Peptic Ulcer: A disruption of the mucosal integrity of the stomach

Peptic Ulcer

A peptic ulcer is defined as a disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation. The word peptic refers to pepsin a stomach enzyme that breaks down proteins. A peptic ulcer in the stomach is called a gastric ulcer.

Epidemiology of Peptic ulcer

Peptic ulcer used to be a rare disease before the 19th century. Acute perforations of gastric ulcers were first reported in young girls at the beginning of the 19th century. With the progress of the 19th century, peptic ulcer disease became frequent both in men and women.

In the West, this disease affects equally men and women whereas men are affected 18 times more commonly than women in India.  Broadly, developing countries like India it is impossible to obtain exact figures of disease incidence, and differences are bound to exist between regions. 

A peptic ulcer is more prevalent in Jammu and Kashmir, followed by Southern India. North India comes next, and East and North East have a comparatively lower prevalence

Pathogenesis of Peptic Ulcer

Peptic ulcers occur because of an imbalance between aggressive factors (gastric acid and pepsin) and defensive factors (gastric mucus, bicarbonate, Prostaglandins). Gastric ulceration occurs when mucosal defenses fail, as when mucosal blood flow drops, gastric emptying is delayed, or epithelial restitution is impaired

The factors produce ulceration by aggravating gastric acid and pepsin secretion- 2 categories:

 a. Endogenous factors: These include different visceral neurotransmitters, hormones (acetylcholine, gastrin, histamine, somatostatin, and cholecystokinin), second messengers (Ca2+), genetic factors.

 b. Exogenous factors: These include bacterial infection (H.pylori), NSAID, alcohol, psychogenic factors, and dietary habits.

Endogenous Factors

1. Acetylcholine (ACh): It causes gastric acid secretion in the gastric phase of acid secretion.

ACh exerts a considerable influence on gastric acid secretion through the direct stimulation of parietal cells, the release of gastrin from the pyloric antrum, and modifies the responsiveness of the parietal cells to gastrin and histamine. It is released from the vagus nerve and parasympathetic ganglion cells, which are located in gastric mucosa, stimulates acid secretion directly by parietal cells and indirectly by stimulating the release of histamine. It also stimulates the secretion of pepsinogen, the inactive precursor of pepsin, which also causes peptic ulcers.

Muscarinic receptors are involved in the vagal stimulation of gastric acid secretion, mediated by Ach. The muscarinic M1 receptors appear to be more substantially involved in stress-evoked gastric ulceration and mast cell degranulation. On the other hand, the muscarinic M2 receptors may contribute to ulcer formation by increasing stomach smooth muscle motility, but not by degranulating the mast cells. Muscarinic M3 receptors play a significant role in ACh-mediated gastrin secretion, which plays a major role in gastric acid secretion.

2. Gastrin: It is a major stimulant of acid secretion. After ingestion of food, the release of gastrin is modulated by the protein content of food and accounts for the acid secretory response but as the acidity of food increases or intragastric pH decreases, the gastrin secretion initiated by protein content diminishes. Serum gastrin concentration in peptic ulcer patients is 120 pg/ml. Gastrinoma (Zollinger-Ellison syndrome) is a disorder that results from the over-secretion of gastrin-producing adenoma of the pancreas. There is a continuous stimulation of HCl secretion which cannot be turned off as with a normal physiological mechanism. Fasting serum gastrin concentration in this syndrome ranges from 500 pg/ml to 7500 pg/ml. So, gastrin oversecretion is an important pathophysiologic factor for peptic ulcer development.                       

3. Histamine: It is a paracrine regulator of gastric acid secretion. It exerts its ulcerogenic effect during abnormal physiology by acting through H2 receptors on parietal cells. Stored in mast cells and endocrine cells. Studies on H2 receptor antagonists suggest histamine as the final common mediator of acid secretion as these antagonists block both histamine stimulation but also block the stimulatory effect by gastrin and ACh. Release mediated by increased levels of Ca2+ by gastrin in the parietal cell.

