Enteropathic arthropathy: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
 
(15 intermediate revisions by the same user not shown)
Line 3: Line 3:
{{CMG}} {{AE}} {{KD}}
{{CMG}} {{AE}} {{KD}}
==Overview==
==Overview==
'''Enteropathic arthropathy''' or Enteropathic arthritis refers to acute or subacute arthritis in association with or as a reaction to an enteric (usually colonic) inflammatory condition.
'''Enteropathic arthropathy''' or Enteropathic arthritis refers to [[acute]] or [[subacute]] [[arthritis]] in association with or as a reaction to an [[enteric]] (usually colonic) [[inflammatory]] condition.
 
==Classification==
*Axial
**[[Sacroiliitis|Sacroilitis]]
**[[Spondylitis]]
 
*Peripheral arthritis
*'''Type I Arthropathy'''
**Less than five joints involved
**[[Acute]]
**Less than 10 weeks
**Asymmetrical
**Shoulder, hips and knee joints are involved
*'''Type II Arthropathy'''
**More than five joints involved
**[[Chronic (medical)|Chronic]]
**Months to years
**Symmetrical
**Small joints are involved.


==Pathophysiology==
==Pathophysiology==
The pathophysiology of Enteropathic arthropathy:<ref name="pmid3649644">{{cite journal |vauthors=Navis ES |title=Controlling violent patients before they control you. Advice on keeping your cool when your patient is losing his |journal=Nursing |volume=17 |issue=9 |pages=52–4 |date=September 1987 |pmid=3649644 |doi= |url=}}</ref><ref name="pmid3495471">{{cite journal |vauthors=Cuvelier C, Barbatis C, Mielants H, De Vos M, Roels H, Veys E |title=Histopathology of intestinal inflammation related to reactive arthritis |journal=Gut |volume=28 |issue=4 |pages=394–401 |date=April 1987 |pmid=3495471 |pmc=1432823 |doi= |url=}}</ref><ref name="pmid3495471">{{cite journal |vauthors=Cuvelier C, Barbatis C, Mielants H, De Vos M, Roels H, Veys E, Thornton JA, Harrison MJ, Wiesmann UN, DiDonato S, Herschkowitz NN, Derksen A, Cohen P, Chiang YL, Kaminsky LS, King TE, Isoun TT, Cuvelier C, Barbatis C, Mielants H, De Vos M, Roels H, Veys E, George JP |title=Histopathology of intestinal inflammation related to reactive arthritis |journal=Gut |volume=28 |issue=4 |pages=394–401 |date=April 1987 |pmid=3495471 |doi= |url=}}</ref><ref name="pmid20485176">{{cite journal |vauthors=Jacques P, Elewaut D, Mielants H |title=Interactions between gut inflammation and arthritis/spondylitis |journal=Curr Opin Rheumatol |volume=22 |issue=4 |pages=368–74 |date=July 2010 |pmid=20485176 |doi=10.1097/BOR.0b013e3283393807 |url=}}</ref><ref name="pmid20485176">{{cite journal |vauthors=Jacques P, Elewaut D, Mielants H |title=Interactions between gut inflammation and arthritis/spondylitis |journal=Curr Opin Rheumatol |volume=22 |issue=4 |pages=368–74 |date=July 2010 |pmid=20485176 |doi=10.1097/BOR.0b013e3283393807 |url=}}</ref><ref name="pmid1001980">{{cite journal |vauthors=Mallas EG, Mackintosh P, Asquith P, Cooke WT |title=Histocompatibility antigens in inflammatory bowel disease. Their clinical significance and their association with arthropathy with special reference to HLA-B27 (W27) |journal=Gut |volume=17 |issue=11 |pages=906–10 |date=November 1976 |pmid=1001980 |pmc=1411211 |doi= |url=}}</ref><ref name="pmid8733445">{{cite journal |vauthors=Brown MA, Pile KD, Kennedy LG, Calin A, Darke C, Bell J, Wordsworth BP, Cornélis F |title=HLA class I associations of ankylosing spondylitis in the white population in the United Kingdom |journal=Ann. Rheum. Dis. |volume=55 |issue=4 |pages=268–70 |date=April 1996 |pmid=8733445 |pmc=1010149 |doi= |url=}}</ref><ref name="pmid10640771">{{cite journal |vauthors=Mertz AK, Wu P, Sturniolo T, Stoll D, Rudwaleit M, Lauster R, Braun J, Sieper J |title=Multispecific CD4+ T cell response to a single 12-mer epitope of the immunodominant heat-shock protein 60 of Yersinia enterocolitica in Yersinia-triggered reactive arthritis: overlap with the B27-restricted CD8 epitope, functional properties, and epitope presentation by multiple DR alleles |journal=J. Immunol. |volume=164 |issue=3 |pages=1529–37 |date=February 2000 |pmid=10640771 |doi= |url=}}</ref><ref name="pmid19468997">{{cite journal |vauthors=Fantini MC, Pallone F, Monteleone G |title=Common immunologic mechanisms in inflammatory bowel disease and spondylarthropathies |journal=World J. Gastroenterol. |volume=15 |issue=20 |pages=2472–8 |date=May 2009 |pmid=19468997 |pmc=2686905 |doi= |url=}}</ref><ref name="pmid7964509">{{cite journal |vauthors=Taurog JD, Richardson JA, Croft JT, Simmons WA, Zhou M, Fernández-Sueiro JL, Balish E, Hammer RE |title=The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats |journal=J. Exp. Med. |volume=180 |issue=6 |pages=2359–64 |date=December 1994 |pmid=7964509 |pmc=2191772 |doi= |url=}}</ref><ref name="pmid15539413">{{cite journal |vauthors=Laukens D, Peeters H, Marichal D, Vander Cruyssen B, Mielants H, Elewaut D, Demetter P, Cuvelier C, Van Den Berghe M, Rottiers P, Veys EM, Remaut E, Steidler L, De Keyser F, De Vos M |title=CARD15 gene polymorphisms in patients with spondyloarthropathies identify a specific phenotype previously related to Crohn's disease |journal=Ann. Rheum. Dis. |volume=64 |issue=6 |pages=930–5 |date=June 2005 |pmid=15539413 |pmc=1755516 |doi=10.1136/ard.2004.028837 |url=}}</ref><ref name="pmid16937463">{{cite journal |vauthors=Rothfuss KS, Stange EF, Herrlinger KR |title=Extraintestinal manifestations and complications in inflammatory bowel diseases |journal=World J. Gastroenterol. |volume=12 |issue=30 |pages=4819–31 |date=August 2006 |pmid=16937463 |pmc=4087615 |doi= |url=}}</ref>
 
