Elderly Peptic Ulcer

　　The etiology of elderly peptic ulcers is not fully understood. The more clear causes are Helicobacter pylori infection (helicobacter pylori, HP), the use of non-steroidal anti-inflammatory drugs (NSAID), and excessive gastric acid secretion.

　　1. Helicobacter pylori (HP) infection

　　It is currently believed that Helicobacter pylori infection is the primary cause of peptic ulcers. The hand may be a key factor in the transmission of Helicobacter pylori. A study of 242 Guatemalans in an isolated village shows that 58% of the serum samples are positive for Helicobacter pylori, and 87% of them have Helicobacter pylori in the gaps around their teeth or tongue. It can be seen that there is a significant positive correlation between tongue infection and finger nail infection.

　　Due to the lack of an ideal animal model for HP infection, the evidence that establishes HP infection as a cause of peptic ulcers mainly comes from a large number of clinical observations and randomized controlled studies.

　　Patients with peptic ulcers have a high detection rate of Helicobacter pylori: Peptic ulcers are a multifactorial disease, with HP infection being the most prominent factor among the pathogenic factors. Clinical observations have found that whether it is duodenal ulcer or gastric ulcer, the surrounding mucosa often has HP infection, which can be observed by ordinary HE staining of pathological sections, and it is easier to find with Warthin-Starry or Giemsa staining. The population infected with HP has a 10% to 20% chance of developing peptic ulcers in their lifetime, with a risk rate 3 to 4 times higher than that of the uninfected population. The infection rate of HP in patients with duodenal ulcer is extremely high, and a comprehensive analysis of 24 well-documented papers involving 1695 cases in foreign countries shows an infection rate of 90% to 100%, with an average of 95%. The HP infection rate in the histological and bacteriological detection of gastric ulcer tissue is lower than that of duodenal ulcer, with a comprehensive survey of 1395 cases in foreign countries showing an infection rate of 60% to 100%, with an average of 84%.

　　HP not only has a high infection rate in patients with peptic ulcers, but also the infection rate in patients with non-ulcer dyspepsia has reached 50% to 85%. Therefore, relying solely on the high infection rate of HP in patients with peptic ulcers is not enough to prove that HP is the main etiological factor of peptic ulcers. It is now clear that eradication of HP can accelerate ulcer healing, reduce the recurrence rate of ulcers, and decrease the incidence rate of complications. This may be the most powerful evidence to prove the role of HP.

　　Clinical practice has shown that the recurrence rate of ulcers healed by the use of H2 receptor antagonists or proton pump inhibitors is 50% to 90% within one year after discontinuation of medication. Eradication of HP can shorten the time for ulcer healing and improve the healing rate of ulcers, significantly reducing the recurrence rate of gastric and duodenal ulcers and the occurrence of ulcer complications. The recurrence rate of ulcers the following year after eradication of HP can be reduced to below 10% (most below 5%). If the patient does not have repeated HP infection, they can maintain ulcer non-recurrence for 5 years or longer. In addition, studies have shown that certain strains of HP are associated with the onset of duodenal ulcers; the rapid activation of neutrophils caused by HP is also related to ulcers.

　　2. Non-steroidal anti-inflammatory drugs

　　With the application of different NSAIDs, the frequency of gastrointestinal (GI) complications such as bleeding, perforation, obstruction, or symptomatic ulcers also varies. Approximately 40% of complications have an increased incidence rate. The damage is mainly caused by inhibiting prostaglandin synthesis, which has a negative impact on several factors of mucosal defense. Many NSAIDs have a local irritant effect on the epithelium, which may play a particularly important role in small intestinal injury. Although the presence of gastric acid in the stomach is not the main factor causing gastrointestinal disease induced by NSAIDs, in an acidic environment, anti-inflammatory drugs such as aspirin cannot be ionized and dissolve in gastric acid as a whole. Aspirin in its original form is liposoluble, so it can penetrate the epithelial cells and destroy the mucosal barrier. The absorbed aspirin can also inhibit the activity of cyclooxygenase and interfere with the synthesis of prostaglandins in the gastric and duodenal mucosa, causing mucosal cells to lose the normal protective effect of prostaglandins. Under the action of other substances that damage the mucosa (such as bile), ulcers may occur. In addition, NSAIDs can damage the repair process, hinder hemostasis, and inactivate several growth factors involved in mucosal defense and repair, causing chronic mucosal injury and bleeding through these factors.

