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| __NOTOC__
| | #REDIRECT:[[Colitis]] |
| {{SI}}
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| {{CMG}}; {{AE}} {{QS}}
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| ==Overview==
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| '''Proctocolitis''' is a general term for [[inflammation]] of the [[rectum]] and [[Colon (anatomy)|colon]] the distal part of the colon 12 to 15cm above the anus ([[sigmoid colon]])<ref>Online Medical dictionary[http://cancerweb.ncl.ac.uk/cgi-bin/omd?proctocolitis]</ref><ref> 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</ref><ref name="pmid17099092">{{cite journal| author=Hamlyn E, Taylor C| title=Sexually transmitted proctitis. | journal=Postgrad Med J | year= 2006 | volume= 82 | issue= 973 | pages= 733-6 | pmid=17099092 | doi=10.1136/pmj.2006.048488 | pmc=2660501 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17099092 }} </ref>. Common causes of proctocolitis include ''[[Chlamydia trachomatis]]'', ''[[Lymphogranuloma Venereum]]'', ''[[Neisseria gonorrhoeae]]'', [[Herpes Simplex Virus|HSV]], and [[Campylobacter]] species. The mainstay of therapy for infectious proctocolitis is [[antimicrobial]] therapy. The preferred regimen is a combination of [[Ceftriaxone]] and [[Doxycycline]]. Proctocolitis may be acute or chronic.
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| ==Historical Perspective==
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| ==Classification==
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| There is no established classification system for proctocolitis. However, it may be classified based on etiology, age and duration of symptom.
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| ===Classification by etiology===
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| *[[Infectious]]
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| **Viral: [[Cytomegalovirus]]
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| **Bacterial: [[Shigella]], [[Campylobacter]]
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| **Fungal: [[Cryptococcus]]
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| **Protozoan: [[Entameba]]
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| **Atypical micro-organism.
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| *[[Allergic]] (Food protein-induced)
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| *[[Vascular]]: Ischemic
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| *[[Autoimmune]]
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| *[[Drug-induced]]
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| *[[Radiation]]
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| *[[Iatrogenic]]
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| *[[Idiopathic]]
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| ===Classification by Age===
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| * '''Infantile''': More common in early infancy (first six months).<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="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="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>
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| * '''Adults'''
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| ===Classification by duration of symptoms===
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| *Acute: Less than three months.<ref name="pmid24686268">{{cite journal| author=Hauer-Jensen M, Denham JW, Andreyev HJ| title=Radiation enteropathy--pathogenesis, treatment and prevention. | journal=Nat Rev Gastroenterol Hepatol | year= 2014 | volume= 11 | issue= 8 | pages= 470-9 | pmid=24686268 | doi=10.1038/nrgastro.2014.46 | pmc=4346191 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24686268 }} </ref>
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| *Chronic: Greater than three months to years.<ref name="pmid24686268">{{cite journal| author=Hauer-Jensen M, Denham JW, Andreyev HJ| title=Radiation enteropathy--pathogenesis, treatment and prevention. | journal=Nat Rev Gastroenterol Hepatol | year= 2014 | volume= 11 | issue= 8 | pages= 470-9 | pmid=24686268 | doi=10.1038/nrgastro.2014.46 | pmc=4346191 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24686268 }} </ref>
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| ==Pathophysiology==
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| The pathophysiology of proctocolitis depends on the cause. Some pathogenetic mechanisms are not clearly understood.
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| ===Pathogenesis===
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| ====Hypothesis regarding pathogenesis of Allergic proctocolitis====
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| *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>
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| *T cell activation results in release of proinflammatory cytokines, such as TNF, attracting Eosinophils and other polymorphonuclear cells (PMN) to the intestinal tract and subsequent inflammation.
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| *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>
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| ====Pathogenesis of Infectious proctocolitis====
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| *Acquired commonly as a sexually transmitted infection (STI) among individuals who practice unsafe anal sex.
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| *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>.
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| *In children, enteric organisms that cause proctocolitis can be acquired through faeco-oral contamination. 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>
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| *May also occur following antibiotic use, especially broad spectrum antibiotics.
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|
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| *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>
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| **The EB form is responsible for inoculation with ''C. trachomatis''.
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| **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>
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| **Once inside the host cell, EBs immediately start differentiating into reticulate bodies (RBs) that undergo replication.
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| **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>
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| *''[[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>
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| *Regarding ''[[Campylobacter jejuni]]'' protocolitis the exact pathogenesis by which it causes protocolitis after transmission is not fully understood.
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| **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>
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| **''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>
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| *Following transmission of ''[[Entameoba histolytica]]'', the trophozoites undergo excystation in the small intestine, after which it migrates to the large intestine using pseudopods.
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| **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>
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| **''E. histolytica'' trophozoites secrete proteases, which induce the release of mucin from goblet cells, resulting in glandular hyperplasia.<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>
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| **''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>
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| *Under normal condition, there is usually a balance in the normal intestinal commensals.
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| **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.
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| **''Clostridium difficile'', an obligate [[anaerobic]] gram positive spore forming bacillus tends to proliferate under such conditions causing pseudomembranous protocolitis.
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| **''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>
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| ====Pathogenesis of radiation proctocolitis====
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| *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>
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| *The DNA is the main site of damage. May also affect RNA, proteins and cell membranes.
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| **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.
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| **This leads to cell death, recruitment and activation of polymorphonuclear (PMN) inflammatory cells, mucosal edema and damage to small blood vessels.
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| **Usually self limiting.
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| **In chronic radiation proctocolitis, mesenchymal tissue is involved.
