The coexistence of gastric ulcers and duodenal ulcers is a compound ulcer. This type of ulcer accounts for about 5% of patients with ulcer disease. The majority of patients suffer from duodenal ulcer first, which leads to functional pyloric obstruction and can cause delayed emptying, gastric dilation and stimulate gastrin secretion, which increases gastric acid secretion and pyloric malfunction causing duodenal fluid to flow back into the stomach, repeatedly stimulating the stomach and forming gastric ulcer. In patients with compound ulcers, the occurrence of gastric ulcers precedes duodenal ulcers, but the proportion is small, and there are more men than women with compound ulcers. The incidence of bleeding in this disease is high, but the rate of malignant transformation is low. The aim of treatment is to eliminate the cause, relieve symptoms, heal the ulcer, prevent recurrence and avoid complications. The etiology and pathogenesis of peptic ulcer vary from patient to patient, so each case should be analyzed for possible causative factors and pathophysiology, and appropriate treatment should be given. I. General treatment Life should be regular, work should be combined with work and rest, avoid overexertion and mental tension, if there is anxiety, should be given guidance, if necessary, can give sedative drugs. In principle, we need to emphasize regular meals, avoid spicy, salty food and strong tea, coffee and other beverages. Although milk and soybean paste can dilute gastric acid for a while, the calcium and protein they contain can stimulate gastric acid secretion, so they should not be drunk too much. If you have a habit of smoking or drinking and it is confirmed to be related to the development of ulcers, you should quit immediately. Even if the patient is not taking such drugs, he should be warned to use them carefully in the future. Before the 1970s, the treatment of this disease mainly relied on antacids and anticholinergics. The introduction of H2RA caused the first change in treatment; the eradication of Hp advocated in recent years is a major milestone in treatment. (A) Hp eradication treatment Hp eradication can make most patients with Hp-associated ulcer fully achieve the treatment purpose. There is an international consensus on the management of Hp-associated ulcers, that is, anti-Hp treatment should be given regardless of the initial or recurrent ulcers, regardless of activity or quiescence, and regardless of the history of complications. 1. Treatment options for Hp eradication Hp infection is not easily eradicated due to the reduced activity of most antimicrobial drugs in the low pH environment of the intestine and their inability to penetrate the mucus layer to reach the bacteria. So far, no single drug can effectively eradicate Hp, and therefore, a combination of gastric acid secretion inhibitors, antibacterial drugs or synergistic colloidal bismuth agents has been developed. Treatment options for Hp eradication can be broadly divided into two categories: proton pump inhibitor (PPI)-based and colloidal bismuth-based. A PPI or a colloidal bismuth agent plus two of the three antibacterial drugs, clarithromycin (methomycin), aspirin (or tetracycline), and metronidazole (or tinidazole), make up the triple therapy. the rate of metronidazole resistance in Hp strains is rapidly increasing. Furazolidone has a strong anti-Hp effect and Hp is less likely to develop resistance. Furazolidone can be used instead of metronidazole at a dose of 200 mg/d, divided into two doses. H2RA can be used instead of PPI to reduce the cost, but the efficacy is also reduced. If the initial treatment fails, a quadruple therapy of PPI and colloidal bismuth combined with two antibacterial drugs can be used. 2. The need to continue anti-ulcer therapy after Hp eradication therapy has not been unified. If the efficacy of the treatment plan is high and the ulcer area is not very large, a single anti-Hp therapy can make the active ulcer heal effectively in 1-2 weeks. If the efficacy of the Hp eradication regimen is slightly low, the ulcer area is large, the patient’s symptoms are not relieved at the end of anti-Hp therapy, or there is a recent history of complications such as bleeding, consideration should be given to continuing treatment with acid suppressants for 2-4 weeks after the end of anti-Hp therapy. 