　　3. Excessive Gastric Acid Secretion

　　Hydrochloric acid is the main component of gastric juice, secreted by parietal cells and regulated by the nervous and humoral systems. It is known that the membrane of parietal cells contains three types of receptors, namely histamine receptors, cholinergic receptors, and gastrin receptors, which respectively accept the activation of histamine, acetylcholine, and gastrin. The increased secretion of gastric acid in duodenal ulcer patients is mainly related to the following factors:

　　Increased number of parietal cells: Normally, there are about one billion parietal cells in the gastric mucosa, while in duodenal ulcer patients, the average number of parietal cells is 1.9 billion, which is twice as high as that of normal individuals. The increase in the number of parietal cells may be due to the long-term effect of genetic factors and/or gastric acid secretion stimulants (such as gastrin).

　　Increased sensitivity of parietal cells to stimulating substances: The response of duodenal ulcer patients to the secretion of gastric acid after stimulation by food or pentagastrin is greater than that of normal individuals. This may be related to an increased affinity of gastrin receptors on the parietal cells of patients or a decrease in substances (such as somatostatin) that inhibit the secretion of gastric acid in response to gastrin stimulation in the body.

　　Defect in the normal feedback inhibitory mechanism of gastric acid secretion: Normally, gastric acid secretion has an intrinsic regulatory function. However, some duodenal ulcer patients have hyperfunction of G cells in the gastric antrum, and their feedback inhibitory mechanism also has a defect. HP infection can lead to hypergastrinemia, and one of the reasons for the blocked feedback inhibition of gastrin secretion by G cells is the infection.

　　Increased vagal tone: The vagus nerve releases acetylcholine, which has the effect of directly stimulating parietal cells to secrete hydrochloric acid and stimulating G cells to secrete gastrin. In duodenal ulcer patients, where the ratio of basic acid output (BAO) to nocturnal acid output (MAO) increases, there is little response to the secretion of gastric acid caused by eating, suggesting that these patients are under the maximum vagal tone.

　　The base and stimulated gastric acid secretion of gastric ulcer patients is mostly normal or even lower than normal. Only in the gastric ulcer patients with an ulcer in the prepyloric area or those with duodenal ulcer, the gastric acid secretion can be higher than normal. Therefore, the change in the amount of gastric acid secretion seems to be insignificant in the occurrence of gastric ulcers.

　　4. Genetic Factors

　　Genetic factors play a more significant role in the onset of duodenal ulcers compared to gastric ulcers. Ulcer disease sometimes shows a familial multi-morbidity trend, indicating a genetic relationship. Recent research has found that the incidence of ulcer disease in individuals with blood type O is 1.5 to 2 times higher than that of other blood types. This is due to the fact that the gastric mucosal cells of these individuals are more susceptible to bacterial invasion. In vitro experiments have shown that the Helicobacter pylori (HP) responsible for ulcers tends to attack cells with O blood antigen on the surface, and after bacteria come into contact with this type of antigen, they enter the cells, causing infection and chronic inflammation, which lead to the development of ulcers (Thomas Boren, 1993).

　　5. Stress and Psychological Factors

　　It is now a consensus that acute stress can cause acute peptic ulcer disease. Currently, it is believed that psychological fluctuations can affect the physiological function of the stomach, and in patients with pre-existing peptic ulcer disease, symptoms may recur or worsen during anxiety and sadness.

　　6. Smoking

　　Epidemiological and clinical observations have shown that smoking and peptic ulcer disease are closely related. The incidence of the disease in long-term smokers is higher than that in non-smokers. Nicotine in tobacco can slightly damage the gastric mucosa and can enhance the damaging effects of alcohol or NSAIDs on the gastric mucosa; it can also reduce the content of prostaglandin E (PGE) in the mucosa. Long-term smoking can cause hyperplasia of parietal cells and excessive secretion of gastric acid. Nicotine reduces the tone of the pyloric sphincter, making it easier for bile to reflux into the stomach, and can inhibit the secretion of HCO3-, thus weakening the neutralizing capacity of the duodenum against gastric acid.

