Peptic ulcer natural history

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2017 ACG Guidelines for Peptic Ulcer Disease

Guidelines for the Indications to Test for, and to Treat, H. pylori Infection

Guidelines for First line Treatment Strategies of Peptic Ulcer Disease for Providers in North America

Guidlines for factors that predict the successful eradication when treating H. pylori infection

Guidelines to document H. pylori antimicrobial resistance in the North America

Guidelines for evaluation and testing of H. pylori antibiotic resistance

Guidelines for when to test for treatment success after H. pylori eradication therapy

Guidelines for penicillin allergy in patients with H. pylori infection

Guidelines for the salvage therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Overview

Peptic ulcers tend to come back if untreated. Cure rates are high and recurrence is low, if patient is compliant to treatment.

Natural History

  • The infection of Helicobacter pylori ,common cause of peptic ulcer disease is acquired usually during the childhood , mainly in those who have low socioeconomic status, increased number of siblings and similar infection in the mother[1][2][3]The duodenal ulcer occurs in 20-50 years of age.The gastric ulcer occurs in the age above 40 years . It start with symptoms such as episodic epigastric pain, indigestion,bloating.Without treatment, the patient will develop symptoms of perforation leading into symptoms of peritionitis.Chronic infection leads to gastric atrophy ,gastric metaplasia and ultimately leads to gastric cancer and MALT lymphoma [4]

Complications

  • Gastrointestinal bleeding is the commonest complication. Sudden large bleeding can be life threatening[5]. It occurs when the ulcer erodes one of the blood vessels.
  • Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into abdominal cavity. Perforation at the anterior surface of stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. Often first sign is sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to back.
  • Penetration is when the ulcer continues into adjacent organs such as liver and pancreas[6].
  • Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting.

Prognosis

References

  1. Opekun AR, Gilger MA, Denyes SM, Nirken MH, Philip SP, Osato MS, Malaty HM, Hicks J, Graham DY (2000). "Helicobacter pylori infection in children of Texas". J. Pediatr. Gastroenterol. Nutr. 31 (4): 405–10. PMID 11045838.
  2. Parkinson AJ, Gold BD, Bulkow L, Wainwright RB, Swaminathan B, Khanna B, Petersen KM, Fitzgerald MA (2000). "High prevalence of Helicobacter pylori in the Alaska native population and association with low serum ferritin levels in young adults". Clin. Diagn. Lab. Immunol. 7 (6): 885–8. PMC 95979. PMID 11063492.
  3. Malaty HM, El-Kasabany A, Graham DY, Miller CC, Reddy SG, Srinivasan SR, Yamaoka Y, Berenson GS (2002). "Age at acquisition of Helicobacter pylori infection: a follow-up study from infancy to adulthood". Lancet. 359 (9310): 931–5. doi:10.1016/S0140-6736(02)08025-X. PMID 11918912.
  4. Kusters JG, van Vliet AH, Kuipers EJ (2006). "Pathogenesis of Helicobacter pylori infection". Clin. Microbiol. Rev. 19 (3): 449–90. doi:10.1128/CMR.00054-05. PMC 1539101. PMID 16847081.
  5. Cullen DJ, Hawkey GM, Greenwood DC; et al. (1997). "Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs". Gut. 41 (4): 459–62. PMID 9391242.
  6. "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Retrieved 2007-10-10.


Template:WikiDoc Sources Associate Editor(s)-in-Chief: Manpreet Kaur, MD [3]

Natural History

  • The Helicobacter pylori is acquired usually during the childhood of life mainly those who have low socioeconomic status, increased number of siblings and similar infection in the mother[1][2][3]The duodenal ulcer occurs in 20-50 years of age.The gastric ulcer occurs in the age above 40 years . It start with symptoms such as episodic epigastric pain, indigestion,oating.Without treatment, the patient will develop symptoms of perforation, which may eventually lead to acute circulatory failure....[4]

Complications

Acute and common complications :

  • Bleeding
  • Perforation
  • Peritonitis
  • Obstruction
  • Stricture

Chronic and rare complications:

  • Gastric cancer-Chronic Helicobacter pylori leads to
  • MALT cell lymphoma
  • Iron deficiency anemia
  • Idiopathic thrombocytopenic purpuras
  • Signs of bleeding:
    • Melena -blood in stools
    • Hematemesis-blood in vomitus
    • Anemia-pale colored skin, shortness of breath during physical activity, tachycardia


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Prognosis

  • This section should detail the prognosis of the disease, both treated and untreated.
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References

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  1. Opekun AR, Gilger MA, Denyes SM, Nirken MH, Philip SP, Osato MS, Malaty HM, Hicks J, Graham DY (2000). "Helicobacter pylori infection in children of Texas". J. Pediatr. Gastroenterol. Nutr. 31 (4): 405–10. PMID 11045838.
  2. Parkinson AJ, Gold BD, Bulkow L, Wainwright RB, Swaminathan B, Khanna B, Petersen KM, Fitzgerald MA (2000). "High prevalence of Helicobacter pylori in the Alaska native population and association with low serum ferritin levels in young adults". Clin. Diagn. Lab. Immunol. 7 (6): 885–8. PMC 95979. PMID 11063492.
  3. Malaty HM, El-Kasabany A, Graham DY, Miller CC, Reddy SG, Srinivasan SR, Yamaoka Y, Berenson GS (2002). "Age at acquisition of Helicobacter pylori infection: a follow-up study from infancy to adulthood". Lancet. 359 (9310): 931–5. doi:10.1016/S0140-6736(02)08025-X. PMID 11918912.
  4. Kusters JG, van Vliet AH, Kuipers EJ (2006). "Pathogenesis of Helicobacter pylori infection". Clin. Microbiol. Rev. 19 (3): 449–90. doi:10.1128/CMR.00054-05. PMC 1539101. PMID 16847081.