Peptic Ulcer Disease
A peptic ulcer is a break in the lining of the gastointestinal tract, extending through to the muscularis mucosae of the bowel wall. Whilst they may technically appear anywhere in the gastrointestinal tract, they are most often located on the lesser curvature of the proximal stomach or the first part of the duodenum.
The incidence of peptic ulcers is estimated to be 0.1-0.19% of the population per annum, with duodenal ulcers typically presenting earlier than gastric by around two decades. A recent systematic review revealed patients are 13 times more likely to bleed from an ulcer if they are over age 70 compared to those under the age of 40
In this article, we shall look at the clinical features, investigations and management of peptic ulcer disease.
The normal gastrointestinal mucosa is protected by numerous defensive mechanisms, such as surface mucous secretion. Ulceration occurs when there is an overwhelming presence of a noxious substance, or when these natural barriers are impaired; such as in the presence of Helicobacter pylori (H. pylori) or Non-Steroidal Anti-Inflammatory Drugs (NSAIDs).
Helicobacter Pylori and Peptic Ulcers
H. pylori is a Gram negative spiral-shaped bacillus, found in the mucous layer of those with duodenal ulcers (90%) or gastric ulcers (70%). It survives in the stomach by producing an alkaline micro-environment, and induces an inflammatory response by:
- Invoking an cytokine and interleukin driven inflammatory response
- Increasing gastric acid secretion in both the acute and chronic phases of infection, increasing the release of histamine which acts on parietal cells
- Damaging host mucous secretion by degrading surface glycoproteins and down-regulating bicarbonate production
NSAIDs can result in peptic ulcers by inhibiting prostaglandin synthesis. This results in a reduced secretion of glycoprotein, mucous and phospholipids by the gastric epithelial cells, which would otherwise normally contribute to the barrier protecting the gastric mucosa.
The two main risk factors are H. pylori infection and prolonged NSAID use. Other risk factors include:
- Gastrinoma (Zollinger Ellison Syndrome)
- Foreign body ingestion e.g batteries
- Steroid use
Zollinger-Ellison Syndrome refers to a triad of (i) severe peptic ulcer disease; (ii) gastric acid hypersecretion; and (iii) gastrinoma. The characteristic finding is a fasting gastrin level of >1000 pg/ml. A third of these cases are discovered as part of Multiple Endocrine Neoplasia Type 1 syndrome (Pancreas/Pituitary/Parathyroid tumours), so further investigations including serum calcium are important.
Up to 70% of peptic ulcers are asymptomatic. Moreover, significant pathological processes, such as malignancy, pancreatitis, and mesenteric angina can all mimic the symptoms of an ulcer. Therefore, a thorough history, examination, and investigation is warranted.
- Epigastric pain
- Typically exacerbated by eating
- Nausea and anorexia
- Weight loss
- Epigastric pain
- Worse around 2-5 hours after consuming after a meal
- Worse when fasting yet can often be alleviated by eating
Less commonly patients may present with complications of peptic ulcer disease, such as bleeding, perforation, or gastric outlet obstruction.
The ALARMS symptoms (Anaemia/Lost weight/Anorexia/Recent rapid onset/Meleana/Swallowing difficulties) is a useful mnemonic that has been historically used as a basis for referral for urgent endoscopy.
Recent NICE guidance recommends urgent endoscopic referral for anyone with dyspepsia who is >55yrs with recent onset symptoms or with any of the following:
- Chronic gastrointestinal bleeding or iron deficiency anaemia
- Progressive unintentional weight loss
- Progressive difficulty swallowing
- Persistent vomiting
- Epigastric mass
All other patients should be managed conservatively prior to any investigation.
Any condition that causes dyspepsia, chest pain, or abdominal pain can be considered a differential for peptic ulcer disease. However, those most important to rule out when assessing the patient include gastric malignancy, pancreatitis, acute coronary syndrome, gastro-oesphageal reflux, and cholecystitis/biliary colic.
Any patient older than 55yrs or with any of the ALARMS symptoms should be referred for an immediate upper GI endoscopy. A upper GI endoscopy allows biopsies to be taken for histology and rapid urease “CLO” test (histological test used for determining presence of H. pylori)
For patients presenting with dyspepsia, younger than 55yrs, without ALARMS symptoms, and who have not responded to lifestyle changes and antacid therapy, non-invasive H. pylori testing is required, such as:
- Carbon-13 urea breath test
- Serum antibodies to H Pylori
- Stool antigen
Importantly, prior to any H. pylori test, patients should stop any current medical therapy for 2 weeks prior to investigation to reduce the risk of false negatives. Once H. pylori is identified, no further investigations are warranted prior to starting eradication therapy.
It may also be advisable to perform a full blood count in patients with suspected peptic ulcer, assessing for any underlying anaemia.
Any patient with dyspepsia should be given lifestyle advice to reduce symptoms, such as smoking cessation, weight loss, and reduction in alcohol consumption. There should also be an avoidance/cessation of NSAIDs where possible.
Any patient with failed conservative management and negative H. pylori testing can be stared on a Proton Pump Inhibitor (such as omeprazole or lansoprazole) for 8 weeks to reduce acid production. Those patients with a positive H. pylori test should be started on triple therapy.
NICE guidance recommends gastric ulcers to be biopsied at presentation due to malignant potential and a repeat endoscopy performed towards the end of PPI therapy to check for resolution. Persistence of symptoms should lead the clinician to suspect failure of H Pylori eradication, malignancy, or rare causes such as Zollinger-Ellison Syndrome.
Any patient with positive H. pylori testing requires eradication therapy (also termed triple therapy), which commonly consists of a PPI with amoxicllin and clarithromycin or metronidazole for 7 days.
Surgery for peptic ulcer disease is now rare, except in emergencies (such as perforation) or in the management of Zollinger Ellison Syndrome.
However, in severe or relapsing disease, the following procedures can be considered:
- Partial gastrectomy – removes the ulcer along with the G-cells contained in the antrum which secrete gastrin, which is followed by either a Bilroth I (end to side gastroduodenostomy) or Bilroth II (side to side gastrojejunostomy) anastamosis
- Selective vagotomy – removal of branches of the vagus nerve to decrease acid secretion, often used in combination with either gastroenterostomy or pyloroplasty (as the vagotomy frequently impairs the ability of the pylorus to relax leading to delayed emptying of the stomach)
The main complications of these procedures include:
- Diarrhoea (due to increased bowel transit time)
- Dumping syndrome – rapid gastric emptying of hyperosmotic chyme into the small bowel can cause fluid shift and bowel distension.
- Alkaline Reflux Gastritis – reflux of duodenal contents into the stomach following Bilroth I or II procedure (can potentially be relieved by conversion to Roux-en-y anastamosis).
The main complications of peptic ulcer disease are perforation, haemorrhage, and pyloric stenosis.