Proctocolitis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [3]
Overview
Proctocolitis is a general term for inflammation of the rectum and colon particularly distal part of the colon(sigmoid)[1]. Common causes of proctocolitis include Chlamydia trachomatis, Lymphogranuloma Venereum, Neisseria gonorrhoeae, 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.
Historical Perspective
Classification
There is no established classification system for proctocolitis. However, it may be classified based on etiology, age and duration of symptom.
Classification by etiology
- Infectious
- Viral
- Bacterial
- Fungal,
- Protozoan
- Atypical micro-organism.
- Allergic (eosinophilic)
- Vascular
- Autoimmune
- Drug-induced
- Radiation
- Chemical
- Idiopathic
Classification by Age
Classification by duration of symptoms
- Acute: for example allergic proctocolitis in infants.
- Chronic: Usually months to years, for example ulcerative colitis.
Pathophysiology
The pathophysiology of proctocolitis depends on the cause. Some of the pathogenetic mechanisms are not fully understood.
Pathogenesis
Hypothesis regarding pathogenesis of Allergic proctocolitis
- It is a non IgE immunological reaction against food protein antigens which is thought to be T cell mediated resulting in Eosinophil accumulation in the intestinal tract and subsequent inflammation.[3][5][6]
- Could also be an autoimmune disease. Atypical p antineutrophil cytoplasmic antibodies (a-pANCA) have been seen in some infants with intestinal infiltration by Neutrophils.[7]
Pathogenesis of Infectious proctocolitis
- Acquired commonly 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.[8].
- 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.[9]
- Inoculation and replication of Chlamydia trachomatis' 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).[10]
- 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.[11]
- 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.[12]
- 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).[13]
- The exact mechanism by which Campy
- 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.[14]
- E. histolytica trophozoites secrete proteases, which induce the release of mucin from goblet cells, resulting in glandular hyperplasia.[14]
- E. histolytica is also said to contain glycosidases that cleave glycsolyated mucin molecules, resulting in mucin degradation.[15][16]
Causes
Proctocolitis has many possible causes. Common infectious causes of proctocolitis include Chlamydia trachomatis, LGV (Lymphogranuloma Venereum), Neisseria gonorrhoeae, HSV, and 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
Cardiovascular | No underlying causes |
Chemical/Poisoning | No underlying causes |
Dental | No underlying causes |
Dermatologic | No underlying causes |
Drug Side Effect | Chlorpropamide |
Ear Nose Throat | No underlying causes |
Endocrine | No underlying causes |
Environmental | No underlying causes |
Gastroenterologic | No underlying causes |
Genetic | No underlying causes |
Hematologic | No underlying causes |
Iatrogenic | No underlying causes |
Infectious Disease | No underlying causes |
Musculoskeletal/Orthopedic | No underlying causes |
Neurologic | No underlying causes |
Nutritional/Metabolic | No underlying causes |
Obstetric/Gynecologic | No underlying causes |
Oncologic | No underlying causes |
Ophthalmologic | No underlying causes |
Overdose/Toxicity | No underlying causes |
Psychiatric | No underlying causes |
Pulmonary | No underlying causes |
Renal/Electrolyte | No underlying causes |
Rheumatology/Immunology/Allergy | No underlying causes |
Sexual | No underlying causes |
Trauma | No underlying causes |
Urologic | No underlying causes |
Miscellaneous | No underlying causes |
Causes in Alphabetical Order
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Differentiating Proctocolitis 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 here.
Surgery
Prevention
See also
References
- ↑ Online Medical dictionary[1]
- ↑ 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.
- ↑ 3.0 3.1 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.
- ↑ 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.
- ↑ Lucarelli S, Di Nardo G, Lastrucci G, D'Alfonso Y, Marcheggiano A, Federici T; et al. (2011). "Allergic proctocolitis refractory to maternal hypoallergenic diet in exclusively breast-fed infants: a clinical observation". BMC Gastroenterol. 11: 82. doi:10.1186/1471-230X-11-82. PMC 3224143. PMID 21762530.
- ↑ Chesworth BM, Hamilton CB, Walton DM, Benoit M, Blake TA, Bredy H; et al. (2014). "Reliability and validity of two versions of the upper extremity functional index". Physiother Can. 66 (3): 243–53. doi:10.3138/ptc.2013-45. PMC 4130402. PMID 25125777.
- ↑ 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.
- ↑ Template:Rompalo AM. Chapter 9: Proctitis and Proctocolitis. In Klausner JD, Hook III EW. CURRENT Diagnosis & Treatment of Sexually Transmitted Diseases. McGraw Hill Professional; 2007
- ↑ Levinson, Warren E (2006). Review of Medical Microbiology and Immunology (9 ed.). McGraw-Hill Medical Publishing Division. p. 30. ISBN 978-0-07-146031-6. Retrieved February 27, 2012.
- ↑ Taraktchoglou M, Pacey AA, Turnbull JE, Eley A (2001). "Infectivity of Chlamydia trachomatis serovar LGV but not E is dependent on host cell heparan sulfate". Infect Immun. 69 (2): 968–76. doi:10.1128/IAI.69.2.968-976.2001. PMC 97976. PMID 11159992.
- ↑ Mabey D, Peeling RW (2002). "Lymphogranuloma venereum". Sex Transm Infect. 78 (2): 90–2. PMC 1744436. PMID 12081191.
- ↑ Moulder JW (1991). "Interaction of chlamydiae and host cells in vitro". Microbiol Rev. 55 (1): 143–90. PMC 372804. PMID 2030670 PMID 2030670 Check
|pmid=
value (help). - ↑ Mounier, Joëlle; Vasselon, T; Hellio, R; Lesourd, M; Sansonetti, PJ (January 1992). "Shigella flexneri Enters Human Colonic Caco-2 Epithelial Cells through the Basolateral Pole". Infection and Immunity. 60 (1): 237–248. PMC 257528. PMID 1729185.
- ↑ 14.0 14.1 Espinosa-Cantellano M, Martínez-Palomo A (2000). "Pathogenesis of intestinal amebiasis: from molecules to disease". Clin Microbiol Rev. 13 (2): 318–31. PMC 100155. PMID 10756002.
- ↑ Müller FW, Franz A, Werries E (1988). "Secretory hydrolases of Entamoeba histolytica". J Protozool. 35 (2): 291–5. PMID 2456386.
- ↑ Spice WM, Ackers JP (1998). "The effects of Entamoeba histolytica lysates on human colonic mucins". J Eukaryot Microbiol. 45 (2): 24S–27S. PMID 9561780.