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| **The damage is progressive with atrophy of the mucosa, fibrosis of the intestinal wall, obliteration of small arteries, chronic ischemia, ulcers, and fistula formation.
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| **This occurs usually after three months to years.
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| ====Pathogenesis of ischemic proctocolitis====
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| *Rare cause of proctocolitis, due to rich collateral vascular supply to the rectum.
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| *Seen in the elderly with compromised cardiovascular status.
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| *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>
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| ====Hypotheses related to the pathogenesis of ulcerative proctocolitis====
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| * Exact pathogenesis not fully clear.
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| *It is a chronic inflammatory disease affecting the innermost part of the lamina propria.
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| *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>
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| *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>
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| *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>
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| *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>
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| ====Other pathogenetic mechanisms of proctocolitis=====
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| *NSAIDS may cause proctocolitis. 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 with 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===
| |
| There is no specific genetic cause for proctocolitis. However, genetic predisposition may play a role in some causes.<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><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>
| |
| | |
| ===Associated conditions===
| |
| | |
| *[[Human Immunodeficiency Virus (HIV)]]/ [[AIDS]]
| |
| *Arterosclerosis
| |
| *Artificial infant feeding
| |
| | |
| ===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>
| |
| **Clostridium difficile proctocolitis. The gross pathologic finding is the presence of diffuse yellowish exudates of 2 to 10mm which may merge giving rise to the characteristic "pseudomembrane" layer on 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 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>
| |
| 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:Radiation proctitis3.jpg|Radiation Proctitis<ref name=Proctocolitis> Wikipedia. Proctitis. https://en.wikipedia.org/wiki/Proctitis#/media/File:Radiation_proctitis3.jpg Accessed on August 31, 2016 </ref>
| |
| Image:Pseudomembranous_colitis.JPG | Pseudomembranous colitis. (WC) <ref name=Pseudomembranous-Proctocolitis> Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/Pseudomembranous_colitis Accessed on August 31, 2016 </ref>
| |
| Image:UC granularity.png| Ulcerative colitis.<ref name=ulcerative_colitis> Ulcerative colitis. Wikidoc. http://www.wikidoc.org/index.php/File:UC_granularity.png#filehistory Accessed on August 31, 2016 </ref>
| |
| </gallery>
| |
| | |
| ===Microscopic pathology===
| |
| <gallery>Image:Ischemic colitis.JPG| Ischemic colitis </gallery><ref name=Ischemic-Proctocolitis> Wikidoc. Ischemic colitis. http://www.wikidoc.org/index.php/File:Ischemic_colitis.JPG Accessed on August 31, 2016 </ref>
| |
| | |
| ==Causes==
| |
| Proctocolitis has many possible causes. Common infectious causes of proctocolitis include ''[[Chlamydia trachomatis]]'', [[Lymphogranuloma Venereum|LGV (Lymphogranuloma Venereum)]], ''[[Neisseria gonorrhoeae]]'', [[Herpes Simplex Virus|HSV]], and [[Campylobacter|Campylobacter species]]. It can also be idiopathic (see [[colitis]]), vascular (as in [[ischemic colitis]]), or autoimmune (as in [[inflammatory bowel disease]]).
| |
| | |
| ===Life Threatening Causes===
| |
| | |
| ===Common Causes===
| |
| | |
| ===Causes by Organ System===
| |
| {|style="width:80%; height:100px" border="1"
| |
| |style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" |'''Cardiovascular'''
| |
| |style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
| |
| |-
| |
| |bgcolor="LightSteelBlue"| '''Chemical/Poisoning'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Dental'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Dermatologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Drug Side Effect'''
| |
| |bgcolor="Beige"| [[Chlorpropamide]]
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Ear Nose Throat'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Endocrine'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Environmental'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Gastroenterologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Genetic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Hematologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Iatrogenic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Infectious Disease'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Musculoskeletal/Orthopedic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Neurologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Nutritional/Metabolic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Obstetric/Gynecologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Oncologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Ophthalmologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Overdose/Toxicity'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Psychiatric'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Pulmonary'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Renal/Electrolyte'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Rheumatology/Immunology/Allergy'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Sexual'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Trauma'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Urologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Miscellaneous'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |}
| |
| | |
| ===Causes in Alphabetical Order===
| |
| {{col-begin|width=80%}}
| |
| {{col-break|width=33%}}
| |
| * [[Chlorpropamide]]
| |
| | |
| {{col-break|width=33%}}
| |
| * Disease B
| |
| | |
| {{col-break|width=33%}}
| |
| * Disease C
| |
| {{col-end}}
| |
| | |
| ==Differentiating {{PAGENAME}} from Other Diseases==
| |
| | |
| ==Epidemiology and Demographics==
| |
| | |
| ==Risk Factors==
| |
| | |
| ==Screening==
| |
| | |
| ==Natural History, Complications, and Prognosis==
| |
| ===Natural History===
| |
| | |
| ===Complications===
| |
| | |
| ===Prognosis===
| |
| | |
| ==Diagnosis==
| |
| ===Diagnostic Criteria===
| |
| | |
| ===History and Symptoms===
| |
| | |
| ===Physical Examination===
| |
| | |
| ===Laboratory Findings===
| |
| | |
| ===Imaging Findings===
| |
| | |
| ===Other Diagnostic Studies===
| |
| | |
| ==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 [[proctitis medical therapy|'''here''']].
| |
| | |
| ===Surgery===
| |
| | |
| ===Prevention===
| |
| | |
| ==See also==
| |
| * [[Colitis]]
| |
| * [[Proctitis]]
| |
| | |
| ==References==
| |
| {{reflist|2}}
| |
| | |
| [[Category:Gastroenterology]]
| |