*Although the pathogenesis of EA has not been plainly clarified, the observation that joint inflammation occurs in genetically predisposed subjects with bacterial gut infections provided an important evidence for a possible relationship between inflammation of the gut mucosa and arthritis.
==Risk factors==
*Current theories provide, in genetically predisposed subjects, an aberrant migration of intestinal lymphocytes or macrophages from inflamed gut mucosa to joints, in which an important role was played by gut bacteria.
*[[HLA-B27]] positive people
*In fact, a dysfunctional interaction between the mucosal immune system and gut bacteria could result in an abnormal state of immunological tolerance toward flora by alterations in mucosal effector cells or by affecting regulatory cells.
*Active [[inflammatory bowel disease]] (IBD)
*A significant evidence for the pathogenic role of gut bacteria in the pathogenesis of SpA is derived from animals models.
*Positive family history
*Genetic factors play a predisposing role while environmental factors, such as infectious agents, may play a causative role.
*Tobacco smoking
*Among the genetic factors, HLA-B27 has the strongest genetic association with SpA and in particular with ankylosing spondylitis (AS).
*This association is reported in more than 90% of cases, also spondylitis in IBD is associated with the presence of HLA-B27, however, in lower frequencies than in AS (30%–80%).
*Pure asymptomatic sacroiliitis in CD is not strongly associated with HLA-B27 and a very recent study indicates a prevalence of 7%.
*In 2000, Orchard et al. described an association with HLA-DR0103, B35, and B27 in type 1 peripheral arthritis and neither B27 nor DR4 associations were observed in type 2 arthritis.
*In order to describe the role of HLA-B27 in the pathogenesis of EA, different theories have been proposed.
*One theory suggests that HLA-B27-expressing macrophages expose specific bacterial antigens that may activate CD4+ T-cells with their migration from gut to joint with the development of arthritis.
*Another theory proposes that homology between HLA-B27 sequences and bacterial antigens may activate T-cell and inflammation by antigen mimicry mechanism.
*Finally, the most recent theory is based on the endoplasmic reticulum stress: under normal conditions, the peptide-loaded HLA class I heavy chain binds the β2-microglobulin (β2m) in the endoplasmic reticulum. The folding process of the HLA-B27 heavy chain is slower than that of other HLA alleles thus leading to the generation of misfolded chains.
*Misfolded chains are usually removed in the endoplasmic reticulum, but in certain conditions, such as viral infection, they accumulate thus activating the protein BiP, the endoplasmic reticulum-unfolded-protein-response (UPR) and the nuclear factor κB (NFκB), which play a critical role in the induction of inflammation.
*Data suggest that deposition of β2m, caused by the high dissociation rate between the HLA-B27 heavy chain and β2m, occurring within synovial tissue, may lead to the initiation of chronic inflammation.
*Other HLA genes have been associated with SpA in IBD: HLA-DrB10103, HLA-B35, HLA-B24 in type 1 peripheral arthritis, and HLA-B44 in type 2 peripheral arthritis.
*Moreover, Mielants et al. showed an association between HLA-Bw62 and chronic gut lesions associated with a family history of AS and CD, with markers of inflammation, reduced axial mobility, the presence of sacroiliitis, destructive joint lesions, and a diagnosis of AS.
*Further confirming the relevance of HLA-B27 in the pathogenesis of enteroarthritis, Hammer et al. studied transgenic rats overexpressing HLA-B27 molecule. These rats developed a multisystemic inflammatory disease that had several clinical and histopathological similarities to SpA and IBD [54]. An important finding was that these rats did not develop joint or gut inflammation when they were in a germ-free environment [55]. This result supports the theory of the participation of microorganisms in the pathogenesis of these diseases.
