High Incidence Of Peptic Ulcer Research Articles

Mast Cells Are Critical for Protection against Peptic Ulcers Induced by the NSAID Piroxicam

Many commonly used non-steroidal anti-inflammatory drugs (NSAIDs) also cause gastrointestinal toxicity, including the development of life-threatening peptic ulcers. We report that mast cell-deficient mice have an extremely high incidence of severe peptic ulceration when exposed to the NSAID piroxicam. This enhanced ulcer susceptibility can be reversed by reconstitution with mast cells. Furthermore, wild type mice treated with diphenhydramine hydrochloride, a commonly used antihistamine that blocks histamine H1 receptors, develop a similarly high incidence of peptic ulcers following piroxicam exposure. The protective effect of mast cells is independent of TNF, blockade of H2 receptors, or acid secretion. These data indicate a critical role for mast cells and the histamine that they produce in prevention and/or repair of piroxicam-induced gastric mucosal injury. Additional studies will be required to determine whether this represents a NSAID class effect that can be exploited to develop novel therapeutic strategies to limit the incidence of NSAID-induced side effects in humans.

Porphyria cutanea tarda and peptic ulcer

A high incidence of peptic ulcer was found in a retrospective study of 199 Bulgarians with porphyria cutanea tarda. Ulcers were found in 35 patients (17.59%), while its incidence in Bulgaria varies between 2.52 and 3.7%. The site of the ulcer was duodenal in 29 porphyriacs, gastric in three, both duodenal and gastric in two and pyloric in one. The pattern of localization was similar to that seen in the general population. Peptic ulcers became symptomatic before the appearance of porphyria in 30 cases. Six (17.1%) of the patients had perforations, while the frequency of this complication in the general population was 1.7-8.5%. Two porphyriacs with perforations died of peritonitis. Ulcers were found in 21 (24.4%) of 86 patients with normal activity of erythrocyte uroporphyrinogen decarboxylase, i.e. they had sporadic (acquired) porphyria cutanea tarda. Two (10%) of 20 patients suffering from the familial form of the disease (with low erythrocyte uroporphyrinogen decarboxylase activity) had ulcers. The examination of 105 unselected porphyriacs showed a significantly higher incidence of blood group B in comparison with the general population (23.8% vs. 16.6%). The association between the porphyriacs with ulcers and blood group B (8 of 21 examined persons) and the rare occurrence of group O (only 4 of 21) was unexpected. An association between porphyria and some of the haptoglobin types could not be established in 98 unselected patients (including those with and without ulcer). More studies are needed to substantiate the validity of blood groups and uroporphyrinogen decarboxylase as genetic markers for porphyria cutanea tarda combined with peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)

Pyloric function five to eleven years after Ramstedt's pyloromyotomy

Pyloric function after Ramstedt's pyloromyotomy was assessed in seven patients aged five to eleven years and compared to that in sixteen normal children. Gastric emptying (T 1/2) of liquid, as measured by the double sampling test, was faster in patients than in normal children. Duodenal reflux was calculated from the sodium content in gastric aspirates. At rest, it was greater in patients than in normal children. In the poststimulatory state, there was no difference. Gastric acid secretion was similar in both groups. Rapid gastric emptying might explain the high incidence of peptic ulcer reported in several series of long-term follow-up patients. Increased duodenal reflux at rest might account for a similar increased incidence in gastritis and dyspepsia.

Effect of cysteamine on gastroduodenal mucosal histamine in rat.

Cysteamine administration to rats is followed by a high incidence of peptic ulceration. The aim of the present study was to investigate the effect of cysteamine on gastric and duodenal mucosal histamine and gastric mucosal histamine formation capacity. After a four hour fast, cysteamine in doses of 50, 100, 200, 300, 400, and 500 mg/kg bodyweight was injected subcutaneously to male Wistar rats; saline injection was used as control. After 24 hours the animals were killed; the stomach and duodenum were removed and examined for ulceration. Mucosal biopsies were taken for histamine studies. Gastric and duodenal ulceration tended to appear with increasing incidence with higher doses. A direct correlation was found between the dose of cysteamine and gastric mucosal histamine (p less than 0.02), and duodenal mucosal histamine (p less than 0.05). Further, a direct relationship was found between gastric mucosal histidine decarboxylase activity and the dose of cysteamine (p less than 0.05). Gastric mucosal histamine and histidine decarboxylase activity showed a direct correlation (p less than 0.001). Gastric and duodenal mucosal histamine and gastric mucosal histamine formation capacity were higher in rats with ulcers than in controls and rats without ulcers. In rat, cysteamine induces dose related changes in mucosal histamine and histidine decarboxylase activity. These changes are related to ulcer formation; histamine may be involved in the pathophysiology of cysteamine induced ulcer formation.

