History

Fact Explanation
Asymptomatic[1] All individuals infected with H. pylori will show histological gastritis. But only a minority will develop clinically apparent symptoms or signs. [1]
Acute and chronic gastritis will cause non specific dyspeptic symptoms[1] Nausea, vomiting, abdominal fullness and abdominal pain occur due to inflammation of proximal and distal gastric mucosa. It is associated with the hypochlorhydria [1].
Peptic ulcer disease when uncomplicated causes epigastric pain, other dyspeptic symptoms. Complicated symptoms due to duodenal ulcer are epigastric pain during fasting and relieved by eating or anti-acids [1,2] H pylori colonizes from the prepyloric antrum to the cardia. Clinical features vary on the pattern of chronic mucosal inflammation [2]. Life time risk of developing peptic ulcer disease in H. pylori positives is 3-10 times higher than culture negative population. [1] Infection of non acid secreting antral portion of the stomach (with sparing of the acid secreting body) induces inflammation of gastric mucosa and stimulates the gastrin release which in turn increases acid secretion. Therefore acid load coming to the duodenum increases, damaging the duodenal mucosa, causing ulceration and gastric metaplasia. [2],[3] In development of a gastric ulcer, both body and antral mucosal inflammation occurs to a similar degree. In gastric ulcer due to the severe involvement of body mucosa acidity can be decreased. [2]
Ulcer complications such as bleeding, Perforation, stricture formation[1] H.pylori infection increase the risk of ulcer complications. [4]
Atrophic gastritis, intestinal metaplasia, and gastric cancer [1] Chronic inflammation caused by H. pylori causes loss of normal gastric mucosa and destruction of gastric glands. This is followed by replacement with fibrosis and an intestinal-type epithelium. This process is called atrophic gastritis and intestinal metaplasia. Chronic active inflammation pattern decides the risk for atrophic gastritis [1]. There is a strong association between H. pylori and gastric cancer especially non cardia gastric cancer. Patients who have both fundic and antral mucosal inflammation that causes mucosal atrophy or intestinal metaplasia have the highest risk of developing cancer. [3]
Gastric MALT (mucosa associated lymphoid tissue) lymphoma [1] Normal gastric mucosa does not contain lymphoid tissue, but MALT nearly always appears in infection of H. pylori .[1] Risk of gastric MALT lymphoma highly increased (72-98%) by H. pylori infection. [5]
Extra digestive manifestations - Ischemic heart disease, ischemic cerebrovascular disorders, functional vascular disorders, autoimmune disorders, chronic urticaria, liver cirrhosis and some diseases of the biliary tract. [6] This may be occur due to the fact that some H. pylori cytotoxic strains may induce local chronic release of cytokines, or vasoactive or procoagulant substances by immune cells in susceptible individuals. [6]
References
  1. KUSTERS JG, VAN VLIET AH, KUIPERS EJ. Pathogenesis of Helicobacter pylori Infection Clin Microbiol Rev [online] 2006 Jul, 19(3):449-490 [viewed 20 May 2014] Available from: doi:10.1128/CMR.00054-05
  2. MALFERTHEINER PETER, CHAN FRANCIS KL, MCCOLL KENNETH EL. Peptic ulcer disease. The Lancet [online] 2009 October, 374(9699):1449-1461 [viewed 23 May 2014] Available from: doi:10.1016/S0140-6736(09)60938-7
  3. MCCOLL KENNETH E.L.. Array. N Engl J Med [online] 2010 April, 362(17):1597-1604 [viewed 23 May 2014] Available from: doi:10.1056/NEJMcp1001110
  4. CULLEN D, HAWKEY G, GREENWOOD D, HUMPHREYS H, SHEPHERD V, LOGAN R, HAWKEY C. Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs Gut [online] 1997 Oct, 41(4):459-462 [viewed 21 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891536
  5. SUERBAUM S, MICHETTI P. Helicobacter pylori infection. New England Journal of Medicine. 2002;347(15):1175-86.
  6. GASBARRINI A, FRANCESCHI F, ARMUZZI A, OJETTI V, CANDELLI M, TORRE E, DE LORENZO A, ANTI M, PRETOLANI S, GASBARRINI G. Extradigestive manifestations of Helicobacter pylori gastric infection Gut [online] 1999 Jul, 45(Suppl 1):I9-I12 [viewed 23 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1766655