4. Somatostatin and Cholecystokinin: Major evidence that cholecystokinin (CCK) acts as an inhibitor of gastric acid secretion is that exogenous CCK infused intravenously in a physiological dose is capable of inhibiting gastric acid secretion. Both receptors subtypes CCK A and CCK B are involved in the inhibition and facilitation of gastrin action respectively. On activation of CCK A receptor, somatostatin is released which acts through somatostatin receptors on gastrin G cells to inhibit gastrin secretion, and CCK B receptor stimulation by CCK causes increased release of gastric acid.

5. Ca2+ as second messengers: Ca2+ plays an important role in the pathogenesis of gastric ulcers. The administration of calcium both orally or intravenously stimulates acid secretion and increases the circulating concentration of gastrin. Cytosolic free calcium increases the effects of ACh and gastrin on the stimulation of acid secretion by parietal cells. Ca2+ also plays an important role in the release of histamine from enterochromaffin-like (ECL) cells, a powerful chemical mediator of gastric acid secretion, which involves both mobilizations of an intracellular calcium pool and the influx of calcium over the ECL cell membrane.

6. Genetics: Increased familial history – 20-50% of patients. Ulcers are also more common in blood group O subjects and in those who do not secrete blood group antibodies into gastric secretions.

Exogenous Factors

1.  H. pylori: Pylori is a curved or S-shaped gram-negative bacterium approximately 0.5 by 3 µm in size containing four to seven sheathed flagella at one pole.

Mechanism of H. pylori Infection

The success of a pathogen depends on both its virulence and its pathogenicity. Virulence is the ability to infect a host, whereas pathogenicity is the ability to cause disease in the host. A sufficient number of H. pylori must survive the gastric acid barrier and colonize the enteric fluid or mucous layer. Examples of important virulence factors are attachment mechanisms and motility in the intestinal mucous layer.

(i) Binding to mucus and epithelial cells: H.pylori have cell wall-associated lectins which allow them to bind selectively to mucus and epithelial cells. Targets of H.pylori lectins exist in the gastric mucus as glycoproteins and glycolipids. H.  pylori appear to bind to all of these, including sulfated (acid) mucins, L-fucose, D-galactose, and sialic acids. H. pylori lectins also attach to red blood cells of various animal species.

(ii) Tight attachment to cells: H.pylori attaches tightly to the epithelial cell, and a characteristic structure called an attachment pedestal forms. This attachment causes localized cell damage characterized by enhancement of microvilli and disruption of cytoskeletal elements of the cell. Actin polymerization also occurs below the sites of attachment pedestals.

(iii) Elaboration of Enzymes

(a) Urease: Most common and virulence-producing enzyme produced by H. pylori is urease. This enzyme is highly active between the pH of 5 and 8. It hydrolyses urea into ammonia. Ammonia thus generated acts as a potent cellular toxin in 3 ways.

Firstly, it combines with α-ketoglutarate to form glutamine, thus depleting the Krebs cycle of an essential intermediate substrate. Secondly, it interacts with hypochlorous acid to form mono-n chloramine, which also acts as a potent cellular toxin.

Thus, the urease enzyme plays an important role in the virulence of H. pylori and its colonization in gastric mucosa. In the course of H. pylori infection, accumulation of phagocytic cells in the gastric mucosa occurs through two distinct mechanisms: (i) neutrophil recruitment through Interleukin (IL) 8 production which is then released by the gastric epithelial cells, and (ii) release by the bacterium itself of substances with chemotactic activity able to attract phagocytes. These phagocytic cells ingest the microorganism and, as in the case of other pathogens, destroy it through oxygen-dependent and oxygen-independent mechanisms. The release of free oxygen radicals by the neutrophils might play a role in the genesis of chronic inflammation and the development of peptic ulcers. 

(b) Phospholipases A2 and C: The epithelial cell membrane consists of a phospholipid bilayer. Phospholipids are similar to triglycerides except that one of the terminal fatty acids is replaced by a phosphate group.

Phospholipase A2 of H. pylori removes a long-chain fatty acid group from the second carbon. It also attacks membrane phospholipids to liberate arachidonic acid which may then be converted to leukotriene, prostaglandin, or thromboxane.

Phospholipase C removes the phosphate group from the third carbon of the phospholipids. The resultant compounds, diacyl glyceride and particularly lysolecithin, are incapable of forming the normal phospholipid bilayers and may form micellar structures instead, potentially affecting the integrity of the epithelial cell membrane. 