3. Review after anti-Hp therapy After anti-Hp therapy, the test to determine whether Hp is eradicated should be performed at no less than 4 weeks after the completion of treatment. Most DU patients treated with a highly effective anti-Hp regimen (eradication rate ≥ 90%) do not need to undergo a test to confirm Hp eradication. Refractory ulcers or DU with a history of complications should establish whether Hp is eradicated. Because of the potential risk of malignancy in GU, in principle, gastroscopy and Hp review should be performed at an appropriate time after treatment. For patients with persistent dyspepsia even after appropriate treatment, whether Hp is eradicated should also be established. (ii) Gastric acid suppressant therapy The healing of ulcers, especially DU, is proportional to the intensity and duration of antacid therapy. Alkaline antacids (such as aluminum hydroxide, magnesium hydroxide and their compound preparations) neutralize gastric acid (with some cytoprotective effect) and have a good effect on relieving pain-like symptoms, but to promote ulcer healing, large doses of multiple doses are required to be effective. The inconvenience of multiple doses and the possible adverse effects of long-term use of high-dose antacids limit their use. Antacids are rarely used as a single treatment for ulcers and can be used as an adjunct to enhance pain relief. The anticholinergic pirenzepine (pipiridiazepine) and the pro-gastrin receptor antagonist proglutamine are not sufficiently effective to treat ulcers and are rarely used for ulcers. The two major types of drugs commonly used in clinical practice to inhibit gastric acid secretion are H2RA and PPI. PPI acts on the production of H+-K+-ATPase, the key enzyme in the terminal step of gastric acid secretion in mural cells, before the mural cells resume acid secretion function. Therefore, PPIs inhibit gastric acid secretion more strongly than H2RA, and their effects are long-lasting. At least four PPIs have been used clinically, namely omeprazole, lansoprazole, pantoprazole and rabeprazole. The general doses are omeprazole 20mg, lansoprazole 30mg, pantoprazole 40mg and rabeprazole 10mg orally once a day; the dose needs to be doubled for Hp eradication therapy. (iii) Gastric mucosal protection therapy There are three main types of gastric mucosal protection agents, namely aluminum thioglycollate, Lizudra (bismuth potassium citrate) and the prostaglandin-like drug misoprostol. These drugs have similar ulcer healing rates to H2RA at 4-8 weeks of treatment. The mechanism of the anti-ulcer effect of aluminum thioglycollate is mainly related to its adhesion to the ulcer surface to prevent the continued attack of the ulcer surface by dispersion and pepsin, promotion of endogenous prostaglandin synthesis and stimulation of epidermal growth factor secretion. Aluminum thioglycollate has few adverse reactions, constipation is its main adverse reaction. In addition to the similar mechanism of action of aluminum thiosemicarbazone, bismuth potassium citrate has a strong anti-Hp effect. Short-term use of bismuth citrate potassium rarely causes adverse reactions except for black tongue; in order to avoid excessive accumulation of bismuth in the body, it should not be taken continuously for a long time. Misoprostol has the effect of inhibiting gastric acid secretion, increasing mucus/bicarbonate secretion in gastroduodenal mucosa and increasing mucosal blood flow. Diarrhea is its main adverse effect and is contraindicated in pregnant women because it can cause uterine contractions. (iv) Treatment and prevention of NSAID ulcers For NSAID-associated ulcers, the NSAID dose should be suspended or reduced as much as possible, and Hp infection should be detected and eradication therapy should be performed. With PPI treatment, the healing of GU or DU may be unaffected or less affected by continued NSAID administration, so when NSAID treatment cannot be discontinued, PPI should be chosen for treatment. Those with a prior history of peptic ulcer or those with severe illness, advanced age, and other factors that are intolerable for ulcers and their complications may be prophylactically treated with concomitant anti-peptic ulcer medications. Misoprostol can prevent NSAID-induced GU and DU. PPI can also play a preventive role, but standard doses of H2RA do not. (E) Prevention of ulcer recurrence Hp infection, NSAID use, and smoking are removable risk factors affecting ulcer