Medicine:Radiation colitis

From HandWiki
Radiation colitis
SpecialtyGastroenterology
CausesRadiation therapy.[1]

Radiation colitis is injury to the colon caused by radiation therapy. It is usually associated with treatment for prostate cancer or cervical cancer.[1] Common symptoms are diarrhea, a feeling of being unable to empty the bowel,[2] gastrointestinal bleeding, and abdominal pain.[1]

If symptoms of radiation colitis onset within 60 days of exposure to radiation, it is referred to as acute; otherwise, it is classified as chronic. Acute radiation colitis may onset within a few hours of radiation exposure, and may clear up within two or three months after radiation ends. Between 5 and 15% of individuals who receive radiation to the pelvis may have chronic radiation colitis.[1] Radiation therapy can also affect the bowel at the small intestine (radiation enteritis) or the rectum (radiation proctitis).[2]

Signs and symptoms

Tenesmus or diarrhea appear to be the most common symptoms in patients with radiation colitis. Patients may also exhibit perforation or obstruction.[2]

Causes

Radiation colitis is typically brought on by radiation therapy administered to the pelvis for prostate, cervix, uterus, anus, rectum, or bladder cancers.[3]

Mechanism

Radiation primarily harms rapidly dividing cells by causing DNA strand loss that results in irreversible DNA changes. Consequently, the G2/M phase of the cell cycle, when the DNA strands are arranged into well-defined chromatin pairs and prepared for division into two daughter cells, is when radiation damage is greatest.[4] Colocytes, the cells that divide quickly that make up the epithelium lining the colon, undergo regeneration every five to six days. Its quick regeneration also makes it more vulnerable to radiation-related damage.[5]

Genetic and cytokine interactions are necessary for the active process of programmed cell death known as apoptosis. Research on animals has demonstrated a significant increase in intestinal crypt apoptosis following low-dose radiation exposure.[6]

Through its strong fibrogenic and proinflammatory effects, TGF-β also plays a significant role in the pathogenesis of chronic radiation colitis. TGF-β levels in irradiated tissues are significantly higher and stay elevated in smooth muscle cells, vascular endothelial cells, and fibrocytes for up to 26 weeks.[7]

Diagnosis

Radiation colitis is characterized histologically by stromal injury followed by progressive fibrosis that results in epithelial atrophy and persistent mucosal ischemia.[3]

References

  1. Jump up to: 1.0 1.1 1.2 1.3 Odze and Goldblum surgical pathology of the GI tract, liver, biliary tract and pancreas. Elsevier Health Sciences. 2014. p. 480. ISBN 9781455733248. 
  2. Jump up to: 2.0 2.1 2.2 "Radiation colitis and proctitis". Clin Colon Rectal Surg 20 (1): 64–72. February 2007. doi:10.1055/s-2007-970202. PMID 20011363. 
  3. Jump up to: 3.0 3.1 Qadeer, Mohammed A.; Vargo, John J. (2008). "Approaches to the prevention and management of radiation colitis". Current Gastroenterology Reports 10 (5): 507–513. doi:10.1007/s11894-008-0093-9. ISSN 1522-8037. PMID 18799128. 
  4. Bernhard, E J; McKenna, W G; Muschel, R J (1999). "Radiosensitivity and the cell cycle". The Cancer Journal from Scientific American 5 (4): 194–204. PMID 10439162. 
  5. Jones, Blake A.; Gores, Gregory J. (December 1, 1997). "Physiology and pathophysiology of apoptosis in epithelial cells of the liver, pancreas, and intestine". American Journal of Physiology-Gastrointestinal and Liver Physiology (American Physiological Society) 273 (6): G1174–G1188. doi:10.1152/ajpgi.1997.273.6.g1174. ISSN 0193-1857. PMID 9435542. 
  6. Metcalfe, Anthony; Streuli, Charles (1997). "Epithelial apoptosis". BioEssays 19 (8): 711–720. doi:10.1002/bies.950190812. ISSN 0265-9247. 
  7. Wang, Junru; Zheng, Huaien; Sung, Ching-Ching; Richter, Konrad K.; Hauer-Jensen, Martin (1998). "Cellular Sources of Transforming Growth Factor-β Isoforms in Early and Chronic Radiation Enteropathy". The American Journal of Pathology (Elsevier BV) 153 (5): 1531–1540. doi:10.1016/s0002-9440(10)65741-0. ISSN 0002-9440. PMID 9811345. 

Further reading

External links