Production of Toxins: H. pylori also produces certain chemo toxins, known as a vacuolating cytotoxin (VacA) which directly act on the epithelial cell surface and damage the defense system. This toxin causes cell injury (characterized by vacuole formation) in vitro and gastric tissue damage in vivo. Vac A renders the cell membrane permeable to urea by causing the formation of transmembrane pores, suggesting it can increase H. pylori pathogenicity by enhancing urease activity. Thus, VacA plays an important role in the pathogenesis of peptic ulcers.

2. Non-steroidal Anti-inflammatory Drugs (NSAID): NSAID use has been associated with the development of gastric ulcers and with the major complications of ulcers i.e., gastrointestinal bleeding, perforation and can even lead to death. NSAID reduces tissue levels of prostaglandins, especially PGE1, PGE2, and PGI2, by inhibiting COX-1, which is the most important mechanism of action. By inhibition of prostaglandin synthesis,

NSAID interfere with the following lines of mucosal defense-

1. Mucous cell secretion of mucin and surface-active phospholipid. Both PGE and PGF induce the secretion of polysaccharide material in the stomach known as mucin, which acts as a protective agent against potential stomach ulceration induced by HCl and pepsin. This implies that NSAIDs cause gastric ulcers by inhibiting the secretion of this cytoprotective substance.

2. Basal bicarbonate secretion from gastric mucosa.

 3. Mucosal proliferation is necessary for ulcer healing.

4. Regulation of mucosal blood flow.

 5. Physiological regulation of gastric acid secretion via feedback inhibition.

NSAID may also cause ulceration by the generation of oxygen-derived free radicals and products of the lipo-oxygenase pathway. COX inhibition by NSAID results in diversion of arachidonic acid metabolism towards lipo-oxygenase pathway, resulting in increased leukotriene synthesis. These leukotrienes can contribute to gastrointestinal ulceration, by two mechanisms, firstly, by a reduction in prostaglandin level and secondly, through the release of oxygen radicals mediated mucosal injury produced in this pathway.

3. Ethanol:  Ethanol damage to the gastrointestinal mucosa starts with micro-vascular injury, namely disruption of the vascular endothelium resulting in increased vascular permeability, edema formation, and epithelial lifting. These effects are secondary to ethanol-induced slowing or cessation of gastric mucosal flow. Alcohol causes the stomach cells to oversecrete both acid and histamine which makes the stomach linings vulnerable to ulcer formation. Ethanol also reduces prostaglandin levels, increases the release of histamine and influx of calcium ions.

Ethanol also produces a marked contraction of the circular muscles of fundic strip. Such a contraction can lead to mucosal compression at the site of the greatest mechanical stress, at the crests of mucosal folds leading to necrosis and ulceration. This reduces the secretion of bicarbonates and the production of mucus and also leads to increased neutrophil infiltration into the gastric mucosa. These neutrophils adhere to endothelial cells, thereby blocking capillaries and induce damage to the endothelial cells through the release of proteases, leukotriene (LTC4), and oxygen-free radicals. These oxygen free radicals also cause increased lipid peroxidation which causes damage to cell and cell membranes, thereby playing a major role in the pathogenesis of acute mucosal injury induced by ethanol. Ethanol promotes oxygen radical attack on proteins at the lipophilic side chain of amino acids.

4. Cigarette Smoking: Continued smoking with advancing age augments the secretion of HCl and pepsin and is also expected to modify the contents of gastric juice and pepsin isoenzyme patterns. The increased gastric acid secretion is mediated through the stimulation of the H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers.

Smoking causes mucosal injury by increasing the content of free oxygen radicals, PAF, pituitary vasopressin, gastric endothelin, and pituitary vasopressin. Smoking and nicotine stimulate pepsinogen secretion also by increasing the chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, NSAID or cold restrain stress. Smoking also alters processes important in gastric and duodenal mucosal integrity or protection such as mucosal bicarbonate secretion, prostaglandin content, mucosal blood flow, or epidermal growth factor.