recurrence and should be removed as much as possible; when ulcer recurrence is frequent, don’t forget to exclude gastrodinoma. Since a great majority of peptic ulcers are Hp-associated ulcers, and the recurrence rate of ulcers can be significantly reduced after Hp is truly eradicated, it is important to determine the presence or absence of Hp infection. It is important to note that after the Hp infection is “eradicated” or after the initial test is negative, there is still a possibility of a positive test. The re-infection rate in adults after Hp eradication is very low, about 1 to 3 % per year. In the treatment of Hp eradication, Hp is still not eradicated in some patients after one or even two courses of treatment due to factors such as adverse drug reactions to resistant strains and poor patient compliance. Ulcers with complications and refractory ulcers are prone to recurrence, and those of advanced age or with severe disease who cannot tolerate ulcers and their complications are priority targets for recurrence prevention. Maintenance therapy was once the main measure to prevent recurrence of ulcers, but compared with Hp eradication therapy, maintenance therapy requires precipitated dosing, and ulcers can recur after discontinuation, and is less effective than the former, so the status of maintenance therapy needs to be re-evaluated. Maintenance therapy still has a place due to the existence of Hp-negative ulcers, the fact that a small number of ulcers recur after Hp eradication, the fact that the efficacy of current eradication regimens is still not 100%, and the fact that there is still a certain rate of reinfection after Hp eradication. In fact, Hp eradication therapy is complemented by maintenance therapy to most effectively reduce ulcer recurrence and complications. Maintenance therapy is usually done with H2RA body antagonists, and the commonly used regimen is a standard dose of half a dose taken at bedtime, or omeprazole 10mg/d or 20mg orally 2-3 times a week for maintenance therapy. The duration of maintenance therapy should be decided on a case-by-case basis, ranging from 3-6 months for short cases to 1-2 years for long cases, or even longer. Third, the strategy of peptic ulcer treatment For DU or GU with a clear diagnosis by gastroscopy or X-ray, the first step is to distinguish between Hp-positive or negative. If positive, anti-Hp therapy should be given first, followed by 2-4 weeks of treatment to suppress gastric acid secretion at the end of anti-Hp therapy if necessary. For Hp-negative ulcers including NSAID-associated ulcers, conventional treatment as in the past, i.e., taking any kind of H2RA or PPI, can be given for 4-6 weeks for DU and 6-8 weeks for GU. As to whether maintenance treatment should be given, the decision should be made based on the presence or absence of risk factors such as recurrence of ulcers, patient’s age, NSAID use, smoking, combination of other serious diseases, and history of ulcer complications. As for surgical treatment, due to the progress of medical treatment, it is currently limited to a small number of patients with complications. The indications for surgery are: (i) when massive bleeding is ineffective by emergency medical treatment; (ii) acute perforation; (iii) scarring pyloric obstruction; (iv) intractable ulcers for which medical treatment is ineffective; and (v) gastric ulcers suspected of being cancerous. Safety tips 1. Avoid ulcer-causing drugs: non-autologous anti-inflammatory drugs, adrenocorticosteroids, pro-adrenocorticosteroids, reserpine and other ulcer-causing drugs should be stopped as far as possible. If the patient also has a disease that necessitates the use of such drugs, enterosol-type and small-dose intermittent dosing should be used as much as possible. Adequate antacid and gastric mucosal protection therapy should be administered throughout the medication period. Antacid treatment even lasts until 2-3 weeks after discontinuation of adrenocorticosteroids. 2.Rational diet: You should eat three meals on time, with more foods such as pasta, noodles, porridge, soy milk, dairy, beans, meat, vegetables and leaves that are less stimulating and easy to digest, and less spicy condiments. 3, quit smoking and alcohol, reduce the consumption of coffee, Coca-Cola and other beverages. 4. Combine work and rest, ensure sufficient sleep, reduce mental stress, and relieve worries about peptic ulcer.