Etiology Of Peptic Ulcer Research Articles

Peptic ulcer is prevalent among shift workers.

To elucidate sleep disturbances in the etiology of peptic ulcers, the prevalence of peptic ulcer disease was compared among shift workers and daytime workers. The subjects (N = 11,657) were employees of various institutions, such as factories, banks, or schools, and had undergone a mass x-ray examination of the upper gastrointestinal tract. With present shift workers (N = 2269), the prevalence of gastric ulcers was 2.38% (N = 54) and that of duodenal ulcers, 1.37% (N = 31). With the past shift workers (N = 2111), the prevalence of gastric ulcers was 1.52% (N = 32) and that of duodenal ulcers, 0.62% (N = 13). On the contrary, with the daytime workers (N = 6525) the prevalence of gastric ulcer was 1.03% (N = 67) and that of duodenal ulcer, 0.69% (N = 45). The working schedule for 752 examinees was unknown. The prevalence of gastric and duodenal ulcers was higher with shift workers than daytime workers. Thus, shift work involving sleep disturbances may play an important role in the development of peptic ulcers.

Peptic ulcer and non-steroidal anti-inflammatory agents.

Aspirin is generally regarded as a cause of gastric ulcer but the role of non-steroidal anti-inflammatory agents and paracetamol in the aetiology of peptic ulcer is unclear. To investigate this we conducted a case control study of 180 matched pairs of peptic ulcer patients and controls obtained from surgical and dermatology outpatient clinics. There were 95 gastric ulcer and 85 duodenal ulcer patients. A statistically and clinically association (relative risk = 5) was found between the regular use of non-steroidal anti-inflammatory agents and gastric ulcer. There was also evidence of positive associations between gastric ulcer and aspirin containing preparations with or without non-steroidal anti-inflammatory agents. By contrast, duodenal ulcer was unrelated to these drugs. Too few patients used paracetamol for any conclusion to be drawn on its role.

Changing demographics of peptic ulcer disease.

The demography of peptic ulcer changed greatly and uniformly in western countries until the middle of this century. The demographic pattern reversed at about the turn of the century, duodenal ulcer becoming the predominant lesion, males the most often affected, and age-distribution shifting towards senior citizens. These changes have not continued beyond the 1950s, in fact a decline in the incidence of duodenal ulcer has been postulated. Although hospital admission rates have declined dramatically, there is no evidence of a general decline in the 'true' incidence of duodenal ulcer in the population. However, major changes are ongoing, but the pattern differs from country to country. These findings indicate that environmental factors other than those characterizing industrialized societies are actively involved in the etiology of peptic ulcer.

Peptic ulcer

The author surveys the pathogenesis and etiology of peptic ulcer; examines the role of autonomic regulation in gastric secretion and notes that more work is needed in this area; considers the role of personality and stress; and discusses treatment with emphasis on psychiatric factors and the role of psychotherapy.

Clinical and Experimental Studies on the Etiology of Peptic Ulcer

Clinical and Experimental Studies on the Etiology of Peptic Ulcer

The geographical distribution and possible factors in the aetiology of peptic ulcer.

The geographical distribution and possible factors in the aetiology of peptic ulcer.

The inactivation by carbenoxolone of individual human pepsinogens and pepsins.

1. Carbenoxolone, in suspension at pH 4·0, inhibits swine pepsin A, and human pepsins 1, 3 and 5. Human pepsin 5 is the most readily inhibited, and human pepsin 1 the least. 2. Inhibition occurs by a process which is time-dependent, temperature-dependent and proportional to the quantity of carbenoxolone suspended. 3. Carbenoxolone, in solution at pH 7·4 and pH 8·0, inhibits the activation of the total pepsinogens of human gastric mucosal extracts and of the individual pepsinogens 1, 3 and 5. Pepsinogen 1 was the most readily inhibited, pepsinogen 5 the least. 4. Chymotrypsin was readily inhibited by carbenoxolone at pH 7·4 and 8·0. Trypsin was not inhibited at pH 7·4 but was inhibited, relatively weakly, at pH 8·0. Pronase was weakly inhibited at pH 7·4 and 8·0 but papain was weakly activated. 5. Carbenoxolone is therefore not a general enzyme inhibitor but shows specificity for enzymes (pepsins and chymotrypsin) which split proteins at the same bonds, rather than for enzymes with similar active centres (chymotrypsin and trypsin). 6. The results suggest that, in vivo, carbenoxolone might diminish peptic activity in three ways: by inactivating pepsinogens irreversibly in the mucosal cells or at some point before their activation to pepsins; by inhibiting pepsins irreversibly in the gastric lumen; and by binding pepsins in the lumen without destroying their activity but decreasing their effective concentration. 7. These results are compatible with the hypothesis that pepsins, and pepsin 1 particularly, are factors in the aetiology of peptic ulcer.

