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 the distal part of the colon 12 to 15cm above the anus (sigmoid colon)[1][2][3]. 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

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]

Pathophysiology

The pathophysiology of proctocolitis depends on the cause. Some pathogenetic mechanisms are not clearly 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.[5][8][9][10]
  • 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.
  • Could also be an autoimmune disease. Atypical p antineutrophil cytoplasmic antibodies (a-pANCA) have been seen in some infants with intestinal infiltration by Neutrophils.[11]

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.[12].
  • 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.[13]
    • May also occur following antibiotic use, especially broad spectrum antibiotics.
Chlamydia trachomatis
    • 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).[14]
    • 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.[15]
    • 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.[16]
Shigella
  • 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).[17]
Campylobacter
    • Regarding Campylobacter jejuni protocolitis the exact pathogenesis by which it causes protocolitis 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.[18]
    • C. jejuni is known to also secrete proteins that may contribute to the ability of the bacterium to invade the host epithelial cells.[18]
Entameoba
    • 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.[19]
    • E. histolytica trophozoites secrete proteases, which induce the release of mucin from goblet cells, resulting in glandular hyperplasia.[19]
    • E. histolytica is also said to contain glycosidases that cleave glycsolyated mucin molecules, resulting in mucin degradation.[20][21]
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, cephalosporins, 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) pseudomembranous colitis.[22]
    • 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.[23][22]
    • 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 proctocolitis

  • Occur following radiation treatment for pelvic tumors.[24][25][26][27]
  • More common with radiation doses higher than 45Gy.[27]
  • 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 proctocolitis, 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 proctocolitis

  • Rare cause of proctocolitis, due to rich collateral vascular supply to the rectum.
  • Seen in the elderly with compromised 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.[28]

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.[29][30][31]
  • Cytotoxic T cells and autoantibodies (IgG and IgE) against the colon, cytoskeleton and bowel smooth muscles are seen.[29]
  • The balance in gut microbes is shifted toward pathogenic microorganism, including colonic sulphate reducing bacteria.[30]
  • 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.[31]

Other pathogenetic mechanisms of proctocolitis=

  • NSAIDS can also cause proctocolitis. The mechanism is not completely understood.[32][33]
    • 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.[34][35]
    • 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.[34]

Genetics

There is no specific genetic cause for proctocolitis. However, genetic predisposition may play a role in some causes.[11][31]

Associated conditions

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.[36][37]
    • 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.[28]
  • Allergic proctocolitis[38]
    Allergic proctocolitis[38]
  • Radiation Proctitis[39]
    Radiation Proctitis[39]
  • Pseudomembranous colitis. (WC) [40]
    Pseudomembranous colitis. (WC) [40]
  • Pseudomembranous colitis. [41]
    Pseudomembranous colitis. [41]
  • Ulcerative colitis.[42]
    Ulcerative colitis.[42]

Microscopic pathology

  • Food protein-induced proctocolitis is characterized by marked eosinophil infiltrates in the mucosa of the rectosigmoid area.[36][43]
    • The mucosa architecture is usually preserved on microscopy.[36]
  • In pseudomembranous colitis microscopy shows[44]
    • 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.
  • Ulcerative colitis. H&E staining showing crypt abscess, a characteristic finding in ulcerative colitis [45]
    Ulcerative colitis. H&E staining showing crypt abscess, a characteristic finding in ulcerative colitis [45]
  • Ulcerative colitis. H&E stain showing marked lymphocytic infiltration (blue/purple) of the intestinal mucosa and distortion of the architecture of the crypts. [46]
    Ulcerative colitis. H&E stain showing marked lymphocytic infiltration (blue/purple) of the intestinal mucosa and distortion of the architecture of the crypts. [46]
  • Ischemic colitis. H&E staining showing changes seen in ischemic colitis [47]
    Ischemic colitis. H&E staining showing changes seen in ischemic colitis [47]
  • Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [48]
    Pseudomembranous colitis. H& E staining showing pseudomembranes in Clostridium colitis [48]

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 of proctocolitis by Organ System