High Incidence of Peptic Ulcer among Shift-laborers

High Incidence of Peptic Ulcer among Shift-laborers

Peptic ulceration and cardiovascular disease.

A post-mortem study of two series, a consecutive series of 513 cases and a retrospective study of 65 cases of peptic ulceration, was carried out to ascertain the relationship of atheroma, calcification and aneurysm of the abdominal aorta, severe atheroma of the coronary arteries and aortic stenosis to peptic ulceration. In the retrospective series, 41 cases had peptic ulceration or atrophic gastric mucosa. There was a high incidence of peptic ulceration associated with severe aortic stenosis, severe atheroma and calcification of the abdominal aorta and severe atteroma of the coronary arteries. In this study, there was no increased incidence of peptic ulceration with aneurysm of the abdominal aorta. It was concluded that in the elderly, giant, silent peptic ulcers were associated with pathological changes in the cardiovascular system resulting in a decrease in blood supply to the gastric and duodenal mucosa.

The Sailor’s Stomach

AbstractThe incidence of peptic ulceration in the Royal Navy is higher than in a comparable civilian population and has been rising. It is highest in sedentary groups and lowest in active groups in which physical activity and job satisfaction appear to be important. Four factors appear directly responsible for the high incidence of peptic ulceration in sailors: the personality of those attracted to a seagoing life; operational conditions associated with tension, responsibility and manpower shortages; inadequate physical activity; a diet rich in refined carbohydrates. Contributory factors are smoking, alcohol, noise, domestic unhappiness and intestinal parasites. Job satisfaction and physical fitness appear to reduce the risk. A link appears to exist between peptic ulceration and urolithiasis in the Royal Navy. Gastric secretory studies have failed to provide meaningful information and high acid levels have been found in groups with the lowest incidence of peptic ulceration. Changes in catering arrangements, diet and conditions of service are unlikely to reduce the incidence of peptic ulceration.

Inactivation of gastrin-like synthetic peptide by the liver and serum, and its clinical significance.

Using the method of gastrin bioassay and its modified technique, the inactivation of gastrin-like synthetic peptide was found to exist both in the liver and serum. The experimental liver damage induced by carbon tetrachloride (CCl4) reduced the gastrin-like peptideinactivation in the liver. These findings may indicate that the high incidence of peptic ulcer among the patients with liver diseases is due in part to hypergastrinemia caused by a disturbed inactivation of endogenous gastrin in the liver.

Gastrointestinal Manifestations of Hyperparathyroidism

INTEREST in the association between endocrine tumors and gastrointestinal lesions has been quite active in the last decade, stimulated mainly by the delineation of the Zollinger-Ellison syndrome.1However, other endocrine-gastrointestinal relationships have been studied as well, in particular, gastrointestinal symptoms with hyperparathyroidism.2Furthermore, a high incidence of peptic ulcer has been found to be associated with the syndrome of multiple endocrine adenomatosis3(adenomas affecting the anterior pituitary, parathyroid, pancreas, adrenal, or thyroid glands). However, the exact mechanism of symptoms, the incidence and the significance of the coexisting lesions, and the relationship between the endocrine tumor and the gastrointestinal lesion remain obscure. Because of the relative rarity of these syndromes and the importance of early diagnosis, we are presenting three case reports of hyperparathyroidism that initially were associated with gastrointestinal symptoms. Report of Cases Case 1. —A 44-year-old woman was first examined at the Cleveland Clinic in September 1963, because of

PORTACAVAL SHUNTING AND UPPER GASTROINTESTINAL BLOOD FLOW.