　　Elderly peptic ulcer disease is prone to complications, and about half of the patients with peptic ulcer disease over 70 years of age have complications. Some patients present with complications as the first manifestation. The use of NSAIDs is one of the reasons why complications are more likely to occur. The mortality rate of complications in elderly peptic ulcer disease is as high as 30%, and its prognosis depends on the patient's age, especially the presence or absence of accompanying diseases.

　　1. Bleeding

　　Bleeding is the most common complication of elderly peptic ulcer disease. Its characteristics are the largest amount of bleeding, easy to recur, and high mortality. Some studies have shown that the mortality rate of bleeding in elderly patients with peptic ulcer disease is 4 to 10 times higher than that in young patients, reaching up to 25%. Some scholars believe that gastric ulcer is more likely to bleed than duodenal ulcer, but opinions are divided on whether the mortality rate is higher.

　　2. Perforation

　　Perforation ranks second among the complications of elderly peptic ulcer disease. Perforation in elderly patients with peptic ulcer disease often does not have typical clinical manifestations. According to statistics, about half of the patients seek medical attention more than 24 hours after onset. 25% to 33% of the patients present with sudden collapse as the first manifestation. 30% to 65% of the patients have no symptoms of peptic ulcer disease before perforation. These factors delay the diagnosis of perforation in elderly patients with peptic ulcer disease. It should be pointed out that the diagnosis of ulcer perforation cannot be excluded because of the absence of free gas under the diaphragm, as 25% to 28% of the patients do not have this sign.

　　3. Pyloric Stenosis

　　The incidence of gastric outlet obstruction caused by peptic ulcer disease has significantly decreased in Western countries, but it is still not uncommon in developing countries. Gastric outlet obstruction is caused by duodenal ulcer-induced deformation of the duodenum, and it is less common in cases caused by gastric ulcer. All patients with peptic ulcer disease complicated by gastric outlet obstruction have a long history of ulceration, and they often have symptoms such as weight loss, emaciation, and metabolic disorders.

　　Older patients with peptic ulcer disease, in addition to upper abdominal pain, may also have other gastrointestinal symptoms such as increased saliva secretion, heartburn, regurgitation, acid regurgitation, belching, nausea, and vomiting. Appetite usually remains normal, but occasionally, due to pain after eating, there may be a fear of eating, leading to weight loss. Systemic symptoms may include insomnia and other neurotic symptoms, or symptoms of autonomic nervous system imbalance such as bradycardia and excessive sweating.
　　Characteristics of peptic ulcer pain:
　　1. Long-term The ulcer can heal itself, but it often recurs after healing, so there is a characteristic of long-term and recurrent upper abdominal pain. The average course of the disease is 6-7 years, and some can last for ten to twenty years or even longer.
　　2. Periodicity The recurrent periodic发作 of upper abdominal pain is one of the characteristics of this type of ulcer, especially prominent in duodenal ulcers. The pain in the upper middle abdomen can last for several days, weeks, or even longer, followed by a longer period of relief. It can occur throughout the year, but it is more common in spring and autumn.
　　3. Rhythmical The relationship between ulcer pain and diet has a significant correlation and rhythm. During the period from 3 am to breakfast, gastric acid secretion is at its lowest, so pain rarely occurs during this time. The pain of duodenal ulcers often occurs between meals and persists until the next meal or after taking antacid drugs. Some duodenal ulcer patients may experience pain in the middle of the night due to higher gastric acid levels at night, especially if they have eaten before going to bed. The occurrence of gastric ulcer pain is irregular, often occurring within one hour after meals, gradually subsiding after 1-2 hours, and reappearing before the next meal, following the same rhythm.
　　4. Location of pain The pain of duodenal ulcers often appears in the upper middle abdomen, or above the navel, or slightly to the right of the navel; the pain of gastric ulcers is also often in the upper middle abdomen, but slightly higher, or below the sternum and slightly to the left of the sternum. The pain range is about several centimeters in diameter. Because the localization of pain from hollow visceral organs on the surface is generally not very accurate, the location of the pain does not necessarily accurately reflect the anatomical location of the ulcer.
　　5. Nature of pain The pain is often dull, burning, or hunger-like, generally mild and tolerable. Persistent severe pain suggests that the ulcer has penetrated or perforated.
　　6. Influencing factors Pain is often induced or exacerbated by factors such as mental stimulation, overfatigue, improper diet, drug effects, and climatic changes; it can be alleviated or relieved by rest, eating, taking antacid drugs, pressing on the painful area with the hand, or vomiting.