5. Diet: All foods are capable of stimulating gastric acid secretion through distention of the stomach, but proteins are the major stimulants. Digested protein in the form of peptides, peptones, and amino acids act primarily through the stimulation of gastrin from antral G cells. The aromatic amino acids are the most potent of the amino acids. Amino acids absorbed into the circulation stimulates acid secretion by directly stimulating parietal cells or via gastrin release in humans. Caffeinated beverages (eg. tea, coffee), cola-type beverages, beer, and milk are potent stimulants of gastric acid secretion. Coffee produces acid output equal to 70 percent of peak acid output as compared to Penta gastrin. 5% aqueous tea and coffee beverages act by decreasing PGI2 synthesis. A low fiber diet, high dietary consumption of salt and red/black peppers also cause peptic ulcers. 

6. Psychological Factor (Stress Ulcers): There is considerable evidence that supports the role of stressful life events in the etiology of PUD. Stress-induced ulcers are due to an increase in free radical generation apart from acid pepsin factors. Stress causes an increase in gastric motility, vagal overactivity, mast cell degeneration, reduces gastric mucosal blood flow. Stress may also produce ulceration by the release of histamine with enhanced acid secretion and reduced mucous production. Cold restrained stress-induced ulcers are the result of autodigestion of gastric mucosal barrier, accumulation of HCl, and generation of free radicals.

Types of Peptic Ulcer

Based on location, peptic ulcers are categorized as follows:

Gastric Ulcer: Occurrence of ulcer in the stomach, more commonly in older age group.

Duodenal Ulcer: Occurrence of ulcer in the duodenum. They occur commonly in younger individuals and are evenly distributed among various socioeconomic groups. These patients have higher than normal levels of acid secretion rates. Depending on the severity, peptic ulcers are classified as:

Acute Peptic Ulcer: These ulcers involve tissues to the depth of the submucosa. They may arise in the form of single or multiple lesions. They are found in many sites of the stomach and the first few centimeters of the duodenum.

Chronic Peptic Ulcer: These ulcers penetrate through the epithelial and muscle layers of the stomach wall and may include the adjacent pancreas or liver. In the majority of cases, they occur singly in the pyloric antrum of the stomach and the duodenum. 

Symptoms

The most common symptom of a peptic ulcer is abdominal discomfort. This discomfort comes and goes for several days of the week, generally occurs 2 to 3 hrs after a meal, in the middle of the night, when the stomach is empty.

Other symptoms include blood loss leading to anemia, weight loss, poor appetite, bloating, burping, nausea, and vomiting.

In patients with an advanced-stage emergency, symptoms are sharp, sudden, persistent accompanied by stomach pain, bloody or black stools, blood in vomit, etc

ACUTE PEPTIC ULCER

They are usually multiple erosions due to disruption of the mucosal barrier.

Causes

Stress, drugs like analgesics, steroids, surgeries.

Clinical Features

• Sudden onset of acute pain and tenderness in epigastric region.
• Vomiting with or without haematemesis.
• Often acute peptic ulcers can lead to perforations.
• Acute ulcers after cerebral trauma or neurosurgeries are called as Cushing ulcers.
• Acute ulcers after major burns are called as curling ulcers.

Diagnosis is by gastroscopy.

Treatment

• Intravenous ranitidine 50 mg, 8th hourly.
• IV fluids.
• Blood transfusions if there is bleeding.

Curling’s ulcers

They are acute ulcers that develop after major burns, presenting as pain in the epigastric region, vomiting, or haematemesis. Treatment is conservative- IV ranitidine. IV pantoprazole 80 mg in 100 ml DNS low, later 40 mg IV maintenance.

Note: curling ulcer occurs when burn injury is more than 35%.

Cushing ulcers

They are acute ulcers that develop after cerebral trauma or after neurosurgical operations. Treatment is conservative by IV Ranitidine. It is commonly a single, deeper ulcer more frequently perforates. It can occur in the esophagus and duodenum also.

GASTRIC ULCER

Etiology

It occurs due to an imbalance between protective and damaging factors of the gastric mucosa.

• Atrophic gastritis.
• Smoking, alcohol.
• Helicobacter pylori infection (70%).
• There is either normo-chlorhydria or hypochlorhydria.
• Altered mucosal barrier mechanism.
• Lower socioeconomic group.

Factors involved in Gastric Ulcer Formation

•  Duodenal-gastric reflux containing bile salts and lysolecithin break the mucosal barrier making it more vulnerable for injury, the action of drugs, and pepsin injury.
• Gastric stasis.

