Causes and Treatment of Gastric Ulcers
Peptic ulcers are small erosions in the wall of the stomach or duodenum. These areas are normally protected from gastric acid by mu-cosal secretions that form a protective barrier. When this barrier breaks down, damage occurs and an ulcer forms. Symptoms are pain, nausea, and bleeding. Ulcers are common, occurring in about one in 15 adults. The causes are multiple stress, poor diet, food sensitivities, and infection of the stomach by Helicobacter pylori can all contribute. Optimum nutrition can maintain the health of the protective lining of the stomach and duodenum. It can also support the immune system to increase resistance to chronic Helicobacter infection.
Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulcerations. Lancet 1984 1 1311-1315. 3. NIH Consensus Development Panel on Helicobacter pylori in peptic ulcer disease. JAMA 1994 272 65-69. 5. Drumm B, Rhoads JM, Sringer DA et al. Peptic ulcer disease in children etiology, clinical findings and clinical course. Pediatrics 1988 82 410-414. 6. Eastham EJ. Peptic ulcer. In Walker WA, Durie P Hamilton JR et al, eds. Pediatric Gastrointestinal Disease Pathophysiology, Diagnosis, Management, vol 1. Philadelphia BC Decker, 1991 438-451. Nord KS, Rossi TM, Lebenthal E. Peptic ulcer in children the predominance of gastric ulcers. Am J Gastroenterol 1981 75 153-157. Megraud F, Brassens-Rabb MP, Denis F et al. Seroepidemiology of Campylobacter pylori infection in various populations. J Clin Microbiol 1989 27 1870-1873. 31. Oderda G, Forni M, Dell'Olio D, Ansaldi N. Cure of peptic ulcer associated with eradication of Helicobacter pylori....
Homeless adults also suffer several medical problems due to undernutrition. Common problems include anemia, dental problems, gastric ulcers, other gastrointestinal complaints, cardiovascular disease, hypertension, hypercholesterolemia, acute and chronic infectious diseases, diabetes, and malnutrition.
Brillat-Savarin's work reflects interactions with philosophers and physicians of his time. While he remained a bachelor all his life, he had many prominent guests sitting at his table for meals, and he often sat at the best tables of Paris. Among his guests were Napoleon's doctor, Jean-Nicolas Corvisart, the surgeon Guillaume Dupuytren, the pathologist Jean Cru-veilhier, and other great minds. Cruveilhier was such an authority on the stomach that gastric ulcers are referred to as Cruveilhier's disease. Through such interactions, Brillat-Savarin undoubtedly gained knowledge about the chemistry of food and how it relates to the physiology of digestion. So passionate was Brillat-Savarin about food that many people identified him more often as a chef rather than a lawyer.
Acid output has long been investigated as a key factor of ulcer development and gastric cancer. Indeed, patients with higher acid output are likely to have antral-predominant gastritis and eventually duodenal ulcer, but they do not show any predisposition towards gastric cancer.116 Patients with lower acid output, on the other hand, are more likely to have a body-predominant gastritis, which predisposes to gastric ulcer and to the multistep progression of disease that, in rare cases, leads to gastric carcinoma. Polymorphisms of the IL-1P promoter have been linked to altered gastric acid secretion and pre-malignant histological features. Severity of the host response to H. pylori infection was related to individual ability to produce IL-1, which has been demonstrated to be a potent inhibitor of gastric acid secretion, as well as a proinflammatory cytokine.117 The histological pathways of H. pylori infection and mechanisms involved in carcinogenesis are shown in Figure 6.8. Genetic as...
Scientists are now looking at several other organisms as possible causes of atherosclerosis. For example, the Helicobacter pylori organism is now known to be the causative organism in most cases of gastric ulcer and a particular form of stomach cancer. Another bacterium, Nanobacterium sanguineum, is smaller than many viruses, can change shape with ease, and appears to be involved in the calcification of arterial walls and heart valves. Incredibly, this bacterium can coat itself with calcium and embed itself deep within the arterial wall. In such a state, it cannot be killed by antibiotics or the immune system, and is even resistant to hydrochloric acid and formaldehyde. There is mounting evidence that it is also associated with renal stones, dental stones, plaque, and even brain calcification. Several laboratories can now test for the presence of the organism.
Dehydration and electrolyte imbalances, constipation, cathartic colon (a condition in which the colon becomes unable to function properly on its own), and steatorrhea (excessive fat in the feces) are common. May be addictive, and athlete can develop resistance, requiring increasingly larger doses to produce the same effect (or even to induce a normal bowel movement) Self-induced vomiting Largely ineffective in promoting weight (body fat) loss. Large body water losses can lead to dehydration and electrolyte imbalances. Gastrointestinal problems, including esophagitis, esophageal perforation, and esophageal and stomach ulcers, are common. May promote erosion of tooth enamel and increase the risk for dental caries. Finger calluses and abrasions are often present
It is well known that acetylsalicylic acid and other non-steroidal anti-inflammatory drugs (NSAIDs) can cause gastric injury including gastritis, gastric ulcers and gastrointestinal hemorrhage. Gastroduodenal damage can be seen at endoscopy in 20-40 of adults taking NSAIDs, and the overall risk for peptic complications (hemorrhage and perforation) in these patients is about three times greater than in controls.15 There are no data on the frequency of upper gastrointestinal injury in children related to NSAID use. Because of the risk of Reye syndrome and the availability of different types of antipyretic drugs, the use of acetylsalicylic acid and NSAIDs in children has significantly diminished. The routine use of these drugs in different clinical conditions is associated with severe complications such as mucosal erosions and ulceration, and gastrointestinal bleeding. Endoscopic features include hemorrhagic gastric erosions (most often in the corpus) and gastric ulcers (mainly in the...
