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The pathophysiology of colitis depends on the cause. Some pathogenetic mechanisms are not clearly understood.
The pathophysiology of colitis depends on the cause. Some pathogenetic mechanisms are not clearly understood.
===Pathogenesis===
====Hypothesis regarding pathogenesis of Allergic colitis====
*It is a non IgE immunological reaction against food protein antigens which is thought to be T cell mediated.<ref name="pmid11264489">{{cite journal| author=Pumberger W, Pomberger G, Geissler W| title=Proctocolitis in breast fed infants: a contribution to differential diagnosis of haematochezia in early childhood. | journal=Postgrad Med J | year= 2001 | volume= 77 | issue= 906 | pages= 252-4 | pmid=11264489 | doi= | pmc=1741985 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11264489  }} </ref><ref name="pmid21762530">{{cite journal| author=Lucarelli S, Di Nardo G, Lastrucci G, D'Alfonso Y, Marcheggiano A, Federici T et al.| title=Allergic proctocolitis refractory to maternal hypoallergenic diet in exclusively breast-fed infants: a clinical observation. | journal=BMC Gastroenterol | year= 2011 | volume= 11 | issue=  | pages= 82 | pmid=21762530 | doi=10.1186/1471-230X-11-82 | pmc=3224143 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21762530  }} </ref><ref name="pmid25125777">{{cite journal| author=Chesworth BM, Hamilton CB, Walton DM, Benoit M, Blake TA, Bredy H et al.| title=Reliability and validity of two versions of the upper extremity functional index. | journal=Physiother Can | year= 2014 | volume= 66 | issue= 3 | pages= 243-53 | pmid=25125777 | doi=10.3138/ptc.2013-45 | pmc=4130402 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25125777  }} </ref><ref name="pmid22050274">{{cite journal| author=Academy of Breastfeeding Medicine| title=ABM Clinical Protocol #24: Allergic Proctocolitis in the Exclusively Breastfed Infant. | journal=Breastfeed Med | year= 2011 | volume= 6 | issue= 6 | pages= 435-40 | pmid=22050274 | doi=10.1089/bfm.2011.9977 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22050274  }} </ref><ref name="pmid23843067">{{cite journal| author=Fagundes-Neto U, Ganc AJ| title=Allergic proctocolitis: the clinical evolution of a transitory disease with a familial trend. Case reports. | journal=Einstein (Sao Paulo) | year= 2013 | volume= 11 | issue= 2 | pages= 229-33 | pmid=23843067 | doi= | pmc=4872900 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23843067  }} </ref>
**T cell (CD8 and TH-2) results in release of proinflammatory cytokines, such as TNF, attracting Eosinophils mainly and other polymorphonuclear cells (PMN) to the intestinal tract and subsequent inflammation.
**Genetic influence may have a role to play, may be seen in families.
*Could also be an autoimmune disease. Atypical p antineutrophil cytoplasmic antibodies (a-pANCA) have been seen in some infants with intestinal infiltration by Neutrophils.<ref name="pmid26484355">{{cite journal| author=Sekerkova A, Fuchs M, Cecrdlova E, Svachova V, Kralova Lesna I, Striz I et al.| title=High Prevalence of Neutrophil Cytoplasmic Autoantibodies in Infants with Food Protein-Induced Proctitis/Proctocolitis: Autoimmunity Involvement? | journal=J Immunol Res | year= 2015 | volume= 2015 | issue=  | pages= 902863 | pmid=26484355 | doi=10.1155/2015/902863 | pmc=4592904 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26484355  }} </ref>
====Pathogenesis of Infectious colitis====
*Enteric organisms that cause colitis are usually acquired through feco-oral contamination especially in children. As few as 100 bacterial cells can be enough to cause an infection.<ref>{{cite book|last=Levinson|first=Warren E|title=Review of Medical Microbiology and Immunology|year=2006|publisher=McGraw-Hill Medical Publishing Division|isbn=978-0-07-146031-6|edition=9|url=http://books.google.ca/books?id=Q_80CUAd_ikC&printsec=frontcover#v=onepage&q&f=false|accessdate=February 27, 2012|page=30}}</ref>
*Can also be acquired as a sexually transmitted infection (STI) among individuals who practice unsafe anal sex.
**The pathogens are transmitted directly through overt abrasions or microabrasions in the rectal mucosa or indirectly during oral-anal contact.<ref name="Rompalo">{{Rompalo AM. Chapter 9: Proctitis and Proctocolitis. In Klausner JD, Hook III EW. CURRENT Diagnosis & Treatment of Sexually Transmitted Diseases. McGraw Hill Professional; 2007 }} </ref>
*May also occur following antibiotic use, especially broad spectrum antibiotics.
:'''Chlamydia trachomatis'''
**Inoculation and replication of ''[[Chlamydia trachomatis]]'' [[Serovar|serovars]] L1, L2, or L3 depends on alternation between two forms of the bacterium: the infectious elementary body (EB) and noninfectious, replicating reticulate body (RB).<ref name="pmid11159992">{{cite journal| author=Taraktchoglou M, Pacey AA, Turnbull JE, Eley A| title=Infectivity of Chlamydia trachomatis serovar LGV but not E is dependent on host cell heparan sulfate. | journal=Infect Immun | year= 2001 | volume= 69 | issue= 2 | pages= 968-76 | pmid=11159992 | doi=10.1128/IAI.69.2.968-976.2001 | pmc=PMC97976 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11159992  }} </ref>
**The EB form is responsible for inoculation with ''C. trachomatis''.
**The ''C. trachomatis'' EB enters the body during sexual intercourse or by crossing [[epithelial cells]] of [[mucous membranes]].<ref name="pmid12081191">{{cite journal| author=Mabey D, Peeling RW| title=Lymphogranuloma venereum. | journal=Sex Transm Infect | year= 2002 | volume= 78 | issue= 2 | pages= 90-2 | pmid=12081191 | doi= | pmc=PMC1744436 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12081191  }} </ref>
**Once inside the host cell, EBs immediately start differentiating into reticulate bodies (RBs) that undergo replication.
**The process of endocytosis and accumulation of RBs within host epithelial cells causes host cell destruction ([[necrosis]]) which leads to the formation of a [[papule]] at the site of inoculation  which may ulcerate, depending on the extent of infection and number or EBs transmitted.<ref name="pmidPMID 2030670">{{cite journal| author=Moulder JW| title=Interaction of chlamydiae and host cells in vitro. | journal=Microbiol Rev | year= 1991 | volume= 55 | issue= 1 | pages= 143-90 | pmid=PMID 2030670 | doi= | pmc=372804 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2030670  }} </ref>
:'''Shigella specie'''
**''[[Shigella]]'' first invades the epithelial cells of the large intestine (the rectosigmoid mucosa) by using M cells as entry ports for transcytosis. Shigella then invades macrophages and induces cellular apoptosis, which results in inflammation, generation of proinflammatory cytokines, and recruitment of polymorphonuclear neutrophils (PMNs).<ref name="Mounier">{{cite journal | title=Shigella flexneri Enters Human Colonic Caco-2 Epithelial Cells through the Basolateral Pole | author=Mounier, Joëlle | journal=Infection and Immunity |date=January 1992 | volume=60 | issue=1 | pages=237–248 | pmc=257528 | first2=T | last3=Hellio | first3=R | last4=Lesourd | first4=M | last5=Sansonetti | first5=PJ | pmid=1729185| last2=Vasselon }} </ref>
:'''Campylobacter'''
