Gastric And Duodenal Ulcer
Gastric and duodenal ulcer (peptic ulcer) represent a circumscribed disruption of gastric or duodenal wall continuity, single or multiple,which is accompanied by a fibrous reaction. These interruptions can penetrate gastric or duodenal mucosa and can reach up to the serous.
Peptic ulcer until recently represented a disease with chronic, cyclical evolution, in which the peptic factor was incriminated. The concepts of this pathology, in recent years, have changed a lot, making peptic ulcer from a disease in which acid secretion was required (“No acid, No ulcer”), a disease caused by an infectious agent (Helicobater pylori).
Besides involvement in the development of peptic ulcers, Helicobacter pylori is involved in the development of chronic gastritis, gastric lymphoma and gastric cancer.
The prevalence of peptic ulcer is 5% – 10% in the general population, but prevalence based on pathological studies is 20% -30% in men and 10% – 20% in women. The current trend is a marked decrease in the prevalence of peptic ulcer due to eradication of Helicobacter pylori infection.
- Infection with Helicobacter pylori, once acquired, remains in the body for life, if is not treated.Helicobacter pylori infection is manifested as a acute gastroduodenitis, which becomes chronic and will be responsible for peptic ulcer development. Helicobacter pylori acts on gastric mucosa, both directly and indirectly by increasing acid secretion. Direct mechanism is determined by the inflammatory process made by toxins secreted by Helicobacter pylori, which generates an acute gastritis, which becomes chronic. Indirect mechanism is represented by the fact that bacteria secrete urease, leading in this way to a alkaline gastric juice, which stimulates secretion of gastrin and acid hypersecretion. Due to, acid hypersecretion that reaches the duodenum, here are some changes which consist in transforming the duodenal epithelium in gastric epithelium (gastric metaplasia). In duodenum, Helicobacter pylori can not develop on the duodenal lining, it can only develop in areas with gastric metaplasia.
- Hypersecretion of acid gastric juice.
- Bile acids, are another aggressive factor with ulcerogenic effect through the mechanism of emulsification of lipids from the lining cells of the stomach.
- Smoking: certainly a factor that is decreasing alkaline pancreatic secretion and stimulate the acid secretion.
- Potentially ulcerogenic drugs: aspirin and NSAIDs and the administration of corticosteroids in large doses and for a long period of time.
- Individual, genetic factors, there are studies showing familial aggregation of peptic ulcer (peptic ulcer prevalence increased in first degree relatives of the patients), and the existence of genetic markers (blood group O).
- Other factors often incriminated, are represented by stress, chronic alcohol consumption and various diets.
Diagnosis of peptic ulcer:
Clinical diagnosis of peptic ulcer is based on the classic symptomatology with rhythmicity and regularity. The character of pain is related to eating (hunger pain), the appearance of pain in spring and autumn is a typical signs that may suggest a peptic ulcer. Lately, more ulcer are frequent discovered by endoscopy in the a
bsence of typical symptoms. Thus, any epigastric dyspepsia should be suspected as an peptic ulcer. Sometimes, the onset may be dramatic with upper gastrointestinal bleeding or perforation.
Other symptoms that may occur in peptic ulcer are vomiting, changes in appetite and dyspeptic symptoms (belching, bloating, early satiety).
Paraclinical diagnosis is made by demonstrating the presence of peptic ulcer and by demonstrating the existence of Helicobacter pylori infection.
- Digestive endoscopy, is a highly sensitive diagnostic method because it allows accurate assessment of the ulcer, by recognizing the lesion, by demonstrating it’s activity and by demonstrating the presence of a hemorrhage. Moreover, endoscopy allows biopsies in peptic ulcers which can highlight the benign or malignant character of the lesion. Evaluation of a healed peptic ulcer is also done by endoscopy which can demonstrate the existence of the scar.
- Radiography of peptic ulcer, may be a complementary method of diagnostic, especially when is suspected a gastric emptying disorder (pyloric stenosis).
- Determination Helicobacter pylori, the causative agent of most peptic ulcers, is a compulsory element in the diagnosis of peptic ulcer. Determination of Helicobacter pylori is made by direct methods and indirect methods.
- Direct methods require endoscopy with biopsy. The presence oh Helicobacter pylori is determined by histological examination.
- Indirect methods dose not require endoscopy and are represented by the determination of Helicobacter pylori antibodies from the plasma and respiratory tests. Helicobacter pylori antibodies, also can be detereminated in saliva and eradication of Helicobacter pylori infection can be demonstrated by determination of bacteria in the stool (fecal test antigen against Helicobacter pylori). The most sensitive indirect methods of diagnosis of infection with Helicobacter pylori are respiratory tests and fecal antigen anti Helicobater pylori.
Evolution of peptic ulcer:
Over the past 20-30 years, the evolution of peptic ulcer was improved and is mostly favorable, complications were reduced significantly, and cases that are requiring surgery are relatively rare. The introduction of anti Helicobacter pylori therapy led to a decrease of ulcer recurrences.
The possible complications of peptic ulcer are:
- Upper gastrointestinal bleeding, is the most common complication, approximately 15%;
- Pyloric stenosis;
- Malignancy of the ulcer, the risk of developing this complication is low.
Peptic ulcer treatment:
In peptic ulcer is generally recommended to be avoided acidic foods and spicy foods. Smoking is banned because it turned out that is delaying ulcer healing, in contrast diet and the abolition of caffeine have not been shown to hasten the healing process of ulcerous lesion. Excluding coffee in full pain relapse may be recommended. In patients with active peptic ulcer is prohibited consumption of NSAIDs, aspirin and corticosteroids.
Drug therapy consists in administration of:
Antisecretory drugs, like histamine H2 receptor blockers (ranitidine, famotidine) or proton pump inhibitors (omeprazole, lansoprazole), for a period of 6-8 weeks.
Treatment schemes for eradication of Helicobacter pylori infection:
Indications for treatment for eradication of Helicobacter pylori infection is contained in the Maastricht European consensus, they are:
- Active peptic ulcer or peptic ulcer in the past and complicated peptic ulcer;
- Gastric lymphoma;
- Atrophic chronic gastritis;
- After gastric resection for gastric cancer;
- First-degree relatives of patients with gastric cancer.
Schemes to eradicate the Helicobacter pylori infection are containing proton pump inhibitors (omeprazole, lansoprazole) combined with two antibiotics. The schemes use triple or quadruple therapy.
Triple therapy is used in practice for a period of 7 to 10 days and in case of failure is passes to quadruple therapy for a period of 10 days.
Checking Helicobacter pylori eradication is done by endoscopy with biopsy.
Endoscopic treatment is aimed especially in peptic ulcer complications.
Surgical treatment of peptic ulcer has decreased greatly, with the appearance of current drug treatment. Absolute indications for surgery are perforation and penetration of the peptic ulcer.