The relationship between the etiology of peptic ulcer and the blood flow and metabolism in the gastric mucosa

The relationship between the etiology of peptic ulcer and the blood flow and metabolism in the gastric mucosa

The Psychosomatic Specificity Hypothesis for the Etiology of Peptic Ulcer

The author reaches the conclusion that the psychosomatic specificity hypothesis for the etiology of peptic ulcer, which was based on physiological, clinical, psycho-analytical and biographical data, has been shown to be compatible with the results of later physiological, behavioral, epidemiological and sociological observations. There have, however, been too few studies in which predictions derived from the hypothesis were systematically tested by apropriate validated methods. As a result the hypothesis still stands more or less at the same degree of probability as when it was formulated. The author indicates how more direct ways of testing would be possible by animal, clinical-investigative, epidemiological, and psycho-therapeutic studies.

Role of south Indian diet in the etiology of peptic ulcer

Experimental studies on the effect of poor south Indian diet, alone and in combination with chilli and tamarind, in relation to experimental peptic ulceration have been made over a period of six months. Plasma protein values were not markedly altered in any of the groups at two, four, or six months. Liver protein values were markedly lowered at 4 and 6 months. Ruminai mucosa showed localized proliferation and hyperkeratinization of the stratified squamous epithe in all the groups at four and six months. Ulcerative lesion of grandular mucosa was observed at four and six months in the animals fed on poor south Indian diet in combination with chilli. It has been observed that the damage to the protective mucous barrier is responsible for the production of glandular ulceration.

Controlling gastric secretion.

Although the etiology of peptic ulcers is not known the removal of hydrochloric acid from the stomach leads to pain reduction and eventual healing of the ulcer. Antiacid therapy usually provides pain relief and contributes toward healing. Preventing ulcer recurrence is much more difficult. A number of new therapeutic methods aimed at controlling gastric secretion are being tested. These new treatments include the use of sodium amylosulfate and X-ray therapy. In the future it is possible that prostaglandins may be used to reduce gastric secretions.

The introductory speech with special reference to the etiology of peptic ulcer

Peptic ulcer is seen frequently among dwellers in the town who suffer from the psychic overwork and irregular eating habit and among persons with autonomic imbalance, abnormal function of diencephalon, nervousness or neurotic character. It is also noticeable that gastric ulcer tends to occur more easily in persons of parasympatheticotonic type than duodenal ulcer. These findings are believed to contribute certainly to establish the ideal treatment and to judge the prognosis of this disease.

ROLE OF SALIVA IN THE AETIOLOGY OF PEPTIC ULCER.

Big differences in the incidence and severity of peptic ulcer in various parts of India have been reported by several workers (Somervell and Orr, 1936 ; Dogra, 1940 ; Hadley, 1959 ; Malhotra, 1964 ; Malhotra et al., 1964). Dogra found there were thirteen times as many cases among the population of Madras as compared with the Punjab. While the ulcer is rare in the arid plains of the Punjab, it is by no means uncommon in its humid hill districts (Wig, 1959). In an earlier communication these striking geographical variations were ascribed to the differences in the food habits producing different kinds of salivary secretions (Malhotra, 1964). In this study these variations in some of the properties of saliva have been examined by quantitative methods.

GASTROINTESTINAL HORMONES IN THE PRODUCTION OF PEPTIC ULCER.

