Cause Of Duodenal Ulcer Research Articles

Is helicobacter pylori a cause of duodenal ulcer? A methodologic critique of current evidence

introduction: Helicobacter pylori (HP) in the gastric antrum has been strongly associated with both duodenal ulcer (DU) and chronic active gastritis (CAG). The relationship between HP and DU has been interpreted as causal by many observers. An alternate hypothesis is that HP coincidently colonizes CAG, which is independently associated with DU by some yet-unknown mechanism. purpose: To assess the extent to which a causal relationship between HP and DU has been demonstrated, we performed a methodologic critique of published clinical studies. We carried out a literature search to identify clinical studies that included at least 25 subjects. Of the eight studies we identified, six used a cross-sectional design and two used a prospective cohort design. We applied methodologic criteria to assess causation: strength of association, biologic gradient, temporality, and experiment. methods: A strong association between HP and DU was demonstrated in all eight studies. Biologic gradient and temporality were not assessed in any study. In the two experimental studies of therapy, loss of antral HP was associated with a decreased rate of DU relapse; however, we did not interpret this as sufficient to support causality because the effect may have been due to a direct mucosal action rather than eradication of HP. conclusion: We conclude that published evidence does not establish HP as a cause of DU. One approach to address causality would be an observational cohort study of ulcer relapse to assess the temporal relationships between HP, CAG, and DU.

Helicobacter pylori, Causation, Change in Natural History, and whyHelicobacter-Positive Duodenal Ulcers Should Not Be Routinely Treated

The relationship between Helicobacter pylori and duodenal ulcer is reviewed with regard to the following epidemiologic issues: causation, change in natural history, and whether there is sufficient evidence to treat H. pylori-positive peptic ulcers routinely. There is mounting evidence for a pivotal role of H. pylori as a precipitating cause of duodenal ulcers. There is insufficient data to conclude that eradication of H. pylori alone will cure peptic ulcer disease--that is, preventing instead of controlling relapse. H. pylori-positive duodenal ulcers should not be routinely treated because eradication rates need to be improved, metronidazole resistance is an increasing problem, and side-effects of currently used triple combination treatments are substantial.

The effect of nonsteroidal antiinflammatory drugs on upper gastrointestinal tract symptoms and mucosal integrity.

Gastrointestinal side effects are the most common adverse reactions to the use of nonsteroidal anti-inflammatory drugs (NSAIDs), but their true incidence is controversial. Studies have shown an approximate 20% incidence of upper gastrointestinal symptoms in patients using aspirin and a 10% incidence in patients using some other NSAIDs, such as ibuprofen. Because symptom assessment is subjective and may correlate poorly with objective evidence of gastroduodenal injury, studies of endoscopic and fecal blood loss have been used to assess mucosal injury. Whereas high doses of aspirin may produce overt mucosal injury in a majority of patients and normal volunteers, ibuprofen causes significantly less qualitative and quantitative damage in a dose-dependent manner. Daily doses of 1,200 mg of ibuprofen may produce endoscopic injury and fecal blood losses similar to placebo. Although epidemiologic evidence shows a strong correlation of daily aspirin use to gastric ulcer and upper gastrointestinal hemorrhage, other NSAIDs have not been definitively linked to these lesions; no epidemiologic study has established NSAIDs as a cause of duodenal ulcer or gastric lesions when given in low doses. NSAIDs, particularly ibuprofen, in low doses can be considered to have low gastroduodenal toxicity.

Liver Biopsy in Asymptomatic Carriers of HBsAg

5as presenting evidence that smoking played a sig­ nificant role in the healing of duodenal ulcer in antacid- and pla­ cebo-treated subjects. Those on placebo who smoked had a lower incidence of healing when compared with the patients who did not smoke. There was no difference in healing between antacid­ treated patients who continued to smoke and the nonsmokers. What is the explanation? It would appear that antacid therapy in adequate amounts can be successful in treating an ulcer patient, regardless of the pathogenic mechanism. What Peterson et aJ.5 failed to mention is whether patients whose ulcers did not heal on placebo and had continued smoking were different from the pa­ ti ents who were nonsmokers or those who stopped smoking and whose ulcers did not heal. Patients with ulcer disease who con­ tinue to smoke are constantly harassed by their physicians and are often threatened that they shall enter purgatory if they don't stop smoking. Practically all patients with ulcers who smoke are ingrained with the idea that smoking is bad. Yet they continue to smoke. Do these basic psychologic traits differ from those of the ulcer healer and are these traits the reason for the therapeutic failure? Although not applicable to duodenal ulcer, Doll et aU showed that smoking impaired gastric ulcer healing. However, those gas­ tric ulcer patients who had smoked and quit when instructed to do so by the authors fared better compared with those who had not smoked before. Healing of the ulcer was similar in the non­ smokers and those who were advised to quit smoking and did not. Again the question arises, are the patients who quit smoking dif­ ferent from those who never smoked or did not stop smoking? Until we know the cause of duodenal ulcer and the reason why people smoke, conclusions as to the relationship between the two are pure speculation. The problem is further confused by the fact that smokers are not aiways truthful about whether they have quit smoking. In a paper entitled "Deception among smokers," Sillett et al.

