Peptic Ulcer Disease

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

The term peptic ulcer refers to both gastric and duodenal ulcers.

Helicobacter pylori infection is associated with about 95% of duodenal ulcers and 80% of gastric ulcers.

Dyspepsia occurs in 40% of the population annually and leads to a primary care consultation in 5% and endoscopy in 1%.

Of those who undergo endoscopy:

In the past, duodenal ulcer was 10 times as common in men as in women and gastric ulcer had a male preponderance of 3:2. Now the frequency is much less, largely because of H. pylori eradication and the sex incidence being more even.

Peptic ulcer disease prevalence is decreasing in the West, except in certain populations such as immigrants.[2] A UK population-based cohort study reported an overall incidence of uncomplicated peptic ulcer was 0.75 cases per 1,000 person-years, declining from 1.1 to 0.52 cases per 1,000 person-years between 1997 and 2005. A reduction in H. pylori-related peptic ulcers, changing patterns in non-steroidal anti-inflammatory drug (NSAID) use and increasing proton pump inhibitor (PPI) use may have contributed to this.[3]

Save time & improve your PDP on Patient.co.uk

  • Notes Add notes to any clinical page and create a reflective diary
  • Track Automatically track and log every page you have viewed
  • Print Print and export a summary to use in your appraisal
Click to find out more »
  • H. pylori.
  • NSAIDs.
  • Pepsin.
  • Smoking.
  • Alcohol.
  • Bile acids.
  • Steroids.
  • Stress.
  • Changes in gastric mucin consistency (may be genetically determined).[5]

Defence mechanisms include mucus, bicarbonate, mucosal blood flow and prostaglandins.

Symptoms

Symptoms of dyspepsia are very nonspecific and diagnosis is unreliable on history alone:

  • Epigastric pain, usually 1 to 3 hours postprandial - it may sometimes wake the patient in the night and be relieved by food.
  • Nausea.
  • Oral flatulence, bloating, distension and intolerance of fatty food - the last is also associated with gallstones.
  • Heartburn sometimes occurs although it is more typically associated with gastro-oesophageal reflux.
  • A posterior ulcer may cause pain radiating to the back.
  • Symptoms are relieved by antacids (very nonspecific).

In Taiwan, silent peptic ulcer disease is not uncommon but in Western countries this is unusual.[6] One study suggests that silent peptic ulcers are more commonly associated with bleeding and may be a manifestation of reduced visceral sensation.[7]

Signs[4]

In uncomplicated cases there is very little to find on examination:

  • There is often epigastric tenderness.
  • If gastric emptying is slow, there may be a succussion splash.
  • FBC may show evidence of iron-deficiency anaemia.
  • Testing for H. pylori.
  • Endoscopy:
    • National Institute for Health and Clinical Excellence (NICE) guidelines state that endoscopy is not required unless the patient is presenting for the first time above the age of 55, or there are warning signs (as below).[1]
    • Irrespective of age, endoscopy is required if there is:
      • Iron-deficiency anaemia.
      • Chronic blood loss.
      • Weight loss.
      • Progressive dysphagia.
      • Persistent vomiting.
      • An epigastric mass.
    • In patients aged over 55 years, referral should also be considered if there is:
      • Previous gastric ulcer.
      • Previous gastric surgery.
      • Pernicious anaemia.
      • NSAID use.
      • Family history of gastric carcinoma.

Modification of behaviour[9]

  • If drugs are the cause then they should be stopped or replaced but this may not be possible. Being more meticulous about the instructions for taking alendronate or taking NSAIDs including aspirin after food may be required.
  • Cessation of smoking should be advised if applicable. Smoking increases the risk of peptic ulcer and delays healing as well as opposing the action of H2-receptor antagonists. It has many effects on other parts of the gut including facilitating gastro-oesophageal reflux.

Healing ulcers - H. pylori-positive[10]

Treatment for H. pylori-associated ulcer disease is mainly directed at eradication of infection. See separate article Helicobacter pylori.