　　The etiology of elderly peptic ulcers is complex, and prevention should be carried out in many aspects such as diet and lifestyle.

　　1. Smoking Smokers have twice the incidence of ulcer disease as non-smokers. Smoking affects the healing of ulcers and can promote the recurrence of ulcers.

　　2. Beverages such as alcohol, coffee, strong tea, and Coca-Cola can stimulate an increase in gastric acid secretion and are likely to trigger ulcer disease. Those who consume refined low-fiber foods have a higher incidence of ulcers than those who consume high-fiber foods. Some believe that fibrous foods may have the effect of promoting the release of epidermal growth factor or prostaglandins.

　　3. People who are long-term tense, anxious, or emotionally unstable are prone to duodenal ulcers. During stress, the secretion and motility of the stomach may be enhanced, leading to increased gastric acid secretion and accelerated emptying of the stomach. At the same time, due to the contraction of the gastric duodenal vessels caused by sympathetic nervous system excitement, the blood flow to the mucosa decreases, weakening the mucosal self-defense function.

　　Approximately 10% to 25% of patients with long-term oral non-steroidal anti-inflammatory drugs develop ulcer disease, with gastric ulcer being more common. In addition to the direct stimulatory effect of the drug on the gastric and duodenal mucosa, it is mainly due to the suppression of cyclooxygenase activity by such drugs, which reduces the synthesis of prostaglandins in the mucosa, weakening the protective effect on the mucosa. Aspirin is liposoluble and can penetrate the epithelial cell membrane to destroy the mucosal barrier.

　　The clinical manifestations of elderly patients with peptic ulcer disease are atypical, in addition to medical history and physical examination, diagnosis is mainly made through the following auxiliary examinations.
　　1. Endoscopic Examination
　　Whether choosing fiberoptic gastroscopy or electronic gastroscopy, both are used as the main method for diagnosing peptic ulcer. Under the direct vision of the endoscope, peptic ulcer usually appears as round, elliptical, or linear, with sharp edges, smooth, covered with grayish white or grayish yellow membrane, with surrounding mucosa congestion, edema, and slight prominence.
　　2. X-ray Barium Meal Examination
　　The main X-ray sign of peptic ulcer is the wall niche or shadow, which refers to the barium suspension filling the凹陷 part of the ulcer. In the frontal view, the shadow is round or elliptical, with a regular edge. It forms a transparent area due to inflammatory edema around the ulcer.
　　The shadow of gastric ulcer is often seen in the lesser curvature of the stomach, and it is often accompanied by a spastic gastric incisure on the opposite side of the ulcer. The shadow of duodenal ulcer is commonly seen in the bulb, usually smaller than that of the stomach. The shadow is a direct sign of the presence of an ulcer. Due to inflammation and local spasm around the ulcer, local tenderness and irritation can be found during X-ray barium meal examination. The healing of ulcers and scar contraction can cause deformation locally, especially in the bulb of the duodenum, which can present in the shape of a clover or a petal-like deformation.
　　3. Detection of HP Infection
　　The detection methods for Helicobacter pylori (HP) infection are generally divided into four categories: ① Directly check HP from the gastric mucosal tissue, including bacterial culture, tissue smear or section staining for bacterial examination; ② Determine the activity of gastric urease by methods such as urease test, respiratory test, and detection of urea nitrogen in gastric juice; ③ Serological examination for anti-HP antibodies; ④ Apply polymerase chain reaction (PCR) technology to detect HP-DNA. Bacterial culture is the most reliable method for diagnosing HP infection.
　　4. Gastric Juice Analysis
　　The basal acid output (BAO) of normal males and females is averaged at 2.5 and 1.3 mmol/h, respectively (0～6 mmol/h), and the BAO of patients with duodenal ulcer in males and females is averaged at 5.0 and 3.0 mmol/h. When BAO is greater than 10 mmol/h, it often suggests the possibility of gastrinoma. After the injection of pentagastrin at a dose of 6 μg/kg, the maximum acid output (MAO) is often over 40 mmol/h in patients with duodenal ulcer. Due to the overlap of gastric acid levels in various types of gastric diseases with those of normal individuals, the diagnosis of ulcer disease is only for reference.