**Regarding ''[[Campylobacter jejuni]]'' colitis the exact pathogenesis by which it causes colitis after transmission is not fully understood.
**However, it is hypothesized that requirement for C. jejuni virulence include (1) motility, (2) drug resistance, (3) host cell adherence, (4) host cell invasion, (5) alteration of the host cell signaling pathways, (6) induction of host cell death, (7) evasion of the host immune system defenses, and (9) acquisition of iron which serves as a micronutrient for growth and works as a catalyst for hydroxyl radical formation.<ref name="pmid4522793">{{cite journal| author=Capra JD, Kehoe JM| title=Variable region sequences of five human immunoglobulin heavy chains of the VH3 subgroup: definitive identification of four heavy chain hypervariable regions. | journal=Proc Natl Acad Sci U S A | year= 1974 | volume= 71 | issue= 3 | pages= 845-8 | pmid=4522793 | doi= | pmc=388111 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4522793  }} </ref>
**''C. jejuni'' is known to also secrete proteins that may contribute to the ability of the bacterium to invade the host epithelial cells.<ref name="pmid4522793">{{cite journal| author=Capra JD, Kehoe JM| title=Variable region sequences of five human immunoglobulin heavy chains of the VH3 subgroup: definitive identification of four heavy chain hypervariable regions. | journal=Proc Natl Acad Sci U S A | year= 1974 | volume= 71 | issue= 3 | pages= 845-8 | pmid=4522793 | doi= | pmc=388111 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4522793  }} </ref>
'''Entameoba histolytica'''
**Following transmission of ''[[Entameoba histolytica]]'', the trophozoites undergo excystation in the small intestine, after which it migrates to the large intestine using pseudopods.
**In the large intestine, the trophozoites invades the intestinal mucosa into the bloodstream. Simultaneously, they form resistant cysts in the large intestines that are then excreted in human stools.<ref name="pmid10756002">{{cite journal| author=Espinosa-Cantellano M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002  }} </ref>
**''E. histolytica'' trophozoites secrete proteases, which induce the release of mucin from goblet cells, resulting in glandular hyperplasia.<ref name="pmid10756002">{{cite journal| author=c M, Martínez-Palomo A| title=Pathogenesis of intestinal amebiasis: from molecules to disease. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 318-31 | pmid=10756002 | doi= | pmc=PMC100155 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10756002  }} </ref>
**''E. histolytica'' is also said to contain glycosidases that cleave glycsolyated mucin molecules, resulting in mucin degradation.<ref name="pmid2456386">{{cite journal| author=Müller FW, Franz A, Werries E| title=Secretory hydrolases of Entamoeba histolytica. | journal=J Protozool | year= 1988 | volume= 35 | issue= 2 | pages= 291-5 | pmid=2456386 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2456386  }} </ref><ref name="pmid9561780">{{cite journal| author=Spice WM, Ackers JP| title=The effects of Entamoeba histolytica lysates on human colonic mucins. | journal=J Eukaryot Microbiol | year= 1998 | volume= 45 | issue= 2 | pages= 24S-27S | pmid=9561780 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9561780  }} </ref>
:'''Pseudomembranous colitis'''
**Under normal condition, there is usually a balance in the normal intestinal commensals.
**Following broad spectrum systemic antibiotics use, especially penicillin-based antibiotic such as [[amoxicillin]], [[cephalosporin]]s, [[fluoroquinolones]] and macrolides this balance is affected with killing susceptible bacteria and allowing for proliferation of the remaining non-susceptible bacteria.
**''Clostridium difficile'', an obligate [[anaerobic]] gram positive spore forming bacillus tends to proliferate under such conditions and is the usual cause (almost 99 percent of cases) of pseudomembranous colitis.<ref name="pmid10095149">{{cite journal| author=Surawicz CM, McFarland LV| title=Pseudomembranous colitis: causes and cures. | journal=Digestion | year= 1999 | volume= 60 | issue= 2 | pages= 91-100 | pmid=10095149 | doi=7633 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10095149  }} </ref>
**''Clostridium difficile'', produces toxin A (enterotoxin), toxin B (cytotoxin), and binary toxin. These toxins are required for it to colonize the gut, intestinal cell disruption, attract inflammatory cells and cause disease.<ref>{{cite journal | title=The role of toxin A and toxin B in''Clostridium difficile'' infection | author= Sarah A. Kuehne, Stephen T. Cartman, John T. Heap, Michelle L. Kelly, Alan Cockayne & Nigel P. Minton | journal=[[Nature (journal)|Nature]] | year=2010 |doi=10.1038/nature09397 | pmid=20844489 | volume=467 | issue=7316 | pages=711–3}}</ref><ref name="pmid10095149">{{cite journal| author=Surawicz CM, McFarland LV| title=Pseudomembranous colitis: causes and cures. | journal=Digestion | year= 1999 | volume= 60 | issue= 2 | pages= 91-100 | pmid=10095149 | doi=7633 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10095149  }} </ref>
**Other reported causes of pseudomembranous colitis include infections such as ''[[Staphylococcus aureus]]'', ''[[Yersinia specie]]'', ''[[Salmonella specie]]'', ''[[Shigella specie]]'', NSAIDs such as indomethacin, chemotherapeutic drugs like - cisplatin and inflammatory bowel disease.
====Pathogenesis of radiation colitis====
*Occur following radiation treatment for pelvic tumors.<ref name="pmid16693707">{{cite journal| author=Keith NM, Whelan M| title=A STUDY OF THE ACTION OF AMMONIUM CHLORID AND ORGANIC MERCURY COMPOUNDS. | journal=J Clin Invest | year= 1926 | volume= 3 | issue= 1 | pages= 149-202 | pmid=16693707 | doi=10.1172/JCI100072 | pmc=434619 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16693707  }} </ref><ref name="pmid27504391">{{cite journal| author=Bansal N, Soni A, Kaur P, Chauhan AK, Kaushal V| title=Exploring the Management of Radiation Proctitis in Current Clinical Practice. | journal=J Clin Diagn Res | year= 2016 | volume= 10 | issue= 6 | pages= XE01-XE06 | pmid=27504391 | doi=10.7860/JCDR/2016/17524.7906 | pmc=4963751 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27504391  }} </ref><ref name="pmid27462390">{{cite journal| author=Nelamangala Ramakrishnaiah VP, Krishnamachari S| title=Chronic haemorrhagic radiation proctitis: A review. | journal=World J Gastrointest Surg | year= 2016 | volume= 8 | issue= 7 | pages= 483-91 | pmid=27462390 | doi=10.4240/wjgs.v8.i7.483 | pmc=4942748 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27462390  }} </ref><ref name="pmid22144997">{{cite journal| author=Do NL, Nagle D, Poylin VY| title=Radiation proctitis: current strategies in management. | journal=Gastroenterol Res Pract | year= 2011 | volume= 2011 | issue=  | pages= 917941 | pmid=22144997 | doi=10.1155/2011/917941 | pmc=3226317 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22144997  }} </ref>