*In humans with reactive arthritis, following Yersinia enterocolitica, Shigella spp. or Salmonella enteritidis and Typhimurium infection, bacterial antigens have been detected in joints [56–59]. Later studies further confirmed this evidence.
*Other molecular studies found similarities between Klebsiella nitrogenase and HLA-B27 and between Klebsiella pullulanase and collagen fibers types I, III, and IV.
*Interestingly, elevated levels of antibodies against Klebsiella and collagen fibers types I, III, IV, and V were detected in patients with CD and AS.
*In addition to HLA-B27, other genes have been identified as being related to SpA and IBD. In fact, several common genetic predispositions between SpA and IBD were identified, of which the association with IL-23R polymorphisms is most prominent.
*The functional role of IL-23 receptor polymorphisms remains unclear, the fact that IL-23 signaling plays a critical role in the Th17-mediated inflammation indicates that Th17 cells may represent a common pathogenetic mechanism in both IBD and SpA.
*The first susceptibility gene that has been identified for CD is CARD15 (or NOD2). Variants within this gene increase the risk for CD by threefold for heterozygous and fortyfold for homozygous individuals.
*An association was also found in SpA patients between the carriage of CARD15 variants and the development of chronic subclinical gut inflammation.
*Although CARD15 mutations do not seem to predispose to arthritis, it might confer a risk towards the development of (sub) clinical gut inflammation in SpA patients, rendering these patients more disposed to develop IBD.
*A CARD15-mediated NFκB-dependent inflammatory reaction might be an important pathogenic process within the joints.
*The protein is expressed in the joint tissue, and bacterial cell wall components have been demonstrated in the synovium of SpA patients, supporting the idea that CARD15 can locally trigger inflammation.
*Recently, additionally shared associations between SpA and IBD were found at chromosome 1q32 near KIF21B (genome-wide significant), STAT3, IL-12B, CDKAL1, LRRK2/MUC19, and chromosome 13q14 (experiment-wise association).
*As the genes IL-23R, STAT3, and IL-12B all influence Th17 lymphocyte differentiation/activation, this provides further evidence implicating the Th17 lymphocyte subset in the pathogenesis of SpA.
*In addition to genetic susceptibility, an important role was also been given to the environmental factors in triggering the onset of disease.
*In fact, bacterial gut infections such as Yersinia enterocolitica, Salmonella typhimurium, Campylobacter jejuni, and Shigella spp may cause joint inflammation in genetically predisposed patients.
*Given the prototypical link between certain bacterial infections and the onset of reactive arthritis, several studies have aimed to assess the role of intestinal flora in disease progression, as well as the resulting changes in mucosal response.
*On the basis of these observations, the possible pathways involved in joint and gut inflammation in EA may be the following: in the acute phase of inflammation, bacterial infections can cause acute intestinal inflammation.
*Certain bacteria may survive intracellularly in macrophages that can traffic to the joint and cause arthritis in a genetically predisposed host. *Proinflammatory cytokines such as TNF and IL-23 are produced locally, with Paneth cells being the most important producers of IL-23 in the intestine.
*This expression can activate innate immune cells (NK) to produce IL-22 that may help control inflammation at mucosal sites.
*Otherwise, damage and pathogen-associated molecular pattern molecules (DAMPs and PAMPs) and cellular stretch might promote initiation of joint inflammation.
*In the transition phase, acute intestinal and articular inflammation can be sustained due to defective immune regulation by TREG cells, or by ER stress, whereas iNKT cells act as regulators to control inflammation. Proangiogenic factors such as PlGF can lead to aberrant neovascularisation. *These events may lead to chronicity, further enhanced or maintained by repetitive cellular stress.
*In this stage, stromal cells become more important, as targets for proinflammatory cytokines (Figure 1).