　　The main points to pay attention to in the diet of elderly patients with peptic ulcers are as follows.

　　1. Develop good eating habits; have meals at regular times.

　　2. Do not eat spicy foods; avoid spices, coffee, strong tea, soda, acidic beverages, glutinous rice products, and excessive fried foods.

　　3. Do not overeat or undereat.

　　4. Quit smoking and drinking.

　　5. Avoid drinking tea.

　　6. Avoid drinking milk.

　　7. Pay attention to dietary hygiene; failing to do so, having a preference for certain foods, overeating, under-eating, or excessive consumption of cold drinks and cold food, or having a fondness for spicy foods such as chili, strong tea, and coffee, can lead to disorders of gastrointestinal digestion and is not conducive to the healing of ulcers. Paying attention to dietary hygiene, having regular meals with a balanced intake, chewing slowly, is a good habit that promotes ulcer healing.

　　After the diagnosis of senile peptic ulcer, general comprehensive treatment measures are usually taken, including basic treatment in internal medicine, medication, treatment of complications, and surgical treatment. The purpose of treating peptic ulcers is: ①Alleviate clinical symptoms; ②Promote ulcer healing; ③Prevent recurrence of ulcers; ④Reduce complications. However, the existing therapies cannot change the natural course of peptic ulcers or completely cure the ulcers.
　　I. Basic treatment in internal medicine
　　1. Life Peptic ulcers belong to the category of typical psychosomatic diseases. Psychological and social factors play an important role in the onset of the disease, so maintaining an optimistic attitude, a regular lifestyle, and avoiding excessive tension and fatigue are important at both the onset and remission stages of the disease. During the active phase of the ulcer, when symptoms are severe, bed rest for several days to 1-2 weeks is recommended.
　　2. Diet Before the advent of H2 receptor antagonists, dietary therapy had been the only or primary treatment for peptic ulcers. In 1901, Lenhartz pointed out that eating less and more frequently was beneficial to patients. Subsequently, the Sippy dietary therapy was introduced and has been used in clinical practice for decades. The Sippy diet mainly consists of milk, eggs, and butter, and later included some 'soft' non-irritating foods. The principle is that these foods can persistently dilute and neutralize gastric acid. The following views are held regarding the diet of patients with peptic ulcers: ①Chew slowly and avoid hurried eating; chewing can increase saliva secretion, which can dilute and neutralize gastric acid and may have a protective effect on the mucosal barrier; ②Have regular meals at fixed times to maintain the rhythm of normal digestive activity; ③During the acute phase, it is advisable to eat less and more frequently, with 4-5 meals a day, but once the symptoms are controlled, it should be encouraged to return to the usual three meals a day as soon as possible; ④Pay attention to nutrition in the diet, but no special diet is required; ⑤Avoid snacks between meals, and do not eat before bedtime; ⑥During the acute phase, quit smoking and drinking, and avoid刺激性 spices or drinks such as coffee, strong tea, strong meat soup, and chili vinegar, as well as drugs that damage the gastric mucosa; ⑦Do not overeat to prevent excessive expansion of the gastric antrum and increase the secretion of gastrin.
　　3. Sedatives For a small number of patients with symptoms such as anxiety, tension, and insomnia, short-term use of some sedatives or tranquilizers may be appropriate.
　　4. Avoid the use of ulcerogenic drugs Patients should be advised to stop using drugs that may induce or worsen peptic ulcer disease or cause bleeding complications, including: ① Salicylates and non-steroidal anti-inflammatory drugs (NSAIDs); ② Adrenal cortical hormones; ③ Erythromycin, etc. If it is necessary to use the aforementioned drugs for conditions such as rheumatoid arthritis or rheumatoid arthritis, they should be used as enteric-coated formulations or in small doses intermittently. At the same time, sufficient antacid treatment and enhanced mucosal protective agents should be administered.
　　Secondly, drug therapy