*More common with radiation doses higher than 45Gy.<ref name="pmid22144997">{{cite journal| author=Do NL, Nagle D, Poylin VY| title=Radiation proctitis: current strategies in management. | journal=Gastroenterol Res Pract | year= 2011 | volume= 2011 | issue=  | pages= 917941 | pmid=22144997 | doi=10.1155/2011/917941 | pmc=3226317 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22144997  }} </ref>
*The DNA is the main site of damage. May also affect RNA, proteins  and cell membranes.
**Injury occurs few hours to days, up to three months  after irradiation in acute radiation proctocolitis. 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.
**Usually self limiting.
**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 occurs usually after three months to years.
====Pathogenesis of ischemic colitis====
*Rare cause of colitis
*Seen in the elderly with low cardiovascular status
*The exact pathogenesis remains unclear. It is characterized by polymorphonuclear (PMN) cells infiltration, extensive mucosal necrosis and bleeding, submucosa edema and absence of lymphocytes and plasma cells in the deeper aspect of the lamina propria.<ref name="pmid18521689">{{cite journal| author=Abhishek K, Kaushik S, Kazemi MM, El-Dika S| title=An unusual case of hematochezia: acute ischemic proctosigmoiditis. | journal=J Gen Intern Med | year= 2008 | volume= 23 | issue= 9 | pages= 1525-7 | pmid=18521689 | doi=10.1007/s11606-008-0673-2 | pmc=2518031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18521689  }} </ref>
====Hypotheses related to the pathogenesis of ulcerative proctocolitis====
* Exact pathogenesis not fully clear.
*It is a chronic inflammatory disease affecting the innermost part of the lamina propria.
*An interplay between hyper-reactive immune system, gut microbiota, Impaired gut mucosa barrier, genetic factors, and environmental factors.<ref name="pmid27499766">{{cite journal| author=Cai M, Zeng L, Li LJ, Mo LH, Xie RD, Feng BS et al.| title=Specific immunotherapy ameliorates ulcerative colitis. | journal=Allergy Asthma Clin Immunol | year= 2016 | volume= 12 | issue=  | pages= 37 | pmid=27499766 | doi=10.1186/s13223-016-0142-0 | pmc=4975874 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27499766  }} </ref><ref name="pmid27493597">{{cite journal| author=Lopez J, Grinspan A| title=Fecal Microbiota Transplantation for Inflammatory Bowel Disease. | journal=Gastroenterol Hepatol (N Y) | year= 2016 | volume= 12 | issue= 6 | pages= 374-9 | pmid=27493597 | doi= | pmc=4971820 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27493597  }} </ref><ref name="pmid26579126">{{cite journal| author=Loddo I, Romano C| title=Inflammatory Bowel Disease: Genetics, Epigenetics, and Pathogenesis. | journal=Front Immunol | year= 2015 | volume= 6 | issue=  | pages= 551 | pmid=26579126 | doi=10.3389/fimmu.2015.00551 | pmc=4629465 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26579126  }} </ref>
*Cytotoxic T cells and autoantibodies (IgG and IgE) against the colon, cytoskeleton and bowel smooth muscles are seen.<ref name="pmid27499766">{{cite journal| author=Cai M, Zeng L, Li LJ, Mo LH, Xie RD, Feng BS et al.| title=Specific immunotherapy ameliorates ulcerative colitis. | journal=Allergy Asthma Clin Immunol | year= 2016 | volume= 12 | issue=  | pages= 37 | pmid=27499766 | doi=10.1186/s13223-016-0142-0 | pmc=4975874 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27499766  }} </ref>
*The balance in gut microbes is shifted toward pathogenic microorganism, including colonic sulphate reducing bacteria.<ref name="pmid27493597">{{cite journal| author=Lopez J, Grinspan A| title=Fecal Microbiota Transplantation for Inflammatory Bowel Disease. | journal=Gastroenterol Hepatol (N Y) | year= 2016 | volume= 12 | issue= 6 | pages= 374-9 | pmid=27493597 | doi= | pmc=4971820 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27493597  }} </ref>
*About 160 genetic loci have been identified for inflammatory bowel disease (IBD) with newer potential loci being identified. Some of these loci are associated with impaired mucosal barrier function.<ref name="pmid26579126">{{cite journal| author=Loddo I, Romano C| title=Inflammatory Bowel Disease: Genetics, Epigenetics, and Pathogenesis. | journal=Front Immunol | year= 2015 | volume= 6 | issue=  | pages= 551 | pmid=26579126 | doi=10.3389/fimmu.2015.00551 | pmc=4629465 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26579126  }} </ref>
====Other pathogenetic mechanisms of colitis====
*NSAIDS can also cause colitis. The mechanism is not completely understood.<ref name="pmid24339669">{{cite journal| author=Tonolini M| title=Acute nonsteroidal anti-inflammatory drug-induced colitis. | journal=J Emerg Trauma Shock | year= 2013 | volume= 6 | issue= 4 | pages= 301-3 | pmid=24339669 | doi=10.4103/0974-2700.120389 | pmc=3841543 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24339669  }} </ref><ref name="pmid3774712">{{cite journal| author=Ravi S, Keat AC, Keat EC| title=Colitis caused by non-steroidal anti-inflammatory drugs. | journal=Postgrad Med J | year= 1986 | volume= 62 | issue= 730 | pages= 773-6 | pmid=3774712 | doi= | pmc=2418853 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3774712  }} </ref>
**Inhibits cyclooxygenase and thus prostaglandin production. Prostaglandin helps maintain mucosal integrity.
**NSAIDS also impair oxidative phosphorylation, increasing risk of oxidative injury to the gut.
**Direct damage to the intestinal mucosa has been suggested in NSAID related injury since the rectum is often spared.
**It is also hypothesized that there is increased intestinal permeability to antigenic materials following NSAID use, causing activation of the immune system and subsequent inflammation.
*Glutaraldehyde, a disinfectant used in cleaning endoscopes is an uncommon cause of proctocolitis.<ref name="pmid7698592">{{cite journal| author=West AB, Kuan SF, Bennick M, Lagarde S| title=Glutaraldehyde colitis following endoscopy: clinical and pathological features and investigation of an outbreak. | journal=Gastroenterology | year= 1995 | volume= 108 | issue= 4 | pages= 1250-5 | pmid=7698592 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7698592  }} </ref><ref name="pmid22208542">{{cite journal| author=Shih HY, Wu DC, Huang WT, Chang YY, Yu FJ| title=Glutaraldehyde-induced colitis: case reports and literature review. | journal=Kaohsiung J Med Sci | year= 2011 | volume= 27 | issue= 12 | pages= 577-80 | pmid=22208542 | doi=10.1016/j.kjms.2011.06.036 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22208542  }} </ref>
**Proctocolitis results from direct mucosa contact with the chemical.
**Improper cleaning of the endoscopes allows the glutaraldehyde disinfectant to remain, subsequently causing a chemical proctocolitis.
**The primary mucosa toxin in glutaraldehyde is not fully known. However, it may be related to the aldehyde.<ref name="pmid7698592">{{cite journal| author=West AB, Kuan SF, Bennick M, Lagarde S| title=Glutaraldehyde colitis following endoscopy: clinical and pathological features and investigation of an outbreak. | journal=Gastroenterology | year= 1995 | volume= 108 | issue= 4 | pages= 1250-5 | pmid=7698592 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7698592  }} </ref>