Diversion of portal venous blood into the systemic circulation is associated with a high incidence of peptic ulcer in man. 1 Gastric secretory levels in patients with portacaval shunts are not above normal, but are probably elevated from preoperative values. 2 In the dog, portacaval shunting definitely enhances the rate of acid secretion by the stomach. 3 This has been shown to be due to a circulating substance, probably histamine. 4 The purpose of the present study was to determine, in the dog, changes in gastric, duodenal, pancreatic, and esophageal blood flows following creation of portacaval shunts. The radioisotope ( 42 K or 86 Rb) distribution method was used to measure tissue blood flows. Materials and Methods End-to-side portacaval anastomoses were constructed in nine healthy mongrel dogs. The control group consisted of 13 normal animals that had undergone no operation. All dogs were fed a standard diet of commercial dry cereal

PEPTIC ULCER AND RHEUMATOID ARTHRITIS: A PROSPECTIVE STUDY.

HERE IS CONFLICTING evidence in the literature about whether or not adrenal corticosteroid hormones can cause peptic ulceration when they are given to patients with rheumatoid arthritis. 1-9 Several reports have shown that there is a high incidence of peptic ulcer in patients with rheumatoid arthritis. It has been assumed that this complication was due to corticosteroid therapy. 2-4,6 Other reports have suggested that an increased incidence of peptic ulceration in patients with rheumatoid arthritis has no relationship to the steroid therapy. 5,7-9 These conflicting findings suggest that the populations of patients studied may have been different with respect to stage, severity, and duration of disease, dosage of steroids, or criteria of diagnosis of either arthritis or peptic ulceration. A re-examination of this problem has been undertaken with a design such that an accurate definition of rheumatoid disease has been made. This is a prospective study in a well-characterized population

ZOLLINGER-ELLISON SYNDROME.

Few clinical states have aroused more interest and curiosity among physicians than has the Zollinger-Ellison syndrome. In the eight years since its description in 1955, pathologists, physiologists, and clinicians have become very much aware of the intriguing relationship between endocrinopathy and peptic ulceration despite the fact that the syndrome is infrequently encountered. In 1954 Wermer 18 called attention to the high incidence of peptic ulceration in patients having polyendocrine adenomatosis, but it was the report of Zollinger and Ellison 23 a year later which stimulated great interest in the syndrome consisting of fulminating peptic ulceration, gastric hyperacidity, and pancreatic islet-cell adenomas. It is now known that multiple endocrine glands are involved in 20% to 30% 8,11 of patients presenting with this clinical state, and it is probable that this figure is conservatively low. Approximately 70 instances of polyendocrine adenomatosis have been reported, and most of the recent reports have been

Adrenocortical function in chronic pulmonary disease.

RECENT reviews have emphasized the fact that in patients with pulmonary emphysema, there is an extraordinarily high incidence of peptic ulceration.1 2 3 4 It has further been shown that complications of peptic ulcer are more common in these patients than in those without pulmonary disease. The incidence of peptic ulcer in subjects with chronic obstructive pulmonary disease ranges in different series from 19 to 43 per cent. It has been postulated that patients with chronic obstructive airway disease are in a state of constant stress that induces hyperadrenocorticism, with a resultant high incidence of peptic ulcer. However, definitive studies to substantiate this . . .

The effect of pancreatic fistula on gastric secretion.

Zollinger and Ellison first called attention to instances of recurrent peptic ulceration associated with islet cell tumors of the pancreas.¹These were characterized by hyperacidity and hypersecretion of acid gastric juice and not controlled by vagotomy and extensive gastric resection. Previous experimental studies have also demonstrated an interrelationship between the pancreas and gastric secretion. Dragstedt reported in 1942 that approximately 100% of dogs with external total pancreatic fistulae developed duodenal ulcer, whereas dogs in whom the pancreatic ducts had been ligated had only a 29% incidence of duodenal ulcer. He further found that dogs upon whom a pancreatectomy had been performed developed ulcer in only 1%-3%.²In all three of these preparations the external secretion of the pancreas is absent from the duodenum. The internal drainage of bile and pancreatic juice to the terminal ileum in the Mann-Williamson dog also results in a high incidence of peptic ulceration.

Peptic ulcer and pulmonary emphysema.

