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 second to fifth decade of life. where as gastric ulcer occurs in the 4th decade of life.
  • Peptic ulcer disease starts with symptoms such as episodic epigastric pain, indigestion, bloating.
  • Without treatment, the patient will develop symptoms of perforation like severe abdominal pain. Chronic infection leads to gastric atrophy, gastric metaplasia and ultimately leads to gastric cancer and MALT lymphoma.[4]

Complications

Acute complications :

  • Bleeding is the commonest complication.
    • Sudden large bleeding can be life threatening.
    • Bleeding occurs when the ulcer erodes one of the blood vessels around the stomach.[5][6].
  • Perforation
    • Perforation is most common occur at the duodenal bulb (62%), followed by the pyloric region (20%), and the gastric body (18%)
    • Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into abdominal cavity leading to catastrophic consequences.
    • 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 also a form of perforation, when the ulcer continues into adjacent organs such as liver and pancreas.[7][8]
  • Obstruction

Chronic complications:

Chronic Helicobacter pylori infection leads to

  • Gastric cancer
  • MALT cell lymphoma
  • Iron deficiency anemia
  • Idiopathic thrombocytopenic purpura

Prognosis

  • Prognosis is generally good if the underlying cause is treated
  • The recurrence rate of patients with peptic ulcer disease is approximately 20%.
  • Depending on the extent of these [tumor/disease progression/etc.] at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor/good/excellent.
  • The presence of [characteristic of disease] is associated with a particularly [good/poor] prognosis among patients with [disease/malignancy].
  • [Subtype of disease/malignancy] is associated with the most favorable prognosis.
  • The prognosis varies with the [characteristic] of tumor; [subtype of disease/malignancy] have the most favorable 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. Milosavljevic T, Kostić-Milosavljević M, Jovanović I, Krstić M (2011). "Complications of peptic ulcer disease". Dig Dis. 29 (5): 491–3. doi:10.1159/000331517. PMID 22095016.
  6. 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.
  7. "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Retrieved 2007-10-10.
  8. "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Retrieved 2007-10-10.


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