Healing ulcers - H. pylori-negative, NSAID-induced

The NSAID should be stopped. More than 90% of gastric or duodenal ulcers heal with eight weeks of standard-dose H2-receptor antagonists, eg ranitidine 150 mg twice a day if NSAID is discontinued.[11]

A large randomised trial has not shown any difference in gastric ulcer healing between groups receiving esomeprazole 40 mg, esomeprazole 20 mg and ranitidine.[12] NICE recommends full-dose PPI for two months.[1]

A systematic review of randomised trials found that double-]dose H2-receptor antagonists reduce risk of both gastric and duodenal ulcers. PPIs are better than standard-dose H2-receptor antagonists and misoprostol for prevention of duodenal ulcers.[11] Patients with high cardiovascular risk should continue to receive prophylactic low-dose aspirin and full-dose naproxen is the preferred NSAID. Co-therapy with a PPI or misoprostol is recommended for these groups.

H. pylori-negative NSAID-negative ulcer[13]

Ulceration of the gastric or duodenal mucosa in the absence of H. pylori infection and NSAID or aspirin usage is rare. A careful history of the use of NSAIDs and aspirin is very important in any patient presenting with gastroduodenal ulceration in the absence of H. pylori infection. The patient might be unaware that several drugs obtainable over the counter as well as some herbal medications contain NSAIDs or aspirin.

To exclude the rare conditions that may cause this, such as Zollinger-Ellison syndrome, samples should be taken from the ulcer and surrounding mucosa.

Bleeding ulcers[14]

Early endoscopic intervention with ablative or mechanical treatment to the bleeding vessels is the treatment of choice. For more information see separate article Upper Gastrointestinal Bleeding.

Management of recurrence and its prevention[1][9]

  • For gastric ulcer with H. pylori infection, NICE recommends eradication therapy followed by proof of eradication and repeat endoscopy. This is a consensus statement. If eradication is successful but the ulcer unhealed then malignancy needs to be considered.
  • Serology tests are applicable only for initial diagnosis, as they remain positive for a long while.
  • If patients are to be given long-term NSAIDs, a review from Hong Kong suggested that stratification of risk should be used to decide the plan for prevention and that all such patients should be checked for H. pylori infection.[15]
  • For patients who have relapses, intermittent therapy and annual review is recommended.

Patients should be reviewed at the end of a course of treatment, especially H. pylori eradication, to confirm a satisfactory outcome.

Repeat endoscopy may be required for:[1]
  • Failure to eradicate symptoms in a duodenal ulcer.
  • Failure to have eradicated H. pylori.
  • Follow-up of a gastric ulcer - this requires repeat endoscopy to confirm healing at 6 to 8 weeks along with confirmation of eradication of H. pylori.
  • NSAID-induced ulcers - these should be treated according to whether they are gastric or duodenal.
If a gastric ulcer persists, referral to secondary care is required. If it is healed but symptoms persist, a course of acid suppression for a limited duration may be in order but, if symptoms persist, referral is necessary.

The NICE guidelines give the following data on the effectiveness of interventions based on a number of sources:

  • In duodenal ulcer, acid suppression for 4 to 8 weeks produces healing of the ulcer in 69%. This rises by an extra 5.4% with eradication therapy too. Number needed to treat (NNT) = 18.
  • In duodenal ulcer, relapse at 3 to 12 months after treatment is 39% after short-term acid suppression alone but eradication increases this by 52% to 91%. NNT = 2.
  • In gastric ulcer, supplementation of acid suppression with eradication therapy does not improve healing rates but it does reduce relapse so that 3 to 12 months later 45% are free of ulcers after just acid suppression but eradication raises this by 32% to 77%. NNT = 3.
  • In patients taking NSAIDs, eradication did not improve the ulcer healing rate but it did halve the number of endoscopically proven ulcers six months later from 18% to 9%.
  • Haematemesis or melaena are associated with erosion of a large blood vessel and significant haemorrhage. Urgent admission to hospital is required. In patients whose ulcers have bled, eradication of H pylori is more effective than even long-term acid suppression without eradication.[17]
  • Perforation of a peptic ulcer causes an acute abdomen with epigastric pain that may progress to generalised rigidity. In the presence of steroids the symptoms of perforation may be suppressed or absent.
  • Scarring of the duodenum may lead to pyloric stenosis with vomiting and weight loss but this is rare these days with effective treatment. The classical feature is that the vomit shows food such as tomato skins that were eaten 12 to 24 hours ago.
  • Adverse reactions to PPIs and H2-receptor antagonists are usually rare and mild but severe problems can arise. Rare but not serious problems may include taste disturbance, peripheral oedema, photosensitivity, fever, arthralgia, myalgia and sweating. Serious problems include liver dysfunction, hypersensitivity reactions (including urticaria, angio-oedema, bronchospasm, anaphylaxis), depression, interstitial nephritis, blood disorders (including leukopenia, leukocytosis, pancytopenia, thrombocytopenia) and skin reactions (including Stevens-Johnson syndrome, toxic epidermal necrolysis, bullous eruption).
  • Misoprostol often causes diarrhoea and abdominal pain, especially at higher doses.