•  Ischaemia of the gastric mucosa.

Pathology

 Gastric ulcer is large in size, usually lies in the lesser curvature, the muscular layer act as a floor.

 Posteriorly it may penetrate the pancreas; it may cause torrential bleeding by eroding left gastric (commonly) vessels or splenic vessels or vessels in the gastric ulcer wall.

 Anteriorly it may perforate or penetrate the liver. It may lead to hourglass contracture or tea-pot deformity.

 Microscopically, it shows ulcer craters with chronic inflammatory cells and granulation tissue, endarteritis obliterans, and epithelial proliferation.

 A gastric ulcer > 3 cm – giant gastric ulcer. It has got 6-23% chances to turn into malignancy

 Grossly, a margin of the benign gastric ulcer is clear; deep; near lesser curve; the edge is not everted with gastric mucosal folds converging towards the base of the ulcer.

 95% of benign gastric ulcer occurs towards lesser curve, as it takes more burden of the passage of food and so more of wear and tear. Benign gastric ulcer is rare in a greater curvature, fundus, and cardia.

Types of Gastric Ulcer (Daintree Johnson)

1      In the antrum, near the lesser curve                                      55%                       Normal

2  Combined gastric ulcer with duodenal ulcer                         25%                       High

3     Prepyloric ulcer                                                                 15%                         High

4    Gastric ulcer in the proximal stomach                             5%                             Normal

                                   or cardia

Note: Often in a lesser curve, saddle-shaped ulcers can occur.

Clinical Features

 Equal in both sexes.

 Pain in the epigastric region after taking food, lasting up to two hours. Pain is uncommon during the night. Relieved by vomiting or by inducing vomiting.

 Periodicity: symptom-free interval maybe 2-6 months. Often with seasonal variation.

 Vomiting relieves pain.

 Haematemesis and melaena: Haematemesis is more common.

 Appetite is good but hesitant to eat because eating induces pain and that results in loss of weight.

Differential diagnosis

Hiatus hernia

Cholecystitis

Chronic pancreatitis

chronic gastritis

 dysphagia

carcinoma stomach

Investigations

• Barium meal X-ray to see niche and notch.
• Gastroscopy – for location, type of ulcer, and also to take a biopsy.
• US abdomen mainly to rule out other diseases and to confirm the associated diseases.

Treatment

• Drugs like H2 blockers, proton pump inhibitors, carbenoxolone helps in reducing or eliminating the symptoms but asymptomatic ulcers may exist silently and may turn into malignancy So surgery is the preferred line of treatment. Partial gastrectomy and Billorth I gastroduodenal anastomosis is done.
• Type 4 proximal gastric ulcer is difficult to manage.

Complications of gastric ulcers

• Hourglass contracture; which occurs exclusively in women is due to cicatricial of lesser curve ulcers.
• Tea-pot deformity: (Hand-Bag stomach) is due to cicatrization and shortening of the lesser curvature.
• They present with features of pyloric stenosis.
• Perforation.
• Bleeding by erosion into the left gastric and rarely splenic vessels or to vessels in the wall of ulcer.
• Penetration posteriorly into the pancreas, anteriorly into the liver.
• Malignant transformation usually into adenocarcinoma of the stomach (2-5%).

 Clinical features

1.  Loss of periodicity.
2.  Persistent pain.
3.  Vomiting.
4.  Loss of appetite and weight.
   
    Diagnosis

 Barium meal: It shows filling only in the proximal stomach or double pouched stomach.

 Gastroscopy.

 Treatment

Partial gastrectomy wherein gastric ulcer with a lower compartment of the stomach is removed and Billroth-I anastomosis is done.

DUODENAL ULCER

Etiology

•  Common in people with blood group O +ve.
• Stress, anxiety hurry, worry, curry.
•  Helicobacter pylori infection is an important etiology for duodenal ulcers (90%).
•  NSAIDs, steroids
•  Endocrine causes: Zollinger Ellison syndrome, MEN syndrome, hyperparathyroidism.
•  Other causes: Alcohol, smoking, vitamin deficiency.