Exhausting talks, discussions, and distractions (TV, radio, reading) burden stomach and spleen, which are especially sensitive to emotional tensions such as brooding, worries, anger, and fear. Negative emotions block and weaken the qi of digestive organs, resulting in loss of appetite, bloating, regurgitation, and stomach pain. It turned my stomach It ruined my appetite The news made me choke on my food are popular ways of describing this all too common situation. Continuous exposure of the stomach spleen network to emotional stress can cause serious eating disorders and digestive problems such as obesity, bulimia, anorexia, or gastric ulcers.
The gut has received the most attention when evaluating the effects of glutamine supplementation. The importance of circulating glutamine in maintaining gut function and integrity was illustrated in a number of animal studies. In one study, the enzyme glutaminase was infused into several animal species to lower blood glutamine levels to nearly undetectable levels 46 . These animals rapidly developed diarrhea, mild villous atrophy, mucosal ulcerations, and intestinal necrosis. Likewise, Hwang et al. demonstrated that glutamine-enriched parenteral solutions increased jejunal mucosal weight and DNA content and significantly decreased the villous atrophy associated with the use of standard TPN 47 . Others have demonstrated the ability of glutamine-supplemented intravenous or enteral diets to increase villous height and mucosal nitrogen content and stimulate intestinal mucosal growth following starvation 48 . Furthermore, enteral or parenteral glutamine may offer some protection against...
Peptic ulcer, esophageal and gastric neoplastic changes in children are extremely rare. In adults, over the past 30 years, a decreased prevalence of gastric cancer and peptic ulcer with an opposite increase of esophageal adenocarcinoma and GERD have been noted.92 This has been attributed to independent factors amongst which are changes in dietary habits such as a higher fat intake, an increased incidence of obesity and a decreased incidence of Helicobacter pylori infection.17,92 Nevertheless, the frequency, severity and duration of reflux symptoms are related to the risk of developing esophageal cancer. Among adults with longstanding and severe reflux the odds ratios are 43.5 for esophageal adenocarcinoma and 4.4 for adenocarcinoma at the cardia.93 It is unknown whether mild esophagitis or GER symptoms persisting from childhood are related to an increased risk for severe complications in adults.
Imagine the body attacking and damaging its own tissues. When a person has a gastric or peptic ulcer, the hydrochloric acid in the stomach attacks the walls of the stomach, damages the mucosa, and may lead to severe bleeding that compromises the body's ability to deliver adequate oxygen to tissues. This bleeding results in severe anemia.
Epidemiological data about peptic ulcer disease (PUD) are scanty and often related to series investigated by X-rays. Endoscopic data appeared after 1980 and showed a three-fold increase of cases of PUD over earlier findings.5 A review of more than 1000 cases stated that the expected number of new PUD cases in a large children's hospital was evaluated as 3.5 per year.6 Others found that the incidence of PUD was 4.4 10 000 children with a frequency of 3-6 in children who had undergone gastroscopy.7
Peptic ulcers are classified as either primary, when they occur in the absence of an underlying systemic disease, or secondary, when they are caused by medications or other diseases. Acute secondary (stress ulcers), which represent the majority of PUD during infancy and early childhood, occur in association with shock, burns, surgery, sepsis, or intracranial hypertension (Cushing's ulcers).62 Chronic PUD secondary to diseases which produce an increase of gastric acid secretion (Table 6.2) are rare at any age. Acute gastritis Chronic gastritis Duodenal ulcer Gastric ulcer Gastric carcinoma B-Lymphoma (MALToma)
Moderate amounts of caffeine have been shown to increase the secretion of stomach acids and relax muscles and blood vessels in the digestive tract (34). As such, caffeine has been implicated in the aggravation of peptic ulcers. However, since decaffeinated coffee creates the same effects, some other component may be a factor (60). Theobromine has no reported effect on the secretion of gastric acids (28).
Fig. 5.4 Vitamin A as adjunctive therapy in gastric ulcer. 56 men with chronic gastric ulcers were given standard antacid therapy (in doses necessary to reduce stomach pain) or antacid therapy plus 150 000 IU day vitamin A for 4 weeks. Ulcer sizes, which did not differ between groups at the beginning of treatment, were reduced in both groups, but healing was significantly greater in the vitamin A group. Complete healing of ulcers occurred in 19 of men treated with antacids alone, compared with 39 from the antacids plus vitamin A group. (Adapted from Patty I, et al. Lancet. 1982 2 876) Fig. 5.4 Vitamin A as adjunctive therapy in gastric ulcer. 56 men with chronic gastric ulcers were given standard antacid therapy (in doses necessary to reduce stomach pain) or antacid therapy plus 150 000 IU day vitamin A for 4 weeks. Ulcer sizes, which did not differ between groups at the beginning of treatment, were reduced in both groups, but healing was significantly greater in the vitamin A group....