===Genetics===
===Genetics===
Line 160: Line 86:


===Gross pathology===
===Gross pathology===
*Gross pathological findings are often limited to the rectosigmoid region and show evidence of acute or chronic inflammation with or without necrosis, ulcers and hemorrhage. In addition, specific changes based on the cause may be seen.
**Food protein-induced proctocolitis (FPIP) shows patchy or diffuse erythematous and friable mucosa. Characteristic circumscribed nodular hyperplasia with central pit-like erosions and ulcers may also be seen.<ref name="pmid24416045">{{cite journal| author=Hwang JB, Hong J| title=Food protein-induced proctocolitis: Is this allergic disorder a reality or a phantom in neonates? | journal=Korean J Pediatr | year= 2013 | volume= 56 | issue= 12 | pages= 514-8 | pmid=24416045 | doi=10.3345/kjp.2013.56.12.514 | pmc=3885785 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24416045  }} </ref><ref name="pmid17449926">{{cite journal| author=Hwang JB, Park MH, Kang YN, Kim SP, Suh SI, Kam S| title=Advanced criteria for clinicopathological diagnosis of food protein-induced proctocolitis. | journal=J Korean Med Sci | year= 2007 | volume= 22 | issue= 2 | pages= 213-7 | pmid=17449926 | doi=10.3346/jkms.2007.22.2.213 | pmc=2693584 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17449926  }} </ref>
**Pseudomembranous colitis. The gross pathologic finding is presence of diffuse, small, 2 to 10mm, raised yellowish (or whitish) lesions. Mucosa in between lesions may appear normal. Lesions may merge giving rise to a characteristic "pseudomembrane" layer over the mucosa.
**Ulcerative colitis. On gross pathology, the inflammation is seen in the innermost part of the lamina propria.
**Ischemic proctocolitis shows marked mucosal congestion with areas of necrosis and ulceration on gross patholgy.<ref name="pmid18521689">{{cite journal| author=Abhishek K, Kaushik S, Kazemi MM, El-Dika S| title=An unusual case of hematochezia: acute ischemic proctosigmoiditis. | journal=J Gen Intern Med | year= 2008 | volume= 23 | issue= 9 | pages= 1525-7 | pmid=18521689 | doi=10.1007/s11606-008-0673-2 | pmc=2518031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18521689  }} </ref>
<gallery>
<gallery>
Image:Allergic proctocolitis.jpg| Allergic proctocolitis<ref name=AP> The Korean Academy of Medical Sciences. Allergic proctocolitis. http://dx.doi.org/10.3346/jkms.2007.22.2.213 Accessed on 31 August, 2016</ref>
Image:Allergic proctocolitis.jpg| Allergic proctocolitis<ref name=AP> The Korean Academy of Medical Sciences. Allergic proctocolitis. http://dx.doi.org/10.3346/jkms.2007.22.2.213 Accessed on 31 August, 2016</ref>
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===Microscopic pathology===
===Microscopic pathology===
*Food protein-induced proctocolitis is characterized by marked eosinophil infiltrates in the mucosa of the rectosigmoid area.<ref name="pmid24416045">{{cite journal| author=Hwang JB, Hong J| title=Food protein-induced proctocolitis: Is this allergic disorder a reality or a phantom in neonates? | journal=Korean J Pediatr | year= 2013 | volume= 56 | issue= 12 | pages= 514-8 | pmid=24416045 | doi=10.3345/kjp.2013.56.12.514 | pmc=3885785 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24416045  }} </ref><ref name="pmidhttp://dx.doi.org/10.1016/S0022-3476(95)70540-6">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=http://dx.doi.org/10.1016/S0022-3476(95)70540-6 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref>
**The mucosa architecture is usually preserved on microscopy.<ref name="pmid24416045">{{cite journal| author=Hwang JB, Hong J| title=Food protein-induced proctocolitis: Is this allergic disorder a reality or a phantom in neonates? | journal=Korean J Pediatr | year= 2013 | volume= 56 | issue= 12 | pages= 514-8 | pmid=24416045 | doi=10.3345/kjp.2013.56.12.514 | pmc=3885785 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24416045  }} </ref>
*In pseudomembranous colitis microscopy shows<ref name =HistologyPC>Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 837-8. ISBN 0-7216-0187-1}} </ref>
**Heaped necrotic tissue
**Polymorphonuclear neutrophils in the lamina propria, breeching the epithelium like a "volcanic eruption".
**With or without capillary thrombi
*On microscopy, the characteristic finding in ulcerative colitis is presence of lymphocytes and plasma cells in the deeper aspect of the lamina propria (basal lymphoplasmacytosis).
**Crypt architecture is destroyed.
**Abscesses may also be seen in the crypts.
<gallery>
<gallery>
Image: Ulcerative colitis (2) active.jpg | Ulcerative colitis. H&E staining showing crypt abscess, a characteristic finding in ulcerative colitis <ref name=ulcerativecolitis1> Libre Pathology. https://librepathology.org/wiki/File:Ulcerative_colitis_(2)_active.jpg Accessed on September 1, 2016 </ref>
Image: Ulcerative colitis (2) active.jpg | Ulcerative colitis. H&E staining showing crypt abscess, a characteristic finding in ulcerative colitis <ref name=ulcerativecolitis1> Libre Pathology. https://librepathology.org/wiki/File:Ulcerative_colitis_(2)_active.jpg Accessed on September 1, 2016 </ref>
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*Systemic lupus erythematosus(SLE)
*Systemic lupus erythematosus(SLE)