Pathology

1.  An ulcer occurs in the first part of the duodenum, usually within the first inch, involving the muscular layer.
2. Sites: a. In the bulb (bulbar)95%.    b. Post bulbar (5%).
3.  Eventually, it shows cicatrization causing pyloric stenosis. Serosa overlying the site of duodenal ulcer shows petechial hemorrhages with speckled red dots, appearing like sprinkled cayenne pepper

Clinical Features

•  In India, the ratio of duodenal ulcer to gastric ulcer is 30: 1. A very high incidence.
• It is common in all socio-economic groups, more with stressed professionals (Type A personality).
• Pain is more before food, in the early morning, and decreases after taking food. Food relive the hunger pain.. Night pains are common.
•  Common in males.
•  Periodicity is more common than in chronic gastric ulcers with seasonal variation.
•  Water brash, heartburn, vomiting may be present.
•  Melaena is more common, haematemesis also can occur.
• Appetite is good and there is a gain in weight.
• It decreases once stenosis develops.
•  Eats more frequently without any restriction.
•  The chronic duodenal ulcer can be uncomplicated or complicated.

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Differences between clinical features of gastric ulcer and duodenal ulcer

Gastric ulcer                                                                    Duodenal ulcer

Pain after food intake                                                     Pain before food intake

Periodicity less common                                                Periodicity more common

Haematemesis more common                                        Malena more common

Weight loss occurs                                                          Weight gain occurs

Equal in both sexes                                                         Common in males

No pain in empty stomach                                                 food realize pain [hunger pain]

Food never reduces pain                                                   Food reduces pain

No pain at night                                                                   Incidence of nocturnal pain

Vomiting is common so it releases the pain                  After taking he feels better so he takes a frequent diet

Tenderness left to the midline of EPG                                Tenderness at duodenal point

Complications of  Duodenal Ulcer

1. Pyloric stenosis: Due to scarring and cicatrization of the first part of the duodenum.

2. Bleeding (10%).

3. Perforation (5%). Both acute and chronic ulcers can perforate. Anterior ulcers perforate.

4. Residual abscess.

5. Penetration to the pancreas.

Investigations

 Barium meal X-ray shows deformed or absence of duodenal cap (because of spasm). The appearance of trifoliate duodenum is due to secondary duodenal diverticula which occurs as a result of scarring of ulcer.

Gastroscopy reveals the type, location of the ulcer, narrowing if any.

Biopsy for the presence of Helicobacter pylori.

 Estimation of serum gastrin level, serum calcium level.

Treatment

I. General measures: Avoid alcohol, NSAIDs, smoking, spicy foods. Have more frequent food.

II. Specific measures:

Drugs

• H2 Blockers: Promotes ulcer healing in 4-8 weeks, by reducing acid secretion.
• Proton pump inhibitors: Inhibit parietal cell H+, K+ ATPase enzyme responsible for acid secretion. . They stop acid secretion completely.
• Antacids: Neutralises the HCl to form water and salt and also inhibits peptic activity.
• Sucralfate is an aluminum salt of sulfated sucrose that provides a protective coat to ulcer craters, promoting healing. It inhibits peptic activity. The dose is 1 g qid for 6 weeks (Before food). It is an effective drug.
• Anti-Helicobacter pylori regime: It is very useful, given for 7-14 days later the proton pump inhibitors are continued.
• Colloid bismuth sulfate is a good drug for ulcers, but it stains the oral cavity and mucosa.
• Misoprostol is the only prostaglandin agonist accepted. Follow-up gastroscopy is a must, to confirm that the ulcer has healed.

Surgery for Uncomplicated DU

•  Highly Selective Vagotomy (HSV).
• Selective vagotomy with pyloroplasty (SV + P).
• Truncal vagotomy with gastrojejunostomy (TV + GJ).
• In HSV, only fibers supplying the parietal cells are ligated. The nerve of the Latar jet which supplies the antrum pump is retained and so no drainage procedure is required in HSV. HSV is also called parietal cell vagotomy or super-selective vagotomy. Here nerve fibers in the last 6 cm of the stomach, just proximal to pylorus are preserved (Crow’s foot). A vagotomy reduces acid secretion, hence ulcer heals. No acid, no ulcer.
• Posterior truncal vagotomy with anterior seromyotomy—Taylor’s operation. It can be done through laparoscopy.