==Causes==
==Causes==
* [[Reactive arthritis]] (Reactive to enteric infection)
* [[Reactive arthritis]] (Reactive to enteric infection)
* Spondyloarthropathies associated with inflammatory bowel disease (Crohn disease and ulcerative colitis)
* [[Spondyloarthropathies]] associated with [[inflammatory bowel disease]] ([[Crohn disease]] and [[ulcerative colitis]])
* Malabsorption related: Intestinal bypass (jejunoileal), Celiac disease, Whipple disease
* [[Malabsorption]] related: Intestinal bypass ([[Jejuno-ileal bypass|jejunoileal]]), [[Celiac disease]], [[Whipple's disease|Whipple disease]]
* Collagenous colitis
* [[Collagenous colitis]]
 
==Differential diagnosis==
The Differential diagnosis of enteropathic arthritis are as follows:
*[[Reactive arthritis]]
*[[Psoriatic arthritis]]
*[[Ankylosing spondylitis]]
*[[Rheumatoid arthritis]]
*[[Lyme disease]]
*[[Behçet's disease|Behcet's disease]]
*[[Gout]]
*[[Sarcoidosis]]
*[[Septic arthritis]]
 
==Signs and Symptoms==
*'''[[Sacroiliitis]] and [[Spondylitis]]'''- Low back pain exacerbated on sitting and standing for a prolonged period and relieved by activity.
*'''[[Enthesitis]]'''-  [[Inflammation]] of the [[tendon]] at the insertion of the bone such as [[tibial tuberosity]], [[achilles tendon]] at the heel.
*'''Dactilitis'''- [[Inflammation]] of the digit.
*'''Type I Arthropathy'''
**Less than five joints involved
**[[Acute]]
**Less than 10 weeks
**Asymmetrical
**Shoulder, hips and knee joints are involved
*'''Type II Arthropathy'''
**More than five joints involved
**[[Chronic (medical)|Chronic]]
**Months to years
**Symmetrical
**Small joints are involved.
*'''Extra Articular'''
**[[Aphthous ulcer|Aphthous ulcers]]
**[[Uveitis]]
**Fever
**Weight loss
**Abdominal pain
**[[Diarrhea]]
**[[Pyoderma gangrenosum]]
**[[Erythema nodosum]]
 
==Physical Examination==
The physical examination findings of a patient with Enteropathic arthropathy include:<ref name="pmid26557891">{{cite journal |vauthors=Ha F, Khalil H |title=Crohn's disease: a clinical update |journal=Therap Adv Gastroenterol |volume=8 |issue=6 |pages=352–9 |year=2015 |pmid=26557891 |pmc=4622286 |doi=10.1177/1756283X15592585 |url=}}</ref><ref name="pmid22230271">{{cite journal |vauthors=Wilkins T, Jarvis K, Patel J |title=Diagnosis and management of Crohn's disease |journal=Am Fam Physician |volume=84 |issue=12 |pages=1365–75 |year=2011 |pmid=22230271 |doi= |url=}}</ref><ref name="pmid23634187">{{cite journal |vauthors=Donnellan CF, Yann LH, Lal S |title=Nutritional management of Crohn's disease |journal=Therap Adv Gastroenterol |volume=6 |issue=3 |pages=231–42 |year=2013 |pmid=23634187 |pmc=3625021 |doi=10.1177/1756283X13477715 |url=}}</ref><ref name="pmid19568370">{{cite journal |vauthors=Baumgart DC |title=The diagnosis and treatment of Crohn's disease and ulcerative colitis |journal=Dtsch Arztebl Int |volume=106 |issue=8 |pages=123–33 |year=2009 |pmid=19568370 |pmc=2695363 |doi=10.3238/arztebl.2009.0123 |url=}}</ref>
 