==Epidemiology and Demographics==
The causes of proctocolitis are diverse and overlap with other diseases.
===Prevalence and Incidence===
*The exact prevalence and incidence of proctocolitis is difficult to establish due to diverse causes and appropriate diagnostic criteria
*The prevalence and incidence of proctocolitis may be influenced by the patient’s age, genetic factors and race
:*[[Food protein-induced proctocolitis]] (FPIP): Exact prevalence unknown
:**Reported to be 1.6 in 1000 children under 1 year for cow-milk protein allergy in a population based study<ref name="pmid23050491">{{cite journal| author=Elizur A, Cohen M, Goldberg MR, Rajuan N, Cohen A, Leshno M et al.| title=Cow's milk associated rectal bleeding: a population based prospective study. | journal=Pediatr Allergy Immunol | year= 2012 | volume= 23 | issue= 8 | pages= 766-70 | pmid=23050491 | doi=10.1111/pai.12009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23050491  }} </ref>
:**Prevalence of FPIP is documented to range from a low of 16 percent to a high of 64 percent among infants with rectal bleeding<ref name="pmid25976434">{{cite journal| author=Nowak-Węgrzyn A| title=Food protein-induced enterocolitis syndrome and allergic proctocolitis. | journal=Allergy Asthma Proc | year= 2015 | volume= 36 | issue= 3 | pages= 172-84 | pmid=25976434 | doi=10.2500/aap.2015.36.3811 | pmc=4405595 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25976434  }} </ref><ref name="pmid16585287">{{cite journal| author=Arvola T, Ruuska T, Keränen J, Hyöty H, Salminen S, Isolauri E| title=Rectal bleeding in infancy: clinical, allergological, and microbiological examination. | journal=Pediatrics | year= 2006 | volume= 117 | issue= 4 | pages= e760-8 | pmid=16585287 | doi=10.1542/peds.2005-1069 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16585287  }} </ref><ref name="pmid15990624">{{cite journal| author=Xanthakos SA, Schwimmer JB, Melin-Aldana H, Rothenberg ME, Witte DP, Cohen MB| title=Prevalence and outcome of allergic colitis in healthy infants with rectal bleeding: a prospective cohort study. | journal=J Pediatr Gastroenterol Nutr | year= 2005 | volume= 41 | issue= 1 | pages= 16-22 | pmid=15990624 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15990624  }} </ref>
:**Sixty percent of infants with FPIP are babies who are on exclusive breastfeeding<ref name="pmid10634300">{{cite journal| author=Lake AM| title=Food-induced eosinophilic proctocolitis. | journal=J Pediatr Gastroenterol Nutr | year= 2000 | volume= 30 Suppl | issue=  | pages= S58-60 | pmid=10634300 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10634300  }} </ref><ref name="pmid25976434">{{cite journal| author=Nowak-Węgrzyn A| title=Food protein-induced enterocolitis syndrome and allergic proctocolitis. | journal=Allergy Asthma Proc | year= 2015 | volume= 36 | issue= 3 | pages= 172-84 | pmid=25976434 | doi=10.2500/aap.2015.36.3811 | pmc=4405595 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25976434  }} </ref>
:**FPIP is the most common cause of non-infectious colitis in infancy <ref name="pmid26484355">{{cite journal| author=Sekerkova A, Fuchs M, Cecrdlova E, Svachova V, Kralova Lesna I, Striz I et al.| title=High Prevalence of Neutrophil Cytoplasmic Autoantibodies in Infants with Food Protein-Induced Proctitis/Proctocolitis: Autoimmunity Involvement? | journal=J Immunol Res | year= 2015 | volume= 2015 | issue=  | pages= 902863 | pmid=26484355 | doi=10.1155/2015/902863 | pmc=4592904 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26484355  }} </ref>
:*The prevalence of proctocolitis from an adults study in a developed country between 1979 and 1983 was 58.4 cases per 100,000<ref name="pmid3685885">{{cite journal| author=Shivananda S, Peña AS, Mayberry JF, Ruitenberg EJ, Hoedemaeker PJ| title=Epidemiology of proctocolitis in the region of Leiden, The Netherlands. A population study from 1979 to 1983. | journal=Scand J Gastroenterol | year= 1987 | volume= 22 | issue= 8 | pages= 993-1002 | pmid=3685885 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3685885  }} </ref>
:**The incidence of proctocolitis from the same study was 6.8 cases per 100,000 individuals per year<ref name="pmid3685885">{{cite journal| author=Shivananda S, Peña AS, Mayberry JF, Ruitenberg EJ, Hoedemaeker PJ| title=Epidemiology of proctocolitis in the region of Leiden, The Netherlands. A population study from 1979 to 1983. | journal=Scand J Gastroenterol | year= 1987 | volume= 22 | issue= 8 | pages= 993-1002 | pmid=3685885 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3685885  }} </ref>
:*Regarding [[radiation proctitis]] the incidence is not fully known due in part to no standard definition and method of reporting<ref name="pmid/10.1155/2011/917941">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=/10.1155/2011/917941 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref>
:**The incidence of radiation proctitis following external beam radiation studies range from 2% to 39%, brachytherapy 8% to 13%, while that of intensity-modulated radiation therapy (IMRT) range from 1% to 9%<ref name="pmid/10.1155/2011/917941">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=/10.1155/2011/917941 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref>
:**Also, the incidence of acute radiation proctitis occurs in 20% of individuals undergoing radiation therapy, while chronic radiation proctitis occurs in 2% to 20% of individuals having radiation therapy<ref name="pmid/10.1155/2011/917941">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=/10.1155/2011/917941 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref>
:*Ischemic proctocolitis  makes up 3% to 5% of cases of ischemic injury to the colon<ref name="pmid18521689">{{cite journal| author=Abhishek K, Kaushik S, Kazemi MM, El-Dika S| title=An unusual case of hematochezia: acute ischemic proctosigmoiditis. | journal=J Gen Intern Med | year= 2008 | volume= 23 | issue= 9 | pages= 1525-7 | pmid=18521689 | doi=10.1007/s11606-008-0673-2 | pmc=2518031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18521689  }} </ref>
===Age===
*[[Food protein-induced proctocolitis]] is mainly a disease of infants, with onset usually in the first two to three months of life<ref name="pmid25976434">{{cite journal| author=Nowak-Węgrzyn A| title=Food protein-induced enterocolitis syndrome and allergic proctocolitis. | journal=Allergy Asthma Proc | year= 2015 | volume= 36 | issue= 3 | pages= 172-84 | pmid=25976434 | doi=10.2500/aap.2015.36.3811 | pmc=4405595 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25976434  }} </ref><ref name="pmid16585287">{{cite journal| author=Arvola T, Ruuska T, Keränen J, Hyöty H, Salminen S, Isolauri E| title=Rectal bleeding in infancy: clinical, allergological, and microbiological examination. | journal=Pediatrics | year= 2006 | volume= 117 | issue= 4 | pages= e760-8 | pmid=16585287 | doi=10.1542/peds.2005-1069 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16585287  }} </ref><ref name="pmid15990624">{{cite journal| author=Xanthakos SA, Schwimmer JB, Melin-Aldana H, Rothenberg ME, Witte DP, Cohen MB| title=Prevalence and outcome of allergic colitis in healthy infants with rectal bleeding: a prospective cohort study. | journal=J Pediatr Gastroenterol Nutr | year= 2005 | volume= 41 | issue= 1 | pages= 16-22 | pmid=15990624 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15990624  }} </ref>. An adolescent form may develop later.<ref name="pmid21922029">{{cite journal| author=Alfadda AA, Storr MA, Shaffer EA| title=Eosinophilic colitis: epidemiology, clinical features, and current management. | journal=Therap Adv Gastroenterol | year= 2011 | volume= 4 | issue= 5 | pages= 301-9 | pmid=21922029 | doi=10.1177/1756283X10392443 | pmc=3165205 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21922029  }} </ref>
*The incidence of infectious proctocolitis that is not acquired as a [[sexually transmitted infection (STI)]] is higher among pediatric age group