Most surgeons are unaware that patients with pulmonary emphysema have an inordinately high incidence of peptic ulceration and that these ulcers are of a peculiarly complicated and resistant nature. This paper is a review of the incidence of peptic ulcer in our own Emphysema Registry, an investigation of gastric secretory activity in 20 patients with marked emphysema, and a study of pathogenic factors that may relate to the two conditions. The clinical implications of these findings are discussed. <h3>I. Frequency of Coexistence of the Diseases</h3><h3>A. Incidence of Peptic Ulcer in Patients with Emphysema.</h3> —Green and Dundee,¹in 1952, found a 19% incidence of ulcer in both a clinical and an autopsy series of patients with proved emphysema. In a similar study, Flint and Warrack²found a 21% incidence of peptic ulceration in 87 autopsy patients with proved emphysema, as compared with an incidence of 1.6% in a

Peptic ulcer and mental disorder—II

1. (1) A total of 2068 male psychiatric patients were investigated for a history of peptic ulcer, and the results compared with findings in a similar survey of actively working men. 2. (2) After correction for age, the incidence of peptic ulcer was found to be lower amongst psychotics and higher amongst neurotics than in mentally normal men. 3. (3) The low incidence amongst psychotics was found to be almost entirely due to the very low incidence amongst schizophrenics. 4. (4) Amongst the neurotics the highest incidence was in those that were depressed. 5. (5) There is a high incidence of peptic ulcer amongst alcoholic addicts. 6. (6) There is a high incidence of peptic ulcer amongst patients suffering from asthma.

Peptic ulcer and mental disorder. I.

Abstract 1. (1) A total of 2068 male psychiatric patients were investigated for a history of peptic ulcer, and the results compared with findings in a similar survey of actively working men. 2. (2) After correction for age, the incidence of peptic ulcer was found to be lower amongst psychotics and higher amongst neurotics than in mentally normal men. 3. (3) The low incidence amongst psychotics was found to be almost entirely due to the very low incidence amongst schizophrenics. 4. (4) Amongst the neurotics the highest incidence was in those that were depressed. 5. (5) There is a high incidence of peptic ulcer amongst alcoholic addicts. 6. (6) There is a high incidence of peptic ulcer amongst patients suffering from asthma.

Peptic ulcer and pulmonary emphysema; their association in hospitalized patients.

For a number of years various clinicians at this institution have been aware of a seemingly high incidence of peptic ulcer in patients with pulmonary emphysema. Little documentation of this association has appeared in the literature, and we have noticed that many physicians are not alert to it. Unrecognized peptic ulceration has been found at postmortem examination in patients with pulmonary emphysema, and in a few instances death has been due to complications of such ulceration. The present review was undertaken to determine the extent of this association in a large representative group of patients. METHODS AND MATERIALS Protocols of all patients with the diagnosis of chronic diffuse pulmonary emphysema hospitalized during the years 1950 to 1953 were reviewed. A total of 586 patients was included. Of these, 479 were studied clinically and 107 were autopsied. The clinical diagnoses were recorded at time of discharge by resident physicians and represent

Experimental Spontaneous Peptic Ulcer

In this work physiological processes other than the occurrence of peptic ulcer were being studied after jejuno-colostomy. A resulting and unexpected high incidence of peptic ulcer, however, has led to a study of this condition. All operations were performed on healthy adult dogs under morphine-ether anesthesia, using aseptic technique. Through a right paramedian incision the jejunum was isolated and sectioned approximately 25 to 30 cm. distal to the ligament of Treitz. Both ends were inverted. A side-to-side anastomosis was then made between the proximal jejunal stump and the caecum, or ascending colon. At no time during the procedure was the stomach, duodenum or upper abdomen handled or explored, thus eliminating the element of trauma. The abdomen was closed. For 3 days after operation the animals were given intravenous saline only. Fluids and solid food were then given by mouth in gradually increasing amounts, until they were receiving the regular stock diet. Seven dogs have died at intervals, longer than 8 days after operation. In 6 of these 7 animals, autopsy revealed on gross examination acute to more chronic forms of peptic ulcers. In one dog autopsied 8 1/2 days after operation an acute gastric ulcer, 2×2 mm., with destruction of the mucosa was found 4 cm. proximal to the pylorus. Two other animals, having died 14 and 27 days after operation, showed gastric ulcers in the pre-pyloric region. The first was an acute ulceration of the mucosa with rounded margins, measuring 2×2 mm., and the other was a large ulcer 1×0.6 cm., having indurated and rolled margins and penetrating deeply into the stomach wall. Near this last ulcer was a second small acute ulceration 2×1.5 mm.