodstream, has been found to be associated with a subgroup of duodenal ulcer patients. Segregation analysis of elevated serum PG I in duodenal ulcer sibships demonstrates familial aggregation consistent with autosomal dominant inheritance. Elevated PG I is also accompanied by gastric hyperacidity and presumably indicates those individuals with an increased mass of chief and parietal cells, and thus an increased capacity for peptic activity, an important element in the pathogenesis of ulcer disease. An evolutionary hypothesis based on selection for peptic activity and acidity is offered to explain several of the epidemiologic and genetic elements of this group of chronic diseases.     

Lactic acid bacteria and streptococci of the human stomach normally and in pathological processes]

Lactic acid bacteria were either absent or present in negligent quantities in the stomach of apparently healthy man. But in case of various pathological processes in the stomach and duodenum lactic acid bacteria accumulated (up to a million cells per 1 ml of gastric contents). Under these conditions coccal forms sharply prevailed over the bacillary ones. In patients with chronic gastritis and peptic ulcer of the stomach the most frequent were Streptococcus faecalis and its variants; in oncological patients--Str. faecium, strains affiliated to Leuconostoc mesenteroides, and sometimes Str. durans.     

Helicobacter pylori associated gastric pathology.

Helicobacter pylori (HP), undoubtedly, the most common world-wide infection plays an important role in pathogenesis of peptic ulcer. Proof for a causal role for HP in peptic ulcer rests in two major points; 1) the majority of ulcer patients are HP infected and the prevalence of this infection for both gastric ulcer (GU) and duodenal ulcer (DU) is much higher than for gender- and age-adjusted controls and 2) the cure of HP infection dramatically reduces ulcer recurrence. Conclusions regarding the mechanisms by which HP induces peptic ulcer are restricted mainly to studies observing the consequences of its eradication by antibiotics combined with gastric inhibitors or bismuth agents. Several specific virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) as well as other noxious substances including ammonia, lipopolysaccharide (endotoxin), platelet activating factor (PAF), nitric oxide (NO) and others have been implicated in gastritis and were found to be significantly more frequent in gastric cancer than in gender- and age-matched controls, especially in younger generation. Chronic inflammation, atrophic gastritis, intestinal metaplasia, impaired defense mechanisms combined with hypergastrinemia, deficiency of vitamin C in the stomach , excessive oxygen metabolites and epithelial cell proliferation have been associated with gastric cancer. This multi-step pathway originally proposed by Correa and his colleagues, long before the HP was discovered in the stomach, leads to cancer but may be reversed by eradication of HP. This is, however, a controversial issue because gastric atrophy and intestinal metaplasia may be also caused by other factors such as bile reflux, dietary irritants, and autoimmunity. The implication of HP in MALT-lymphoma is based on the observations that eradication of HP in early stage of low-grade of this tumor leads to complete remission. The significance of HP in non-ulcer dyspepsia remains questionable and requires further studies.     

SUBTOTAL GASTRIC RESECTION FOR PEPTIC ULCER—Preliminary Report of a Variation in Technique

Internists as well as surgeons agree that subtotal gastric resection is a satisfactory method of treatment for a selected group of patients with intractable or complicated peptic ulcer.A short historical review of the development of the operation is given.The importance of removing a large portion of the acid pepsin-secreting area of the stomach is stressed. A variation from the usual method of resection accomplishes this and at the same time leaves a satisfactory gastric pouch and lessens the incidence of the dumping syndrome.     

Subtotal gastric resection for peptic ulcer; preliminary report of a variation in technique

Internists as well as surgeons agree that subtotal gastric resection is a satisfactory method of treatment for a selected group of patients with intractable or complicated peptic ulcer.A short historical review of the development of the operation is given. The importance of removing a large portion of the acid pepsin-secreting area of the stomach is stressed. A variation from the usual method of resection accomplishes this and at the same time leaves a satisfactory gastric pouch and lessens the incidence of the dumping syndrome.     

Lesions Associated with Gastroduodenal Haemorrhage,in Relation to Aspirin Intake

The incidence of aspirin ingestion during the week preceding overt gastroduodenal bleeding was recorded in 582 patients. A positive aspirin history was found in 80% of patients with acute gastric lesions, in 63% of those in whom no lesion was found, in 52% of those with a chronic duodenal ulcer, and in 49% of patients with a chronic gastric ulcer. In a control series of 542 consecutive patients without overt bleeding admitted to the same wards during part of the time of this investigation the aspirin incidence was 32%.The difference in aspirin habits between these two series confirms that aspirin is a factor in precipitating overt haemorrhage in acute and chronic peptic ulcers, and that it is an important cause of bleeding from the stomach or duodenum, or both, in the absence of a chronic peptic ulcer.     

Critical Evaluation of the Tetracycline Fluorescence Test in the Diagnosis of Gastric Carcinoma

Exfoliative cytology is a useful tool in the differential diagnosis of gastric lesions. The simplified method developed by Klinger and Katz⁴ using tetracycline fluorescence was subjected to a critical evaluation. Five cases of gastric carcinoma, two of esophageal carcinoma, 21 of benign peptic ulcer, one case of carcinoma eroding into the bile duct, one case of carcinoma of the pancreas penetrating into the stomach, five normal controls on no medication and two normal controls taking vitamin B₂ were studied. The most apparent drawback of this technique is the number of false negatives encountered in cases of gastric carcinoma (three negative results in five cases of carcinoma). One false-positive test was recorded among 21 patients with benign ulcer. Vitamin B₂ if taken a half hour prior to the test will also produce a false-positive test. It is concluded, therefore, that the tetracycline fluorescence test is inferior to accurate studies of exfoliative cytology.     