*Ischemic proctocolitis is more common among the elderly with average age range of 65 to 70 years<ref name="pmid18521689">{{cite journal| author=Abhishek K, Kaushik S, Kazemi MM, El-Dika S| title=An unusual case of hematochezia: acute ischemic proctosigmoiditis. | journal=J Gen Intern Med | year= 2008 | volume= 23 | issue= 9 | pages= 1525-7 | pmid=18521689 | doi=10.1007/s11606-008-0673-2 | pmc=2518031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18521689  }} </ref><ref name="pmid8931407">{{cite journal| author=Bharucha AE, Tremaine WJ, Johnson CD, Batts KP| title=Ischemic proctosigmoiditis. | journal=Am J Gastroenterol | year= 1996 | volume= 91 | issue= 11 | pages= 2305-9 | pmid=8931407 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8931407  }} </ref>
*Other causes of proctocolitis are more common among the adult population than pediatric age group
===Gender===
*Infectious proctocolitis from [[sexually transmitted infections|STI]] is more common in men<ref name="pmid22783058">{{cite journal| author=Gallegos M, Bradly D, Jakate S, Keshavarzian A| title=Lymphogranuloma venereum proctosigmoiditis is a mimicker of inflammatory bowel disease. | journal=World J Gastroenterol | year= 2012 | volume= 18 | issue= 25 | pages= 3317-21 | pmid=22783058 | doi=10.3748/wjg.v18.i25.3317 | pmc=3391771 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22783058  }} </ref><ref name="pmid27583686">{{cite journal| author=de Voux A, Kent JB, Macomber K, Krzanowski K, Jackson D, Starr T et al.| title=Notes from the Field: Cluster of Lymphogranuloma Venereum Cases Among Men Who Have Sex with Men - Michigan, August 2015-April 2016. | journal=MMWR Morb Mortal Wkly Rep | year= 2016 | volume= 65 | issue= 34 | pages= 920-1 | pmid=27583686 | doi=10.15585/mmwr.mm6534a6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27583686  }} </ref><ref name="pmid21160459">{{cite journal| author=Workowski KA, Berman S, Centers for Disease Control and Prevention (CDC)| title=Sexually transmitted diseases treatment guidelines, 2010. | journal=MMWR Recomm Rep | year= 2010 | volume= 59 | issue= RR-12 | pages= 1-110 | pmid=21160459 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21160459  }} </ref><ref name="pmid16410585">{{cite journal| author=Williams D, Churchill D| title=Ulcerative proctitis in men who have sex with men: an emerging outbreak. | journal=BMJ | year= 2006 | volume= 332 | issue= 7533 | pages= 99-100 | pmid=16410585 | doi=10.1136/bmj.332.7533.99 | pmc=1326936 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16410585  }} </ref>
*The other causes of proctocolitis have no sex predilection
===Race===
*There is no racial predilection for proctocolitis
==Risk Factors==
Common risk factors for developing proctocolitis include:
===Risk factors for food protein-induced proctocolitis (FPIP)===
:*Family history of atopy/ previous sibling with FPIP
:*Use of formula feeds
===Risk factors for ischemic proctocolitis===
:*Elderly or debilitated patients who have multiple comorbidities.
:*Cardiovascular disease including atherosclerotis and peripheral vascular disease
:*Diabetes mellitus
:*Aortoiliac surgery
:*Hemodialysis
:*Pulmonary vascular disease
:*Shock
:*Sepsis
===Risk factors for radiation proctocolitis===
:*Dose of radiation > 54 Gy
:*Diabetes
:*Peripheral vascular disease
:*Co-existing inflammatory bowel disease
:*HIV/AIDS
===Risk factors for sexually transmitted infectious proctocolitis===
:*Men who have sex with men
:*Unprotected anal sex
:*HIV/AIDS
:*Previously diagnosed sexually transmitted infection
:*Casual sex acquaintance especially meeting on the internet/ multiple 
:*Recent foreign travel
:*Co-existing ulcerative colitis
===Risk factors for Clostridium difficile proctocolitis===
:*Elderly
:*Use of antimicrobials especially broad spectrum antibiotics such as penicillins, cephalosporins, clindamycin and fluoroquinolones
:*Chemotherapy
:*Immune hypo-function
:*Gastrointestinal surgery including proctocolectomy
:*Mechanical bowel preparation
:*Constipation
:*Gut ischemia
:*Hirschsprung disease
:*Altered gut motility
:*Malnutrition
===Risk factors for drug/ chemical related proctocolitis===
:*Elderly age group
:*Prolonged medication use e.g NSAIDs
:*Improper cleaning/ rinsing of glutaraldehyde disinfectant used in endoscopes
==Screening==
'''Proctocolitis in  [[men who have sex with men|MSM]]'''<ref name="pmid21160459">{{cite journal| author=Workowski KA, Berman S, Centers for Disease Control and Prevention (CDC)| title=Sexually transmitted diseases treatment guidelines, 2010. | journal=MMWR Recomm Rep | year= 2010 | volume= 59 | issue= RR-12 | pages= 1-110 | pmid=21160459 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21160459  }} </ref>
*According to the CDC routine screening, at least annually for common sexually transmitted diseases should be done in sexually active MSM
*A test for rectal infection with N. gonorrhoeae and C. trachomatis in men who have had receptive anal intercourse during the preceding year (using nucleic acid amplification testing (NAAT) of a rectal swab is the preferred approach)
*More frequent STD screening at 3-6 month intervals is indicated for MSM who have multiple or anonymous partners and in those who use illicit drug (particularly methamphetamine use) or whose sex partners participate in these activities
'''Other causes of proctocolitis'''
*Screening is not recommended for the other causes of proctocolitis
==Natural History, Complications, and Prognosis==
===Natural History===
The natural history of proctocolitis depends on the cause
'''Food protein-induced proctocolitis (FPIP)'''
*The symptoms of FPIP typically develop in the first two or three months of life in an exclusively breastfed infant. Symptoms resolve within 48hrs to 96 hrs following avoidance of trigger protein. Spontaneous resolution of symptoms may occur in 20% of the children without elimination of the offending protein. Most infants will be able to tolerate the offending protein by 1 to 3 years of age.<ref name="pmid25976434">{{cite journal| author=Nowak-Węgrzyn A| title=Food protein-induced enterocolitis syndrome and allergic proctocolitis. | journal=Allergy Asthma Proc | year= 2015 | volume= 36 | issue= 3 | pages= 172-84 | pmid=25976434 | doi=10.2500/aap.2015.36.3811 | pmc=4405595 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25976434  }} </ref><ref name="pmid22569527">{{cite journal| author=Koletzko S, Niggemann B, Arato A, Dias JA, Heuschkel R, Husby S et al.| title=Diagnostic approach and management of cow's-milk protein allergy in infants and children: ESPGHAN GI Committee practical guidelines. | journal=J Pediatr Gastroenterol Nutr | year= 2012 | volume= 55 | issue= 2 | pages= 221-9 | pmid=22569527 | doi=10.1097/MPG.0b013e31825c9482 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22569527  }} </ref><ref name="pmid21762530">{{cite journal| author=Lucarelli S, Di Nardo G, Lastrucci G, D'Alfonso Y, Marcheggiano A, Federici T et al.| title=Allergic proctocolitis refractory to maternal hypoallergenic diet in exclusively breast-fed infants: a clinical observation. | journal=BMC Gastroenterol | year= 2011 | volume= 11 | issue=  | pages= 82 | pmid=21762530 | doi=10.1186/1471-230X-11-82 | pmc=3224143 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21762530  }} </ref>
*The natural history of FPIP that develop in adolescence or early adulthood is not fully characterized<ref name="pmid21922029">{{cite journal| author=Alfadda AA, Storr MA, Shaffer EA| title=Eosinophilic colitis: epidemiology, clinical features, and current management. | journal=Therap Adv Gastroenterol | year= 2011 | volume= 4 | issue= 5 | pages= 301-9 | pmid=21922029 | doi=10.1177/1756283X10392443 | pmc=3165205 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21922029  }} </ref>
===Ischemic colitis===
The presentation depends on the degree of bowel involvement. Mortality is high among those with full thickness bowel ischemia.<ref name="pmid18521689">{{cite journal| author=Abhishek K, Kaushik S, Kazemi MM, El-Dika S| title=An unusual case of hematochezia: acute ischemic proctosigmoiditis. | journal=J Gen Intern Med | year= 2008 | volume= 23 | issue= 9 | pages= 1525-7 | pmid=18521689 | doi=10.1007/s11606-008-0673-2 | pmc=2518031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18521689  }} </ref>
===Complications===
===Prognosis===
==Diagnosis==
===Diagnostic Criteria===
===History and Symptoms===
===Physical Examination===
===Laboratory Findings===
===Imaging Findings===
===Other Diagnostic Studies===