The Influence of Geography on Duodenal Ulcers

This editorial is prompted by my reading of the paper entitled "Peptic Ulcer in Africa" by Clarence A. Snyder and Merton J. Alexander in this issue of theArchivesas well as by reflections on reported geographical factors influencing duodenal ulcer in India and in Norway. While there have been many significant contributions in recent years dealing with the pathogenesis of duodenal ulcer, some factors still remain obscure. One of these is the high incidence of ulcer reported in certain areas, while neighboring regions inhabited by the same race of people remain relatively free from the disease. In my own view a hypersecretion of gastric juice of nervous origin has been established as the sufficient cause of duodenal ulcer in the overwhelming majority of patients in the United States and in Europe. These patients regularly display a hypersecretion of gastric juice in the empty stomach which, if reproduced in the

Observations based on two hundred forty-five consecutive gastrectomies for duodenal ulcer disease at Brooke Army Hospital; comparison of two groups of Billroth II gastrectomies.

Introduction Years of experience and clinical investigation into the cause of duodenal ulcer and the results of treatment have resulted in some general agreement as to factors involved in the pathogenesis of the ulcer and the general methods of management of patients. With respect to the technical aspects of surgical operations designed to cure duodenal ulcer, however, there remains a wide diversity of opinion. There are advocates of Billroth I and Billroth II types of operation, large- or small-stoma, vagotomy with or without gastroenterostomy, antecolic or retrocolic anastomosis, and recently even a proponent of staged procedures for treatment of the disease beginning with gastroenterostomy as a preliminary procedure.1 True comparisons between the end-results of operations which are technically different, but performed on the same general type of patient population by surgeons with similar equipment and treatment facilities, are not often reported. This analysis is thought to be of value

The rationale of antrectomy and vagotomy for duodenal ulcer.

ALTHOUGH the basic cause of duodenal ulcer remains unknown, the importance of gastric acidity is a generally accepted premise motivating the treatment of this lesion. On this basis, in recent years, the surgical treatment of most cases of duodenal ulcer has consisted of more or less radical subtotal gastrectomy and of vagotomy combined with a drainage procedure. More recently some interest has been aroused by the favorable results following combined antrectomy and vagotomy in the treatment of this lesion. To date this procedure has been attended by diminished incidence of weight loss and anemia than in subtotal gastrectomy, less motility disturbances than in vagotomy and gastroenterostomy, and less marginal ulcers than in both procedures. Experience has shown that nothing short of total gastrectomy will completely prevent the occurrence of marginal ulcer. This, of course, is too radical a procedure for a benign lesion. It seems feasible then that more consideration

A theory of pathogenesis of duodenal ulcer.

1. The regular occurrence of hyperacidity in duodenal ulcer cases is emphasized and the cause of this coincidence discussed. Hyperacidity may be the predecessor and cause of duodenal ulcer. 2. The theory of psychosomatic origin of peptic ulcers is criticized. 3. Hyperacidity may be produced by antrum gastritis. 4. Antrum gastritis may develop through excessive use of seasonings in food. 5. As vigorous individuals lean toward excessive use of spices and vigor of constitution is inherited, the frequent occurrence of duodenal ulcers in certain families seems to be explained.

PARTIAL OBSTRUCTION AT DUODENOJEJUNAL JUNCTION AS CAUSE OF ULCER OF DUODENUM

The most frequent cause of partial obstruction at the duodenojejunal angle is the mesocolic band, described by W. J. Mayo in 1908. Until that time the vicious circle following gastro-enterostomy was the terror of all operators. Since Mayo published his description of this band and advocated its separation before gastro-enterostomy is performed, the vicious circle after gastro-enterostomy has been rarely seen. However, he seemed to attach no importance to the presence of this band as the cause of duodenal ulcer. My attention was drawn to its presence as a cause of duodenal ulcer in 1910. After separation of the band that extended down for 5% or 6 inches below the duodenojejunal flexure, the contents of the stomach and duodenum were seen immediately to pass down into the jejunum. The patient appeared to be dying on the table, and the abdomen was closed without the performance of a gastro-enterostomy, although the