Examination

Fact Explanation
Unremarkable physical examination.[1] Many of those infected with H.pylori are asymptomatic. [1]
Weight loss [1] Not common, can occur if there is a gastric carcinoma due to H. pylori infection.[1]
Anemia [1] Bleeding is a common complication in peptic ulcer disease[2]. Chronic blood loss from GI tract is a main cause for iron deficiency anemia[3].
Hematemesis/melena Upper GI bleeding is a common complication in peptic ulcer disease. [2] This may present as hematemesis or melena (passage of tarry black stools).
Features of gastric outlet obstruction (GOO)[2] This can occur due to ulcer induced fibrosis but it is rare. If symptoms such as projectile vomiting, early satiety, bloating is present it should raise the suspicion of malignancy. Characteristic examination finding is a succussion splash. [2]
Epigastric mass [1], [4] This may occur in gastric cancer, but it is a relatively late sign. [4]
References
  1. BOON N, DAVIDSON S ed. Davidson's principles & practice of medicine. Edinburgh New York: Elsevier/Churchill Livingstone. 2006.
  2. MALFERTHEINER PETER, CHAN FRANCIS KL, MCCOLL KENNETH EL. Peptic ulcer disease. The Lancet [online] 2009 October, 374(9699):1449-1461 [viewed 23 May 2014] Available from: doi:10.1016/S0140-6736(09)60938-7
  3. MCINTYRE AS, LONG RG. Prospective survey of investigations in outpatients referred with iron deficiency anaemia. Gut [online] 1993 Aug, 34(8):1102-7 [viewed 23 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/8174963
  4. BOWLES MJ, BENJAMIN IS. Cancer of the stomach and pancreas BMJ [online] 2001 Dec 15, 323(7326):1413-1416 [viewed 23 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1121865

Differential Diagnoses

Fact Explanation
NSAID induced gastritis/ gastric ulcers [1] NSAID induced gastric ulcers also cause symptoms similar to H.pylori infection. It is the most common cause of peptic ulcer disease in those without H. pylori infection. Especially in elderly patients with a history of chronic NSAID use. [1]
Pancreatitis [2] Epigastric pain develops rapidly in acute pancreatitis. Pain radiates directly to the back and is relived when leaning forward. [2]
Cholecystitis [2] Pain occurs in right upper quadrant or in the epigastric area. Colicky, dull and constant pain which is aggravated by fatty foods.[2]
Cholangitis [2] Shows a collection of symptoms called 'Charcot's triad', it consist of abdominal pain (epigastric or right hypochondrial pain), jaundice and fever with chills and rigors.[2]
Gastroesophageal reflux disease[3] Shows symptoms of regurgitation, epigastric pain, nausea and vomiting. [3]
Myocardial infarction[4] Occurs with central/retrosternal tightening chest pain/discomfort which patients may describe as heartburn. [4]
Lower lobe pneumonia[5] The patient is febrile with chills and a productive cough. If the pleura is involved pleuritic chest pain (sharp chest pain during inspiration) may occur. Up to 20% of patients may have gastrointestinal symptoms such as nausea, vomiting, and/or diarrhea. [5]
References
  1. RAMAKRISHNAN K, SALINAS RC. Peptic ulcer disease. Am Fam Physician [online] 2007 Oct 1, 76(7):1005-12 [viewed 26 May 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17956071
  2. WILLIAMS, N., BULSTRODE, C., CONNELL, P., ed. Bailey & Love's Short Practice of Surgery. 25th ed. London: Hodder Arnold, 2008. p1120 - 1140
  3. KAHRILAS PETER J.. Gastroesophageal Reflux Disease. N Engl J Med [online] 2008 October, 359(16):1700-1707 [viewed 26 May 2014] Available from: doi:10.1056/NEJMcp0804684
  4. THYGESEN KRISTIAN, ALPERT JOSEPH S., WHITE HARVEY D.. Universal Definition of Myocardial Infarction. Journal of the American College of Cardiology [online] 2007 November, 50(22):2173-2195 [viewed 26 May 2014] Available from: doi:10.1016/j.jacc.2007.09.011
  5. FAUCI, A ed. Harrison's principles of internal medicine. 17th edition. New York: McGraw-Hill Medical, 2008. p1621

Investigations - for Diagnosis

Fact Explanation
Non invasive: Urea breath test [1],[2],[3] The test involves drinking 13-C or 14 - C labeled urea, which is converted to labeled carbon dioxide by urease in H. pylori. In the breath sample the labeled gas is measured[1]. Sensitivity and specificity of the test is more than 90% [1],[2]. It is used as an alternative gold standard test. It is a very useful and reliable test to evaluate the success of H. pylori eradication treatment. [3]
Invasive: Histology [1],[3] Gold standard in routine diagnosis. It requires an endoscopy to obtain a biopsy sample. Specificity and sensitivity is >95% [1],[3]
Invasive: Culture biopsy [1],[3] This is an alternative gold standard test. It can also provide information on antibiotic sensitivity. Requires an endoscopy to obtain the biopsy. Specificity and sensitivity is >95% [1],[3]
Invasive: Rapid urease test[1],[3] A rapid and cost effective test. Endoscopic biopsy specimen is placed in a solution of urea and pH sensitive dye. However it requires an additional test to confirm the presence of H. pylori. Specificity and sensitivity is>90% [1],[3]
Non invasive: Stool antigen test [1],[2],[3] Proton-pump inhibitors to be stopped two weeks prior, H2 receptor antagonists stopped 24 hours prior and antimicrobials stopped 4 weeks prior to the test. As these medications may suppress the infection and reduce the sensitivity of the test. [1] The stool antigen test is is not reliable to evaluate H. pylori eradication after therapy. [3] Sensitivity and specificity is 95% with good patient preparation. [2]
References
  1. MCCOLL KENNETH E.L.. Array. N Engl J Med [online] 2010 April, 362(17):1597-1604 [viewed 26 May 2014] Available from: doi:10.1056/NEJMcp1001110
  2. SUERBAUM SEBASTIAN, MICHETTI PIERRE. Array. N Engl J Med [online] 2002 October, 347(15):1175-1186 [viewed 26 May 2014] Available from: doi:10.1056/NEJMra020542
  3. KUSTERS JG, VAN VLIET AH, KUIPERS EJ. Pathogenesis of Helicobacter pylori Infection Clin Microbiol Rev [online] 2006 Jul, 19(3):449-490 [viewed 22 May 2014] Available from: doi:10.1128/CMR.00054-05