==Treatment==
==Treatment==

Revision as of 19:10, 9 January 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M.Umer Tariq [2]; Maham Khan [3]; Ogheneochuko Ajari, MB.BS, MS [4]; Rim Halaby, M.D. [5]; Qasim Salau, M.B.B.S., FMCPaed [6]

Synonyms and keywords: Proctocolitis, Proctitis, Enterocolitis.

Overview

Colitis is the inflammation of the colon, that can be either acute or chronic. Causes of colitis include infectious causes such as Chlamydia trachomatis, Neisseria gonorrhoeae, Shigella dysenteriae, HSV, allergy ( food potein-induced proctocolitis) and radiation. Colitis may co-exist with enteritis (inflammation of the small bowel), proctitis (inflammation of the rectum) or both. The mainstay of therapy for infectious proctocolitis is antimicrobial therapy. The preferred regimen is a combination of Ceftriaxone and Doxycycline.

Classification

There is no established classification system for colitis. However, it may be classified based on etiology, age and duration of symptom.

Classification by etiology

Classes of Colitis Disorders
Autoimmune
Allergic
Infectious colitis
Idiopathic
Iatrogenic
Vascular
Drug induced
Unclassifiable

Classification by Anatomy

Colitis may co-exist with inflammation involving other parts of the gastrointestinal tract. It can be classified based on anatomy into;

  • Proctitis: When it involves the rectum
  • Colitis: When it involves the inflammation is limited to the colon
  • Proctocolitis: When it involves the rectum and colon (usually the distal part of the colon 12cm to 15cm above the anus (sigmoid colon)[1][2]
  • Enterocolitis: When it involves the small intestine in addition to the colon

Schematic of Anatomical Classification of Colitis

Affected anatomical areas:[3]
*Regions 4 to 6: Enterocolitis
*Region 6: Colitis
*Regions 6 to 8: Proctocolitis
*Regions 7 to 8:Proctitis

Classification by Age

  • Infantile: More common in early infancy (first six months).[4][5][6]
  • Adults

Classification by duration of symptoms

  • Acute: Less than three months.[7]
  • Chronic: Longer than three months. Often months to years.[7]

Notes:

  • Fulminant colitis is any colitis with a rapid downhill clinical course; in addition to the diarrhea, fever, and anemia seen in colitis, the patient has severe abdominal pain and presents a clinical picture similar to that of septicemia, where shock is present.
  • Irritable bowel syndrome, a separate disease, has been called spastic colitis or spastic colon. This name causes confusion, since colitis is not a feature of irritable bowel syndrome.
  • Immune mediated colitis is the experimental name in animal studies of ulcerative colitis. It is a synonym of ulcerative colitis, but it should not be used as a synonym when referring to ulcerative colitis.

Pathophysiology

The pathophysiology of colitis depends on the cause. Some pathogenetic mechanisms are not clearly understood.

Genetics

There is no specific genetic cause for proctocolitis. However, genetic predisposition may play a role in some causes.[8][9]

Associated conditions

Gross pathology

  • Allergic proctocolitis[10]

    Allergic proctocolitis[10]

  • Radiation Proctitis[11]

    Radiation Proctitis[11]

  • Pseudomembranous colitis. (WC) [12]

    Pseudomembranous colitis. (WC) [12]

  • Pseudomembranous colitis. [13]

    Pseudomembranous colitis. [13]

  • Ulcerative colitis.[14]

    Ulcerative colitis.[14]

Microscopic pathology

  • Ulcerative colitis. H&E staining showing crypt abscess, a characteristic finding in ulcerative colitis [15]

    Ulcerative colitis. H&E staining showing crypt abscess, a characteristic finding in ulcerative colitis [15]

  • Ulcerative colitis. H&E stain showing marked lymphocytic infiltration (blue/purple) of the intestinal mucosa and distortion of the architecture of the crypts. [16]

    Ulcerative colitis. H&E stain showing marked lymphocytic infiltration (blue/purple) of the intestinal mucosa and distortion of the architecture of the crypts. [16]

  • Ischemic colitis. H&E staining showing changes seen in ischemic colitis [17]

    Ischemic colitis. H&E staining showing changes seen in ischemic colitis [17]

  • Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [18]

    Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [18]

Causes

Common Causes

Common causes of Proctocolitis include infectious agents such as Chlamydia trachomatis (which causes LGV (Lymphogranuloma Venereum), Neisseria gonorrhoeae, HSV, Shigella dysenteriae and Campylobacter species. It can also be allergic (for example food protein-induced proctocolitis), idiopathic (for example microscopic colitis), vascular (for example ischemic colitis), or autoimmune (for example inflammatory bowel disease).

Causes by Organ System

Cardiovascular EVAR, vasculitis
Chemical / poisoning Chemical colitis from Glutaraldehyde, Coffee enema, Hydrogen peroxide, lanthanum
Dental Dental braces
Dermatologic Albinism, Behcet disease, scleroderma, vasculitis
Drug Side Effect Alosetron, ampicillin Oral, auranofin, azithromycin, aztreonam Injection, cefaclor, cefadroxil, cefamandole Nafate Injection, cefazolin Sodium Injection, cefepime Injection, cefepime, cefoperazone Sodium Injection, cefotaxime Sodium Injection, cefotetan Disodium Injection, cefoxitin Sodium Injection, cefpodoxime, ceftazidime Injection, ceftazidime, ceftizoxime Sodium Injection, ceftriaxone Sodium Injection, cefuroxime Sodium Injection, cephalexin, cephalosporin, cephradine Oral, cidofovir, cilansetron, clindamycin, co-amoxiclav, corticosteroid, darifenacin, desogestrel and ethinyl estradiol, dicloxacillin, dirithromycin, enoxacin, ertapenem, erythromycin and Sulfisoxazole, flucytosine, glycopyrrolate, hyoscyamine, idelalisib, imipenem and Cilastatin Sodium Injection, ipilimumab, ixabepilone, levofloxacin Oral, lincomycin hydrochloride, linezolid, lomefloxacin, loracarbef, methotrexate, miconazole Injection, moxifloxacin, nafcillin Sodium Injection, nivolumab, norfloxacin, ofloxacin injection, oxacillin Sodium Injection, oxcarbazepine, oxybutynin, peginterferon alfa-2a, penicillin, pergolide, piperacillin sodium injection, pramipexole, prednisolone, procyclidine, propantheline, pseudoephedrine, quinolone, ramosetron, reserpine, solifenacin, sparfloxacin, tegaserod
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic Aganglionic megacolon, alpha 1-antitrypsin deficiency, autistic enterocolitis, bacterial gastroenteritis, cap polyposis, chemical colitis, colitis ulcerosa, collagenous colitis, colonic ischemia, Crohn's disease, diversion colitis, diverticulosis, Gerson diet, infectious colitis, inflammatory bowel disease, intestinal ischemia, irritable bowel syndrome, ischemic colitis, lymphocytic colitis, microscopic colitis, multiple organ dysfunction syndrome, primary sclerosing cholangitis, protein losing enteropathy, pseudomembranous colitis, radiation colitis, radiation proctitis, solitary rectal ulcer syndrome, toxic megacolon, typhlitis, ulcerative colitis
Genetic Albinism, alpha 1-antitrypsin deficiency
Hematologic No underlying causes
Iatrogenic Diversion colitis, EVAR, radiation colitis, radiation proctitis
Infectious Disease Bacillary dysentery, bacterial gastroenteritis, balantidium coli, campylobacter jejuni, chlamydia trachomatis, clostridium difficile, cryptosporidiosis, cytomegalovirus, entamoeba histolytica, escherichia coli O157:H7, giardiasis, infectious colitis, isosporiasis, neisseria gonorrhoeae, neonatal necrotizing enterocolitis, pigbel, salmonella, schistosoma, sepsis, shigella, strongyloides stercoralis, syphilis, treponema pallidum, yersinia enterocolitica
Musculoskeletal / Ortho Ankylosing Spondylitis
Neurologic No underlying causes
Nutritional / Metabolic Gerson diet, lysinuric protein intolerance, milk allergy, pigbel, soy protein
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric Autistic enterocolitis
Pulmonary Multiple organ dysfunction syndrome
Renal / Electrolyte Multiple organ dysfunction syndrome
Rheum / Immune / Allergy Ankylosing spondylitis, Behcet disease, common variable immunodeficiency, allergic colitis (Food protein-induced colitis), scleroderma, vasculitis, Ulcerative colitis
Sexual Typical STI such as Chlamydia trachomatis, Neisseria gonorrheae, Treponema pallidum, HSV, CMV, Unusual STI Shigella dysenteriae
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Microscopic colitis

Causes in Alphabetical Order

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3

Life Threatening Causes

Example include toxic megacolon, ischemic colitis, infectious colitis such as escherichia coli O157:H7 and shigella.