　　The drugs used to treat peptic ulcers mainly include medications to reduce gastric acid, drugs to eradicate Helicobacter pylori infection, and drugs to enhance the protective function of the gastric mucosa.
　　1. Medications to reduce gastric acid They include antacids and antisecretory drugs.
　　Antacids react with gastric hydrochloric acid to form salts and water, thereby reducing gastric acid levels. There are many types, including sodium bicarbonate, calcium carbonate, magnesium oxide, aluminum hydroxide, magnesium trisilicate, etc. Their therapeutic effects are as follows: ① Combine and neutralize H+, thereby reducing the retrodiffusion of H+ into the gastric mucosa, and can also reduce the amount of gastric acid entering the duodenum; ② Increase the pH of gastric juice, reducing the activity of pepsin. When the pH of gastric juice is 1.5 to 2.5, the activity of pepsin is strongest.
　　Antacids are divided into two major categories: water-soluble and insoluble. Sodium bicarbonate belongs to the water-soluble category, while others belong to the insoluble category. The former has a quick pain-relieving effect, but has significant side effects when used in large quantities or for a long time. Antacids containing calcium, bismuth, and aluminum can cause constipation, while magnesium preparations can cause diarrhea. It is common to combine two or more antacids into a composite preparation to offset their side effects.
　　2. Treatment of HP infection The treatment of HP infection mainly involves the use of drugs with bactericidal effects. 'Cleared' refers to the disappearance of HP at the end of drug treatment, while 'eradication' refers to the absence of HP recurrence for at least 4 weeks after the end of drug treatment. Clinically, achieving HP eradication can greatly reduce the recurrence rate of peptic ulcers. In vitro drug sensitivity tests show that HP is most sensitive to penicillin under neutral pH conditions, and is highly sensitive to aminoglycosides, tetracyclines, cephalosporins, ofloxacin, ciprofloxacin, erythromycin, rifampin, etc.; moderately sensitive to macrolides, furans, chloramphenicol, etc.; and highly resistant to vancomycin. However, HP is moderately sensitive to bismuth salts.
　　3. Medications to strengthen the protective function of the gastric mucosa The weakening of the protective function of the gastric mucosa is an important factor in the formation of ulcers. Recent research believes that strengthening the protective function of the gastric mucosa and promoting the repair of the mucosa are important links in the treatment of peptic ulcers.
　　4. Gastric motility-promoting drugs In cases of peptic ulcer, if there are obvious symptoms such as nausea, vomiting, and bloating, and laboratory tests show signs of gastric stasis, delayed emptying, bile reflux, or gastroesophageal reflux, gastric motility-promoting drugs should be administered simultaneously.
　　5. Choice of drug treatment There are many types of drugs used to treat peptic ulcers today, and new drugs are constantly being introduced. How to choose is not yet standardized, the following suggestions can be referred to in clinical practice.
　　(1) Principles of drug selection: H2 receptor antagonists can be used as the first-line drug for gastric and duodenal ulcers. Antacids and sucralfate can also be used as first-line drug treatment, but their efficacy is not as good as that of H2 receptor antagonists. Misoprostol, a prostaglandin analog, is mainly used to prevent the occurrence of NSAIDs-related ulcers. Omeprazole can be used as a first-line drug, but in more cases, it is used for refractory ulcers that fail to respond to other drug treatments. In cases with positive HP, a dual or triple therapy should be used to eradicate HP infection.
　　(2) Treatment of refractory and stubborn ulcers: Ulcers that do not heal after regular medical treatment, or symptoms recur during maintenance treatment, or complications occur, are called refractory ulcers; duodenal ulcers that do not heal after 8 weeks of treatment and gastric ulcers that do not heal after 12 weeks of treatment are called stubborn ulcers. At this time, it can be tried to increase the dose of H2 receptor antagonists or use omeprazole, which can heal 90% of stubborn ulcers. The combination of bismuth preparations and antibiotics to clear HP infection has a certain effect on some refractory ulcers. If drug treatment fails, surgery should be considered.