===General Appearance===
*[[Weakness]]
*[[Fatigue]]
 
===Vitals===
*[[Fever]]
*[[Tachycardia]]
 
===HEENT===
*[[Aphthous ulcers]]
*[[Episcleritis]] and [[uveitis]]
 
===Cardiovascular System===
*Normal S1 and S2 sounds
*[[Tachycardia]]
 
===Gastrointestinal System===
*Abdominal tenderness in the right lower quadrant
*Abdominal distension
 
===Skin===
*[[Erythema nodosum]]
*[[Pyoderma gangrenosum]]
 
===Musculoskeletal System===
*Inflammation of the joints.
*[[Enthesitis]]
*[[Dactilitis]]
 
==Laboratory Findings==
The laboratory tests for the Enteropathic arthritis are as follows:<ref>{{cite journal | last = Kaila | first = B. | coauthors = K. Orr and C. N. Bernstein | year = 2005 | month = December | title = The anti-Saccharomyces cerevisiae antibody assay in a province-wide practice: accurate in identifying cases of Crohn's disease and predicting inflammatory disease | journal = The Canadian Journal of Gastroenterology | volume = 19 | issue = 12 | pages = 717-21 | id = PMID 16341311 | url =http://www.pulsus.com/Gastro/19_12/kail_ed.htm | accessdate = 2006-07-02 }}</ref><ref>{{cite journal | last = Israeli | first = E. | coauthors = I. Grotto, B. Gilburd, R. D. Balicer, E. Goldin, A. Wiik and Y. Shoenfeld | year = 2005 | month = September | title = Anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease | journal = Gut | volume = 54 | issue = 9 | pages = 1232-6 | doi =10.1136/gut.2004.060228 | id = PMID 16099791 }}</ref>
{| class="wikitable"
!Laboratory tests
!Findings
|-
|CBC
|
* [[Anemia]]
* [[Leucocytosis]]
* [[Thrombocytosis]]
|-
|Iron studies
|
* + [[Iron deficiency anemia]]
|-
|Serum Vit B12
|
* Normal or low
|-
|[null Serum folate]
|
* Normal or low
|-
|CMP
|
* [[Hypoalbuminemia]]
* [[Hypocalcemia]]
 
|-
|CRP and ESR
|
* Elevated
|-
|Stool testing
|
* Negative for infectious elements
|-
|Yersinia serology
|
* Negative
|}
 
==Diagnostic test of choice==
 
 
==Medical Therapy==
'''Non-Pharmacological therapy'''
*[[Physiotherapy]] including spinal mobility exercises
*Diet specific for IBD patients
*Referral to [[Ophthalmologist]] for the [[Anterior uveitis|anterior uveitis.]]
 
'''Pharmacological therapy'''
*[[Non-steroidal anti-inflammatory drug|Non-steroidal anti-inflammatory drug (NSAIDS]])
*[[Corticosteroids]]
**[[Intraarticular|Intraarticular corticosteroids]]
**Systemic corticosteroids
*[[Sulfasalazine]]
*[[Methotrexate]]
*[[Azathioprine]]
*[[Pamidronate]]
*[[Cyclosporine|Ciclosporin]]
*[[Tumor necrosis factors|Tumour necrosis factor (TNF) antagonists]]
 




Latest revision as of 21:47, 19 April 2018

WikiDoc Resources for Enteropathic arthropathy

Articles

Most recent articles on Enteropathic arthropathy

Most cited articles on Enteropathic arthropathy

Review articles on Enteropathic arthropathy

Articles on Enteropathic arthropathy in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Enteropathic arthropathy

Images of Enteropathic arthropathy

Photos of Enteropathic arthropathy

Podcasts & MP3s on Enteropathic arthropathy

Videos on Enteropathic arthropathy

Evidence Based Medicine

Cochrane Collaboration on Enteropathic arthropathy

Bandolier on Enteropathic arthropathy

TRIP on Enteropathic arthropathy

Clinical Trials

Ongoing Trials on Enteropathic arthropathy at Clinical Trials.gov

Trial results on Enteropathic arthropathy

Clinical Trials on Enteropathic arthropathy at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Enteropathic arthropathy