Diagnosis

Symptoms

Physical Examination

Diagnostic Tests

Colitis is associated with the following findings:

Common tests which reveal these signs include:

Additional tests include stool cultures and blood tests, including blood chemistry tests. A high erythrocyte sedimentation rate (ESR) is one typical finding in acute exacerbations of colitis.

Treatment

Medical Therapy

Treatment of colitis may include the administration of antibiotics and general anti-inflammatory medications such as Mesalamine or its derivatives, steroids, or one of a number of other drugs that ameliorate inflammation.

Changes in diet can be effective at treating the symptoms of colitis and easing the side effects. These can include reducing the intake of carbohydrates, lactose products, soft drinks, and caffeine. This approach has been championed by Elaine Gottschall.

Hygienic and naturopathic doctors have taken the diet approach further, attributing bowel inflammation to toxemia stemming from high-protein, fatty diets and other dietary irritants. Changing to a low-fat, minimally-processed, whole-foods diet per the Natural Hygiene self-healing system has been effective in eliminating symptoms and rebuilding health. Dr. Zarin Azar, MD,, is one advocate of this healing system.

Infliximab (or REMICADE) - a drug originally produced to treat Rheumatoid Arthritis - has recently been approved for the treatment of Colitis where traditional treatments have failed. REMICADE is a biologic therapy that recognizes, attaches to, and blocks the action of a protein in your body called tumor necrosis factor alpha (TNF-alpha). TNF-alpha is made by certain blood cells in your body. It is administered through a series of infusions.

Surgery

Approximately half of patients with fulminant colitis require surgery. Surgery usually entails removing the colon and bowel and creating a "pouch" with portions of the small intestine.

Differentiating Colitis from Other Diseases

Causes of proctocolitis are diverse and may overlap with other disease. The differential diagnosis of proctocolitis can be classified into two according to age group.

Differential diagnosis in Infants

Differential diagnosis in Infants

  • Colorectal malignancy
  • Crohn's disease
  • Behcet's disease
  • Arteriovenous malformation
  • Diverticuclosis
  • Infection
  • Coagulopathy
  • Systemic lupus erythematosus(SLE)


Treatment

Medical Therapy

  • All patients with proctocolitis should be treated.
  • Treatment of proctocolitis is similar to that of proctitis.
  • Generally, the following regimen is recommended:
Preferred regimen: Ceftriaxone 250 mg IM AND Doxycycline 100 mg PO bid for 7 days

To view additional treatment and special considerations for the management of proctitis/proctocolitis, click here.

Surgery

Prevention

See also

References

  1. ↑ 2015 Sexually Transmitted Diseases Treatment Guidelines. Centers for Disease Control and Prevention (2015).http://www.cdc.gov/std/tg2015/proctitis.htm Accessed on August 29, 2016
  2. ↑ Hamlyn E, Taylor C (2006). "Sexually transmitted proctitis". Postgrad Med J. 82 (973): 733–6. doi:10.1136/pmj.2006.048488. PMC 2660501. PMID 17099092.
  3. ↑ WikiMedia Commons https://commons.wikimedia.org/wiki/File:Gastro-intestinal_tract.png. Accessed on September 09, 2016
  4. ↑ Nowak-Węgrzyn A (2015). "Food protein-induced enterocolitis syndrome and allergic proctocolitis". Allergy Asthma Proc. 36 (3): 172–84. doi:10.2500/aap.2015.36.3811. PMC 4405595. PMID 25976434.
  5. ↑ Pumberger W, Pomberger G, Geissler W (2001). "Proctocolitis in breast fed infants: a contribution to differential diagnosis of haematochezia in early childhood". Postgrad Med J. 77 (906): 252–4. PMC 1741985. PMID 11264489.
  6. ↑ Alfadda AA, Storr MA, Shaffer EA (2011). "Eosinophilic colitis: epidemiology, clinical features, and current management". Therap Adv Gastroenterol. 4 (5): 301–9. doi:10.1177/1756283X10392443. PMC 3165205. PMID 21922029.
  7. ↑ 7.0 7.1 Hauer-Jensen M, Denham JW, Andreyev HJ (2014). "Radiation enteropathy--pathogenesis, treatment and prevention". Nat Rev Gastroenterol Hepatol. 11 (8): 470–9. doi:10.1038/nrgastro.2014.46. PMC 4346191. PMID 24686268.
  8. ↑ Sekerkova A, Fuchs M, Cecrdlova E, Svachova V, Kralova Lesna I, Striz I; et al. (2015). "High Prevalence of Neutrophil Cytoplasmic Autoantibodies in Infants with Food Protein-Induced Proctitis/Proctocolitis: Autoimmunity Involvement?". J Immunol Res. 2015: 902863. doi:10.1155/2015/902863. PMC 4592904. PMID 26484355.
  9. ↑ Loddo I, Romano C (2015). "Inflammatory Bowel Disease: Genetics, Epigenetics, and Pathogenesis". Front Immunol. 6: 551. doi:10.3389/fimmu.2015.00551. PMC 4629465. PMID 26579126.
  10. ↑ The Korean Academy of Medical Sciences. Allergic proctocolitis. http://dx.doi.org/10.3346/jkms.2007.22.2.213 Accessed on 31 August, 2016
  11. ↑ Wikipedia. Proctitis. https://en.wikipedia.org/wiki/Proctitis#/media/File:Radiation_proctitis3.jpg Accessed on August 31, 2016
  12. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/Pseudomembranous_colitis Accessed on August 31, 2016
  13. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org Accessed on September 1, 2016
  14. ↑ Ulcerative colitis. Wikidoc. http://www.wikidoc.org/index.php/File:UC_granularity.png#filehistory Accessed on August 31, 2016
  15. ↑ Libre Pathology. https://librepathology.org/wiki/File:Ulcerative_colitis_(2)_active.jpg Accessed on September 1, 2016
  16. ↑ Libre Pathology. https://librepathology.org/wiki/File:Ulcerative_colitis_(2)_endoscopic_biopsy.jpg Accessed on September 1, 2016
  17. ↑ Wikipedia. Ischemic colitis. https://en.wikipedia.org/wiki/Ischemic_colitis#/media/File:Ischemic_colitis_-_high_mag.jpg Accessed on August 31, 2016
  18. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/File:Colonic_pseudomembranes_low_mag.jpg Accessed on September 1, 2016
  19. ↑ Mohan P, Ramakrishnan MK, Revathy S, Jayanthi V (2011). "Granulomatous colitis in oculocutaneous albinism". Dig Liver Dis. 43 (1): e1. doi:10.1016/j.dld.2009.09.006. PMID 19833565.
  20. ↑ Gié O, Clerc D, Giulieri S, Demartines N (2014). "[Clostridial colitis: diagnosis and strategies for management]". Rev Med Suisse. 10 (434): 1309–13. PMID 25073304.

References


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