Prognosis is excellent if the underlying cause such as H. pylori infection or drugs can be addressed.

Eradication of H. pylori decreases the ulcer recurrence rate from 60-90% to 10-20%. This is still higher than previously reported and this is thought to be due to an increase in NSAID-related ulcers. The mortality rate is 1 in 100,000, a figure which has decreased modestly in the last few decades.

Further reading & references

  1. Dyspepsia: Managing dyspepsia in adults in primary care; NICE Clinical Guideline (2004)
  2. Vakil N; Dyspepsia, peptic ulcer, and H. pylori: a remembrance of things past. Am J Gastroenterol. 2010 Mar;105(3):572-4.
  3. Cai S, Garcia Rodriguez LA, Masso-Gonzalez EL, et al; Uncomplicated peptic ulcer in the UK: trends from 1997 to 2005. Aliment Pharmacol Ther. 2009 Nov 15;30(10):1039-48. Epub 2009 Aug 26.
  4. Anand BS et al, Peptic Ulcer Disease, Medscape, Jun 2011
  5. Niv Y; H. pylori/NSAID--negative peptic ulcer--the mucin theory. Med Hypotheses. 2010 Nov;75(5):433-5. Epub 2010 May 4.
  6. Lu CL, Chang SS, Wang SS, et al; Silent peptic ulcer disease: frequency, factors leading to "silence," and implications regarding the pathogenesis of visceral symptoms.; Gastrointest Endosc. 2004 Jul;60(1):34-8.
  7. Gururatsakul M, Holloway RH, Talley NJ, et al; Association between clinical manifestations of complicated and uncomplicated J Gastroenterol Hepatol. 2010 Jun;25(6):1162-9.
  8. Peptic ulcer disease; Surgical-tutor.org.uk
  9. Dyspepsia - proven peptic ulcer, Prodigy (June 2008)
  10. Helicobacter pylori guidelines (various), Health Protection Agency (2008)
  11. Malfertheiner P, Chan FK, McColl KE; Peptic ulcer disease. Lancet. 2009 Oct 24;374(9699):1449-61. Epub 2009 Aug 13.
  12. Goldstein JL, Johanson JF, Hawkey CJ, et al; Clinical trial: healing of NSAID-associated gastric ulcers in patients continuing Aliment Pharmacol Ther. 2007 Oct 15;26(8):1101-11.
  13. McColl KE; Helicobacter pylori-negative nonsteroidal anti-inflammatory drug-negative ulcer. Gastroenterol Clin North Am. 2009 Jun;38(2):353-61.
  14. Holster IL, Kuipers EJ; Update on the endoscopic management of peptic ulcer bleeding. Curr Gastroenterol Rep. 2011 Dec;13(6):525-31.
  15. Chan FK, Graham DY; Review article: prevention of non-steroidal anti-inflammatory drug gastrointestinal complications--review and recommendations based on risk assessment. Aliment Pharmacol Ther. 2004 May 15;19(10):1051-61.
  16. Hermansson M, Ekedahl A, Ranstam J, et al; Decreasing incidence of peptic ulcer complications after the introduction of the BMC Gastroenterol. 2009 Apr 20;9:25.
  17. Gisbert JP, Khorrami S, Carballo F, et al; H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer. Cochrane Database Syst Rev. 2004;(2):CD004062.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Hayley Willacy
Current Version:
Peer Reviewer:
Dr Hannah Gronow
Last Checked:
19/01/2012
Document ID:
3105 (v27)
© EMIS