THE ETIOLOGY OF PEPTIC ULCER remains a mystery. The search for the cause has been and continues to be an exciting hygeria. The study of patients with the common garden variety of peptic (ie duodenal) ulcer has taught us frustratingly little other than that in most of the victims there is hypersecretion of acid and pepsin. However, in the experimental laboratory it has been possible to produce ulcers in animals (dogs) which do not ordinarily develop them spontaneously, and nature in its own ingenuous fashion has produced ulcers in man in association with a variety of other conditions—all of which may, with continued study and keener insight, shed some light on the vexing problem of ulcerogenesis. This presentation will concern itself with the possible role of certain gastrointestinal hormones in the production of peptic ulcers and, I have, for the sake of broadening the scope of the subject, taken the liberty of including gastrointestinal humoral

Aetiology of Peptic Ulcer

Aetiology of Peptic Ulcer

Aetiology of Peptic Ulcer

Aetiology of Peptic Ulcer

Etiology of peptic ulcer

HE IMPORTANCE OI peptic activity (pepsin and acid) in the etiology o[ peptic ulcer is implicit in the very name of the disease. Although it is generally agreed that acid and pepsin are a siple qua ,lott tot the development of peptic ulcer, it is important that this not be construed to mean that peptic activity alone determines whether a chronic peptic ulcer develops. Ahhough a "peptic ulcer does not torm in the absence of peptic activity, a number of other factors hel t) to determine whether an ulcer forms when peptic activity is present. There is no single etiologic tactor responsible for this lesion, and each factor that influences the final outcome does so only in a contrihutory cal)acity. Aclually, the development of a chronic peptic ulcer is determined by

The Story of Peptic Ulcer.

In this small volume, Dr. Tonkin holds the reader's interest by keeping him amused while presenting the essentials of what is known about peptic ulcer. The light breezy style of the text, together with the many cartoon-type illustrations, sets the stage for transmitting the author's ulcer prescription, which calls for large quantities of common sense well mixed in a vehicle of philosophy. The factors usually considered in the etiology of peptic ulcer are presented with a broad-minded point of view. The reader is left with the proper impression that numerous facts regarding this disease have accumulated and yet we do not have sufficient information to tie all the facts into a universally accepted etiological mechanism. In my opinion, the majority of our leaders in the field of gastroenterology will take no major exception to the program of management presented in this book as regards uncomplicated duodenal ulcer. However, it is

The role of the sphincter of Oddi in the etiology of peptic ulcer. II. Effects of sectioning the sphincter of Oddi on the resistance of cats to histamine-induced peptic ulcer.

In a previous report, 1 the anatomy, physiology, and pharmacology of the sphincter of Oddi are reviewed in relation to its possible role in the etiology of peptic ulcer. The strategic location of the sphincter is stressed and its function in the control of the flow of important acid-neutralizing juices, pancreatic and biliary, into the duodenum is emphasized. It was found to be sensitive to a wide variety of chemical, pharmacological, and nervous stimuli, most of which tended to induce a state of spasm or hypertonia, which could be relaxed only by very few agents. While the pitfalls of making deductions from animal experiments and applying them to the analysis of clinical peptic ulcer in man are realized it was nevertheless considered indicated to explore the effects of sectioning the sphincter of Oddi in the experimental animal subjected postoperatively to a potent ulcer-inducing stimulus. TECHNIQUE Adult cats each weighing about

The role of the sphincter of Oddi in the etiology of peptic ulcer. I. Evidence from a review of the literature.

The sphincter of Oddi occupies a key position anatomicaly. Situated as it is at the terminus of the main pancreatic and common bile ducts, it regulates the flow of pancreatic juice and bile into the duodenum in response to a wide variety of stimuli. This important sphincter is subject to many influences, mechanical, chemical, pharmacological, hormonal, and nervous. Its role in the etiology of acute and recurrent pancreatitis has been repeatedly stressed in the literature of the past 30 years, with recent reemphasis on section of the sphincter as an operative maneuver of therapeutic value.* The etiologic relationship of the sphincter of Oddi to biliary dyskinesia, cholecystitis, and the postcholecystectomy syndrome is also mentioned, and, in the recent literature, section of the sphincter of Oddi has been recommended in the last-named condition.† It is the intent of this review to stress in addition the possible critical role of the sphincter