Cardiovascular Ischemic colitis
Chemical/Poisoning Glutaraldehyde, Coffee enema, Hydrogen peroxide
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Chlorpropamide; NSAIDS such as Flufenamic acid, mefenamic acid, naproxen, ibuprofen, indomethacin; Antibiotics (especially penicillins, cephalosporins, fluoroquinolones, clindamycin) but any antibiotic can cause it and penicillin
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 Radiation, Glutaradehyde
Infectious Disease Chlamydia trachomatis, Neisseria gonorrheae, Treponema pallidum, HSV, CMV, Shigella dysenteriae, Salmonella, Enterohemorrhagic Escherichia coli, Clostridium difficile, Campylobacter species, Yersinia, Entameoba histolytica
Musculoskeletal/Orthopedic No underlying causes
Neurologic No underlying causes
Nutritional/Metabolic Food protein-induced proctocolitis
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 Food protein-induced protocolitis, Ulcerative colitis
Sexual Chlamydia trachomatis, Neisseria gonorrheae, Treponema pallidum, HSV, CMV, 'Shigella dysenteriae
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Microscopic colitis

Causes in Alphabetical Order

Differentiating Proctocolitis 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

  • Swallowed maternal blood syndrome
  • Anal fissure
  • Necrotizing enterocolitis especially in preterm babies
  • Vitamin K dependent hemorrhage
  • Other Coagulopathies: (hereditary such as coagulation factor deficiency or acquired such as disseminated intravascular coagulopathy)
  • Food protein-induced enterocolitis
  • Intussusception
  • Gastrointestinal Infections
  • Meckel diverticulum
  • Intestinal duplication cysts
  • Vascular malformations
  • Inflammatory bowel disease(early onset)
  • Hirschsprung disease complicated by enterocolitis
  • Volvolus
  • Gastro-duodenal ulcers
  • Gastrointestinal duplication cyst
  • Liver disease with clotting factor deficiency
  • Lymphonodular hyperplasia