Properties and clinical application of quasi-liquid form of lysozyme

The course of transendoscopic quasi-liquid form of lysozyme treatment of the relapse of peptic ulcer was microbiologically and clinically substantiated. A high antimicrobial and sorption activity of the quasi-liquid form of lysozyme with respect to the microflora isolated from the mucous membrane of the stomach and the duodenum was shown. The transendoscopic introduction of this form of lysozyme significantly reduces the time of the cicatrization of ulcers and the stay of patients in the hospital.     

Plants of the American continent with antiulcer activity.

Peptic ulcer is a chronic and appalling disease. Today, it is dominant among the diseases that affect the world's population. The principal factors causing this disease are inadequate dietetic habits, prolonged use of non-steroidal anti-inflammatory drugs, stress and infection by Helicobacter pylori, in addition to other factors of genetic origin. The present work is a literature survey of plant extracts from the American continent that have been reported to show antiulcer activity. This review refers to 58 plants with their families, parts used, type of extract used, model bioassays and their activity. This work intends to aid the researchers in the study of natural products appropriate to the treatment of stomach and intestinal diseases, in general, and peptic ulcer in particular.     

The immunity characteristics of men with gastric and duodenal peptic ulcer associated with Helicobacter pylori

In males with peptic ulcer of the stomach and the duodenum, associated with H. pylori, the population and subpopulation spectrum of peripheral blood lymphocytes was studied by the method of CD typing with the use of monoclonal antibodies manufactured by the Research Institute "Preparat" (Nizhny Novgorod, Russia). The study revealed the development of disturbances in the amount of populations and subpopulations of peripheral blood lymphocytes, accompanied by a decrease in the absolute number of T lymphocytes (CD3, CD7), T helpers (CD4), T cytotoxic lymphocytes (CD8), B lymphocytes (CD22) and the ratio of CD4/CD8 cells. A decrease in the amount of IgA, IgG, the key complement components C1, C3, C5 was established. In peptic ulcer the immunological characteristics of gastric juice were found to essentially differ from those of saliva by a lower content of mucin, IgA and a higher content of SIgA and IgM in gastric secretions, which may form prerequisites for the colonization of the gastric mucosa by H. pylori.     

Helicobacter pylori infection and perforated peptic ulcer prevalence of the infection and role of antimicrobial treatment

Although the role of Helicobacter pylori infection on noncomplicated peptic ulcer disease has been definitively established, the precise relationship between the organism and complicated ulcer has hardly been studied. The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is of only about 65-70%, which contrasts with the almost 90-100% figure reported in noncomplicated ulcer disease. However, H. pylori infection rates in various studies range markedly from 0% to 100%, suggesting that differences in variables as number and type of diagnostic methods used to diagnose H. pylori infection, or frequency of nonsteroidal anti-inflammatory drug intake, may be responsible for the low prevalence reported in some studies. Recurrent ulcer disease after peptic ulcer perforation mainly occurs in patients with H. pylori infection, which suggests that the microorganism plays an important role in this complication. All patients with perforated peptic ulcer should be treated by simple closure of the perforation and with therapy aimed at healing of the ulcer and eradicating the H. pylori infection, as disappearance of the organism prevents, or at least decreases, ulcer recurrence and ulcer perforation in patients with H. pylori-associated perforated ulcers after simple closure. Therefore, H. pylori eradicating treatment should be started during the immediate postoperative period. The patients with intractable recurrent symptoms of peptic ulcer despite adequate medical treatment, but without H. pylori infection (e.g. a patient using nonsteroidal anti-inflammatory drugs), is probably the only remaining indication for elective definitive surgical treatment of peptic ulcer disease.     

The Pathogenesis of Peptic Ulcer

Peptic ulcers of the stomach and duodenum look much alike and the reaction around them is nonspecific, yet other evidence indicates that ulcers in the two locations do not represent the same disease. It is suggested that a common causal factor is the digestive effect of gastric juice, and that hypersecretion may produce duodenal ulcer without any predisposing change in the relatively susceptible duodenum. The development of a gastric ulcer, which may occur without hypersecretion, presumably requires some previous alteration of the normally resistant gastric mucosa. Focal metaplasia of the gastric mucosa to tissue resembling the lining of the small intestine, which is observed frequently in association with gastric ulcer, may be a factor in providing decreased resistance to peptic injury.     

Twenty five years since the first prospective study by Forman et al. (1991) on Helicobacter pylori and stomach cancer risk

Stomach cancer is one of the leading causes of cancer death worldwide, despite its incidence and mortality falling in many places. The discovery in 1984 that a bacterial infection with Helicobacter pylori could cause stomach and duodenal ulcers prompted work in its role in causing gastritis, and led to the first prospective study in 1991 by Forman et al., showing that infection with H.pylori increased the risk of stomach cancer in those infected by almost three-fold. Prior to then, it was hypothesized that stomach was caused by poor diets. While diets may still play a role, the falls in stomach cancer incidence have been associated with reductions in population prevalence of H. pylori. Discovery of the link was accelerated by the use of stored sera from other unrelated studies, and the use of serological assays.Since those discoveries the treatment landscape of gastric disorders has changed significantly, with a rapid uptake of antibiotic and proton pump inhibitors (triple) therapies in those who are H. pylori positive. Over time we have seen falls in gastric cancer, peptic and duodenal ulcers and in many of the procedures previously used to cure peptic ulcer disease, such as vagotomies and gastrectomies.Further still, an oral vaccine against H. pylori, first trialled in China, holds much promise of being the third vaccine against a cancer causing infection. If successful this would lead to a further reduction in H. pylori related conditions, and ultimately gastric cancer, an otherwise lethal disease.