Alcohol is not a nutrient, but 80 percent of consumed alcohol is absorbed in the small intestine. The other 20 percent is absorbed into the stomach. Alcohol is absorbed by simple diffusion, which explains why gastric ulcers are not uncommon in people who drink excessively.
Both research and therapeutic interven-tional studies were directed towards evaluating and suppressing acid secretion (according to the theory 'no acid, no ulcer') until the discovery of H. pylori. The demonstration that duodenal ulcer is almost invariably associated with H. pylori infection, and recurrence depends on its persistence, established the importance of H. pylori as the main etiological factor in PUD.3,29 Indeed, H. pylori infection has been demonstrated in 92 (33-100 ) of children with duodenal ulcer in 14 studies, and in 25 (11-75 ) of children with gastric ulcer in four studies.30 Recurrence of ulcer after healing has been reported in 47 of children where Helicobacter was not eradicated, but it is rare, if not exceptional, in patients in whom eradication was achieved.31 H. pylori is the main known etiological factor in chronic gastritis in adults as well as in children.30
Antibiotics or antacids usually are prescribed to treat stomach ulcers antibiotics to destroy the bacteria, or antacids to suppress stomach acids. In addition, your doctor may recommend dietary treatment. To heal an ulcer, you don't need to eat bland foods, as once thought. Instead, this advice is generally given
Vitamin C plays a role in controlling body and blood his-tamine levels, and blood histamine levels increase when vitamin C status is poor. High levels of histamine can aggravate allergies, asthma, stomach ulcers, and certain psychiatric disorders.
The diagnosis of bile reflux gastropathy should be considered in adults with abdominal pain and bile-stained vomiting, who had previously undergone partial gastric resection or drainage procedures, even though reflux of duodenal contents has been linked to the development of a number of pathological gastric conditions, such as nonspecific gastritis, gastric ulcer, gastric carcinoma and non-ulcer dyspepsia. In adults, an association between bile reflux and intestinal metaplasia in the gastric and cardiac mucosa has been reported, suggesting that the latter represents a defense response against a sustained adverse environment, in the same way that gastric metaplasia develops in the duodenum when subjected to a high acid
Figure 6.3 Endoscopic appearance of a Helicobacter pylori-associated peptic ulcer of the posterior wall of the duodenal bulb in an 11-year-old girl. Figure 6.3 Endoscopic appearance of a Helicobacter pylori-associated peptic ulcer of the posterior wall of the duodenal bulb in an 11-year-old girl. Figure 6.4 Endoscopic appearance of Helicobacter pylori-associated multiple peptic ulcers of the gastric body and hyperplastic regeneration of the surrounding mucosa in a 12-year-old girl. Figure 6.4 Endoscopic appearance of Helicobacter pylori-associated multiple peptic ulcers of the gastric body and hyperplastic regeneration of the surrounding mucosa in a 12-year-old girl. H. pylori-associated gastritis is the most frequent microscopic finding. It is predominantly an antral gastritis, but in some patients, and particularly in adults, inflammation may involve the entire stomach (pangastritis). In children, its severity is usually less, and features of activity (presence of polymorphonuclear...
Basal acid output has been found to be normal in children with PUD in all39-41 but one study.42 Although children with PUD have been shown to have a higher average maximal acid output compared to age-matched controls, the occasional child with peptic ulcer may well have a completely normal maximal acid output. Similarly, control children may occasionally show increased maximal acid output.39-42 This important overlap of values between children with or without ulcer is similar to that reported in adults. Interestingly, children with more severe PUD (requiring surgery, or presenting severe digestive bleeding) have been reported to have values of maximal acid output significantly higher than those with milder forms of disease or in remis-sion.40,42 Basal41 or meal-stimulated serum gastrin43 can be normal or slightly increased in children with ulcer.
A study investigating the presence of gastro-esophageal reflux in children with recurrent abdominal pain concluded that pathological gastroesophageal reflux is a frequent finding in such children.109 Treatment of gastroesophageal reflux in this group of patients resulted in resolution or improvement of abdominal pain in 71 of cases. Another study evaluating findings on endoscopic examinations in 62 Indonesian children with recurrent abdominal pain revealed pathological abnormalities including esophagitis, erosions and duodenitis in 50 of the patients.110 In the absence of peptic ulcers, it is unclear how much these pathological findings contribute to the patients' symptoms. Endoscopy and biopsy performed in children evaluated for dyspepsia demonstrated that most children did not have significant mucosal disease. Inflammation without evidence of peptic ulceration was found in 38 of the patients with H. pylori being identified in only five cases.111 Follow-up at 6 months to 2 years...