Differential diagnosis in Infants

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

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

  1. ↑ Online Medical dictionary[1]
  2. ↑ 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
  3. ↑ 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.
  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. ↑ 5.0 5.1 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.
  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. ↑ 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.
  9. ↑ 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.
  10. ↑ Academy of Breastfeeding Medicine (2011). "ABM Clinical Protocol #24: Allergic Proctocolitis in the Exclusively Breastfed Infant". Breastfeed Med. 6 (6): 435–40. doi:10.1089/bfm.2011.9977. PMID 22050274.
  11. ↑ 11.0 11.1 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.
  12. ↑ 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
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ Mabey D, Peeling RW (2002). "Lymphogranuloma venereum". Sex Transm Infect. 78 (2): 90–2. PMC 1744436. PMID 12081191.
  16. ↑ 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).
  17. ↑ 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.
  18. ↑ 18.0 18.1 Capra JD, Kehoe JM (1974). "Variable region sequences of five human immunoglobulin heavy chains of the VH3 subgroup: definitive identification of four heavy chain hypervariable regions". Proc Natl Acad Sci U S A. 71 (3): 845–8. PMC 388111. PMID 4522793.
  19. ↑ 19.0 19.1 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.
  20. ↑ Müller FW, Franz A, Werries E (1988). "Secretory hydrolases of Entamoeba histolytica". J Protozool. 35 (2): 291–5. PMID 2456386.
  21. ↑ Spice WM, Ackers JP (1998). "The effects of Entamoeba histolytica lysates on human colonic mucins". J Eukaryot Microbiol. 45 (2): 24S–27S. PMID 9561780.
  22. ↑ 22.0 22.1 Surawicz CM, McFarland LV (1999). "Pseudomembranous colitis: causes and cures". Digestion. 60 (2): 91–100. doi:7633 Check |doi= value (help). PMID 10095149.
  23. ↑ Sarah A. Kuehne, Stephen T. Cartman, John T. Heap, Michelle L. Kelly, Alan Cockayne & Nigel P. Minton (2010). "The role of toxin A and toxin B inClostridium difficile infection". Nature. 467 (7316): 711–3. doi:10.1038/nature09397. PMID 20844489.
  24. ↑ Keith NM, Whelan M (1926). "A STUDY OF THE ACTION OF AMMONIUM CHLORID AND ORGANIC MERCURY COMPOUNDS". J Clin Invest. 3 (1): 149–202. doi:10.1172/JCI100072. PMC 434619. PMID 16693707.
  25. ↑ Bansal N, Soni A, Kaur P, Chauhan AK, Kaushal V (2016). "Exploring the Management of Radiation Proctitis in Current Clinical Practice". J Clin Diagn Res. 10 (6): XE01–XE06. doi:10.7860/JCDR/2016/17524.7906. PMC 4963751. PMID 27504391.
  26. ↑ Nelamangala Ramakrishnaiah VP, Krishnamachari S (2016). "Chronic haemorrhagic radiation proctitis: A review". World J Gastrointest Surg. 8 (7): 483–91. doi:10.4240/wjgs.v8.i7.483. PMC 4942748. PMID 27462390.
  27. ↑ 27.0 27.1 Do NL, Nagle D, Poylin VY (2011). "Radiation proctitis: current strategies in management". Gastroenterol Res Pract. 2011: 917941. doi:10.1155/2011/917941. PMC 3226317. PMID 22144997.
  28. ↑ 28.0 28.1 Abhishek K, Kaushik S, Kazemi MM, El-Dika S (2008). "An unusual case of hematochezia: acute ischemic proctosigmoiditis". J Gen Intern Med. 23 (9): 1525–7. doi:10.1007/s11606-008-0673-2. PMC 2518031. PMID 18521689.
  29. ↑ 29.0 29.1 Cai M, Zeng L, Li LJ, Mo LH, Xie RD, Feng BS; et al. (2016). "Specific immunotherapy ameliorates ulcerative colitis". Allergy Asthma Clin Immunol. 12: 37. doi:10.1186/s13223-016-0142-0. PMC 4975874. PMID 27499766.
  30. ↑ 30.0 30.1 Lopez J, Grinspan A (2016). "Fecal Microbiota Transplantation for Inflammatory Bowel Disease". Gastroenterol Hepatol (N Y). 12 (6): 374–9. PMC 4971820. PMID 27493597.
  31. ↑ 31.0 31.1 31.2 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.
  32. ↑ Tonolini M (2013). "Acute nonsteroidal anti-inflammatory drug-induced colitis". J Emerg Trauma Shock. 6 (4): 301–3. doi:10.4103/0974-2700.120389. PMC 3841543. PMID 24339669.
  33. ↑ Ravi S, Keat AC, Keat EC (1986). "Colitis caused by non-steroidal anti-inflammatory drugs". Postgrad Med J. 62 (730): 773–6. PMC 2418853. PMID 3774712.
  34. ↑ 34.0 34.1 West AB, Kuan SF, Bennick M, Lagarde S (1995). "Glutaraldehyde colitis following endoscopy: clinical and pathological features and investigation of an outbreak". Gastroenterology. 108 (4): 1250–5. PMID 7698592.
  35. ↑ Shih HY, Wu DC, Huang WT, Chang YY, Yu FJ (2011). "Glutaraldehyde-induced colitis: case reports and literature review". Kaohsiung J Med Sci. 27 (12): 577–80. doi:10.1016/j.kjms.2011.06.036. PMID 22208542.
  36. ↑ 36.0 36.1 36.2 Hwang JB, Hong J (2013). "Food protein-induced proctocolitis: Is this allergic disorder a reality or a phantom in neonates?". Korean J Pediatr. 56 (12): 514–8. doi:10.3345/kjp.2013.56.12.514. PMC 3885785. PMID 24416045.
  37. ↑ Hwang JB, Park MH, Kang YN, Kim SP, Suh SI, Kam S (2007). "Advanced criteria for clinicopathological diagnosis of food protein-induced proctocolitis". J Korean Med Sci. 22 (2): 213–7. doi:10.3346/jkms.2007.22.2.213. PMC 2693584. PMID 17449926.
  38. ↑ The Korean Academy of Medical Sciences. Allergic proctocolitis. http://dx.doi.org/10.3346/jkms.2007.22.2.213 Accessed on 31 August, 2016
  39. ↑ Wikipedia. Proctitis. https://en.wikipedia.org/wiki/Proctitis#/media/File:Radiation_proctitis3.jpg Accessed on August 31, 2016
  40. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/Pseudomembranous_colitis Accessed on August 31, 2016
  41. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org Accessed on September 1, 2016
  42. ↑ Ulcerative colitis. Wikidoc. http://www.wikidoc.org/index.php/File:UC_granularity.png#filehistory Accessed on August 31, 2016
  43. ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID http://dx.doi.org/10.1016/S0022-3476(95)70540-6 Check |pmid= value (help).
  44. ↑ 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}}
  45. ↑ Libre Pathology. https://librepathology.org/wiki/File:Ulcerative_colitis_(2)_active.jpg Accessed on September 1, 2016
  46. ↑ Libre Pathology. https://librepathology.org/wiki/File:Ulcerative_colitis_(2)_endoscopic_biopsy.jpg Accessed on September 1, 2016
  47. ↑ Wikipedia. Ischemic colitis. https://en.wikipedia.org/wiki/Ischemic_colitis#/media/File:Ischemic_colitis_-_high_mag.jpg Accessed on August 31, 2016
  48. ↑ Libre Pathology. Pseudomembranous colitis. https://librepathology.org/wiki/File:Colonic_pseudomembranes_low_mag.jpg Accessed on September 1, 2016
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