NICE Guidance on Enteropathic arthropathy

NHS PRODIGY Guidance

FDA on Enteropathic arthropathy

CDC on Enteropathic arthropathy

Books

Books on Enteropathic arthropathy

News

Enteropathic arthropathy in the news

Be alerted to news on Enteropathic arthropathy

News trends on Enteropathic arthropathy

Commentary

Blogs on Enteropathic arthropathy

Definitions

Definitions of Enteropathic arthropathy

Patient Resources / Community

Patient resources on Enteropathic arthropathy

Discussion groups on Enteropathic arthropathy

Patient Handouts on Enteropathic arthropathy

Directions to Hospitals Treating Enteropathic arthropathy

Risk calculators and risk factors for Enteropathic arthropathy

Healthcare Provider Resources

Symptoms of Enteropathic arthropathy

Causes & Risk Factors for Enteropathic arthropathy

Diagnostic studies for Enteropathic arthropathy

Treatment of Enteropathic arthropathy

Continuing Medical Education (CME)

CME Programs on Enteropathic arthropathy

International

Enteropathic arthropathy en Espanol

Enteropathic arthropathy en Francais

Business

Enteropathic arthropathy in the Marketplace

Patents on Enteropathic arthropathy

Experimental / Informatics

List of terms related to Enteropathic arthropathy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

Overview

Enteropathic arthropathy or Enteropathic arthritis refers to acute or subacute arthritis in association with or as a reaction to an enteric (usually colonic) inflammatory condition.

Classification

  • Peripheral arthritis
  • Type I Arthropathy
    • Less than five joints involved
    • Acute
    • Less than 10 weeks
    • Asymmetrical
    • Shoulder, hips and knee joints are involved
  • Type II Arthropathy
    • More than five joints involved
    • Chronic
    • Months to years
    • Symmetrical
    • Small joints are involved.

Pathophysiology

Risk factors

Causes

Differential diagnosis

The Differential diagnosis of enteropathic arthritis are as follows:

Signs and Symptoms

Physical Examination

The physical examination findings of a patient with Enteropathic arthropathy include:[1][2][3][4]

General Appearance

Vitals

HEENT

Cardiovascular System

Gastrointestinal System

  • Abdominal tenderness in the right lower quadrant
  • Abdominal distension

Skin

Musculoskeletal System

Laboratory Findings

The laboratory tests for the Enteropathic arthritis are as follows:[5][6]

Laboratory tests Findings
CBC
Iron studies
Serum Vit B12
  • Normal or low
[null Serum folate]
  • Normal or low
CMP
CRP and ESR
  • Elevated
Stool testing
  • Negative for infectious elements
Yersinia serology
  • Negative

Diagnostic test of choice

Medical Therapy

Non-Pharmacological therapy

Pharmacological therapy


References

  1. ↑ Ha F, Khalil H (2015). "Crohn's disease: a clinical update". Therap Adv Gastroenterol. 8 (6): 352–9. doi:10.1177/1756283X15592585. PMC 4622286. PMID 26557891.
  2. ↑ Wilkins T, Jarvis K, Patel J (2011). "Diagnosis and management of Crohn's disease". Am Fam Physician. 84 (12): 1365–75. PMID 22230271.
  3. ↑ Donnellan CF, Yann LH, Lal S (2013). "Nutritional management of Crohn's disease". Therap Adv Gastroenterol. 6 (3): 231–42. doi:10.1177/1756283X13477715. PMC 3625021. PMID 23634187.
  4. ↑ Baumgart DC (2009). "The diagnosis and treatment of Crohn's disease and ulcerative colitis". Dtsch Arztebl Int. 106 (8): 123–33. doi:10.3238/arztebl.2009.0123. PMC 2695363. PMID 19568370.
  5. ↑ Kaila, B. (2005). "The anti-Saccharomyces cerevisiae antibody assay in a province-wide practice: accurate in identifying cases of Crohn's disease and predicting inflammatory disease". The Canadian Journal of Gastroenterology. 19 (12): 717–21. PMID 16341311. Retrieved 2006-07-02. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  6. ↑ Israeli, E. (2005). "Anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease". Gut. 54 (9): 1232–6. doi:10.1136/gut.2004.060228. PMID 16099791. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Enteropathic_arthropathy&oldid=1464382"