Radiation colitis: Difference between revisions

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*The main site of damage is the DNA. May also affect RNA, proteins  and cell membranes.
*The main site of damage is the DNA. May also affect RNA, proteins  and cell membranes.
**Injury occur few hours to days, up to three months after irradiation in acute radiation colitis. It affects rapidly dividing cells of the epithelium and mucosa. This leads to cell death, recruitment and activation of polymorphonuclear (PMN) inflammatory cells, mucosal edema and damage to small blood vessels. It is usually transient and self limiting, with regeneration of the epithelium.
**Injury occur few hours to days, up to three months after irradiation in acute radiation colitis. It affects rapidly dividing cells of the epithelium and mucosa. This leads to cell death, recruitment and activation of polymorphonuclear (PMN) inflammatory cells, mucosal edema and damage to small blood vessels. It is usually transient and self limiting, with regeneration of the epithelium.
**In chronic radiation colitis, mesenchymal tissue is involved. The damage is progressive with atrophy of the mucosa, fibrosis of the intestinal wall, obliteration of small arteries, chronic ischemia, ulcers, and fistula formation. This changes usually occur three months to years after radiation. Secondary colonic malignancy may occur.
**In chronic radiation colitis, mesenchymal tissue is involved. The damage is progressive with atrophy of the mucosa, fibrosis of the intestinal wall, obliteration of small arteries, chronic ischemia, ulcers, strictures and fistula formation. This changes usually occur three months to years after radiation. Secondary colonic malignancy may occur.


==Differentiating radiation colitis from other Diseases==
==Differentiating radiation colitis from other Diseases==

Revision as of 20:44, 5 November 2016

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Synonyms and keywords:

Overview

Radiation therapy is a common treatment modality for Abdominal and pelvic malignancy. Radiation colitis may complicate this radiotherapy. Radiation colitis tends to develop insidiously and it is often progressive.

Historical Perspective

Classification

Pathophysiology

  • Occur following radiation therapy for Abdominal and pelvic malignancies .[1][2][3][4]
  • More common with radiation doses higher than 45Gy.[4]
  • The main site of damage is the DNA. May also affect RNA, proteins and cell membranes.
    • Injury occur few hours to days, up to three months after irradiation in acute radiation colitis. It affects rapidly dividing cells of the epithelium and mucosa. This leads to cell death, recruitment and activation of polymorphonuclear (PMN) inflammatory cells, mucosal edema and damage to small blood vessels. It is usually transient and self limiting, with regeneration of the epithelium.
    • In chronic radiation colitis, mesenchymal tissue is involved. The damage is progressive with atrophy of the mucosa, fibrosis of the intestinal wall, obliteration of small arteries, chronic ischemia, ulcers, strictures and fistula formation. This changes usually occur three months to years after radiation. Secondary colonic malignancy may occur.

Differentiating radiation colitis from other Diseases

Symptoms of acute radiation proctitis may overlap with other causes of acute colitis, but prior history of radiation will help in distinguishing the cause. Differential diagnosis of acute radiation colitis include:

  • Allergic colitis
  • Chemical colitis
  • NSAID induced colitis
  • Ischemic colitis

Differential diagnosis of chronic radiation colitis include:

  • Ischemic colitis
  • Inflammatory bowel disease

Epidemiology and Demographics

Age

Gender

Race

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

Symptoms

Physical Examination

Laboratory Findings

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

  • There are no primary preventive measures available for [disease name].
  • Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].


References

  1. Keith NM, Whelan M (1926). "A STUDY OF THE ACTION OF AMMONIUM CHLORID AND ORGANIC MERCURY COMPOUNDS". J Clin Invest. 3 (1): 149–202. doi:10.1172/JCI100072. PMC 434619. PMID 16693707.
  2. Bansal N, Soni A, Kaur P, Chauhan AK, Kaushal V (2016). "Exploring the Management of Radiation Proctitis in Current Clinical Practice". J Clin Diagn Res. 10 (6): XE01–XE06. doi:10.7860/JCDR/2016/17524.7906. PMC 4963751. PMID 27504391.
  3. Nelamangala Ramakrishnaiah VP, Krishnamachari S (2016). "Chronic haemorrhagic radiation proctitis: A review". World J Gastrointest Surg. 8 (7): 483–91. doi:10.4240/wjgs.v8.i7.483. PMC 4942748. PMID 27462390.
  4. 4.0 4.1 Do NL, Nagle D, Poylin VY (2011). "Radiation proctitis: current strategies in management". Gastroenterol Res Pract. 2011: 917941. doi:10.1155/2011/917941. PMC 3226317. PMID 22144997.

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