Investigations - Followup

Fact Explanation
Non invasive: Urea breath test [1,2,3] Reliable test to evaluate the success of eradication treatment of H. pylori but it has limited availability in some centers due to poor availability of equipment. [1,2,3]
Non invasive: Stool antigen [1,2,3] Even though this is a simple, non invasive test it is not reliable enough for the routine evaluation H. pylori eradication therapy. [3]
References
  1. MCCOLL KENNETH E.L.. Array. N Engl J Med [online] 2010 April, 362(17):1597-1604 [viewed 26 May 2014] Available from: doi:10.1056/NEJMcp1001110
  2. SUERBAUM SEBASTIAN, MICHETTI PIERRE. Array. N Engl J Med [online] 2002 October, 347(15):1175-1186 [viewed 26 May 2014] Available from: doi:10.1056/NEJMra020542
  3. KUSTERS JG, VAN VLIET AH, KUIPERS EJ. Pathogenesis of Helicobacter pylori Infection Clin Microbiol Rev [online] 2006 Jul, 19(3):449-490 [viewed 22 May 2014] Available from: doi:10.1128/CMR.00054-05

Investigations - Screening/Staging

Fact Explanation
Non invasive: Serological test [1,2,3] Is a widely available, low cost test, however a positive result indicates past infection rather than an ongoing infection. Therefore it is not recommended for diagnosis of confirmation of eradication, but is used for epidemiology survey[1,2,3]. Sensitivity is 85% while specificity is 79%. [1]
References
  1. MCCOLL KENNETH E.L.. Array. N Engl J Med [online] 2010 April, 362(17):1597-1604 [viewed 26 May 2014] Available from: doi:10.1056/NEJMcp1001110
  2. SUERBAUM SEBASTIAN, MICHETTI PIERRE. Array. N Engl J Med [online] 2002 October, 347(15):1175-1186 [viewed 26 May 2014] Available from: doi:10.1056/NEJMra020542
  3. KUSTERS JG, VAN VLIET AH, KUIPERS EJ. Pathogenesis of Helicobacter pylori Infection Clin Microbiol Rev [online] 2006 Jul, 19(3):449-490 [viewed 22 May 2014] Available from: doi:10.1128/CMR.00054-05

Management - General Measures

Fact Explanation
Advise on hygienic practices [1] Poor socioeconomic status, crowded living conditions and poor food hygiene have been identified as major risk factors for developing H.pylori infection. [1]
References
  1. KUSTERS JG, VAN VLIET AH, KUIPERS EJ. Pathogenesis of Helicobacter pylori Infection Clin Microbiol Rev [online] 2006 Jul, 19(3):449-490 [viewed 22 May 2014] Available from: doi:10.1128/CMR.00054-05

Management - Specific Treatments

Fact Explanation
First line therapy: Proton Pump Inhibitor (PPI) based triple therapy [1],[2] 20mg Omeprazole twice daily + 1g amoxicillin and 500mg Clarythromycin or 400mg Metronidazole together with 250mg Clarythromycin for a duration of seven days. [1],[2]
First line therapy: Ranitidine Bismuth Citrate based therapy [1],[2] Ranitidine bismuth citrate in dual therapy with Clarithromycin for two weeks. Advantage of using this regimen is that it is influenced less by antibiotic resistance than PPI based triple therapy. [2]
First line therapy: Ranitidine Bismuth based non Clarithromycin therapy [1],[2] In this regimen Metronidazole or Tetracycline is used as the antimicrobials. [2]
Second line therapy [1,2] In this regimen Levofloxacin 500 mg twice a day, and Amoxicillin 1 g twice a day, is combined with a PPI twice a day [1].
Adjuvant therapy [1] If the regimens cause side-effects that affect patient compliance. Adjuvant therapy using probiotins such as Streptococcus faecium can be used. [1]
References
  1. BRUCE Michael G, MAAROOS Heidi Ingrid. Epidemiology of Helicobacter pylori Infection. Helicobacter [Online] 13 (Suppl. 1): 1–6. [Viewed on 26 May 2014]. Available from: http://www.helicobacter.org/content/publications/helicobacter_2008/Hel_v13_s1_YearInHelicobacter2008.pdf#page=41
  2. SUERBAUM SEBASTIAN, MICHETTI PIERRE. Array. N Engl J Med [online] 2002 October, 347(15):1175-1186 [viewed 26 May 2014] Available from: doi:10.1056/NEJMra020542