　　(3) Treatment of NSAIDs-related ulcers: Aspirin and other NSAIDs can inhibit the synthesis of prostaglandins in the mucosa, weaken the protective effect of cells, increase the sensitivity of the mucosa to injury, leading to peptic ulcers, especially gastric ulcers. A considerable number of gastric ulcer patients, especially the elderly, have a history of taking NSAIDs. NSAIDs-related ulcers often have no symptoms (50%), and many patients present with bleeding as the first symptom.
　　After NSAIDs-induced ulcers occur, NSAIDs should be discontinued as soon as possible, or the dose should be reduced, or other preparations should be used. H2 receptor antagonists are much less effective for this type of ulcer than for general ulcers. Some people believe that omeprazole (40mg/d) has a good effect, whether NSAIDs are discontinued or not, it can promote ulcer healing. Misoprostol alone or in combination with H2 receptor antagonists has been proven to be helpful for ulcer healing.
　　(4) Prevention and treatment of ulcer recurrence: Gastric ulcer is a chronic recurrent disease, about 80% of ulcer patients will relapse within a year after treatment, and the recurrence rate reaches 100% within five years. How to prevent recurrence is still an unresolved issue. It has been recognized that smoking, high gastric secretion, long history of illness, previous complications, use of ulcerogenic drugs, and Helicobacter pylori infection are important risk factors for ulcer recurrence. Clinically, every patient with peptic ulcer should be carefully analyzed for medical history and relevant examinations, and the above risk factors should be eliminated or reduced as much as possible.
　　(5) Maintenance treatment for peptic ulcers: Due to the high recurrence rate after the cure of peptic ulcers and the high incidence of complications, and the natural course lasting for 8 to 10 years, drug maintenance therapy is an important implementation. There are the following three options for treatment: ①Regular maintenance treatment: Suitable for those with recurrent recurrence, persistent symptoms without relief, coexisting multiple risk factors, or complications. Maintenance method: Cimetidine 400mg, ranitidine 150mg, famotidine 20mg, taken once at bedtime, or oral sucralfate 1g, twice a day. The ideal duration of regular long-term maintenance therapy is still difficult to determine, with most advocating at least 1 to 2 years, and lifelong maintenance for the elderly or those with serious consequences expected from ulcer recurrence. ②Intermittent full-dose treatment: When severe symptoms recur or endoscopy confirms ulcer recurrence, a full-dose treatment course can be given, with reports indicating that more than 70% of patients can achieve satisfactory results. This method is simple and easy to implement, and is easily accepted by most patients. ③Demand-based treatment: This method involves short-term treatment when symptoms recur, and medication is stopped after symptoms disappear. For those with symptoms, short-term drug treatment is used to control symptoms while allowing the ulcer to heal spontaneously. In fact, a considerable number of patients with peptic ulcers stop taking medication automatically after symptoms disappear. Although the healing of ulcers is slower with demand-based treatment, the overall efficacy is no different from that of full-course treatment. The following situations are not suitable for this method: those over 60 years old with a history of ulcer bleeding or perforation, those with more than 2 recurrences per year, and those with other serious diseases.
　　Third, surgical treatment
　　Most of the peptic ulcers, after active treatment by internal medicine, symptoms are relieved, ulcers heal. If HP infection can be eradicated and drug maintenance therapy is continued, recurrence of ulcers can be prevented. Surgical treatment is mainly applicable to: ①Acute ulcer perforation; ②Penetrating ulcer; ③Large or recurrent bleeding, where internal medicine treatment is ineffective; ④Organic pyloric obstruction; ⑤Gastric ulcer with canceration or where canceration cannot be ruled out; ⑥Intractable or refractory ulcers, such as pyloric channel ulcers and postpyloric ulcers, mostly belong to this category.