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Crohn's disease

Crohn's disease(Clone,British: Crohn's disease,Abbreviation: CD) Is mainlyOral cavityからanusAll up toDigestive tractIn addition, discontinuous chronic granulomatousInflammationUnexplained causeInflammatory disease[1],Ministry of Health, Labor and WelfareThanSpecific diseaseIs specified in[2].

Ulcerative colitis(English: ulcerative colitis, Stands for: UC) WithInflammatory bowel disease(English: Inflammatory bowel disease, Stands for: IBD)are categorized.Crohn's disease does not always have a high case fatality rate,Ulcerative colitisInflammation occurs only in the large intestine, whereas in Crohn's disease, inflammation can occur in all gastrointestinal tracts and the frequency of complications tends to be higher than that in ulcerative colitis.It is also strict in the treatment of Crohn's diseaseDietary restrictionsIs often required[3].


1932ToNew York University OfMount Sinai HospitalReported as localized ileitis by Burrill Bernard Crohn et al.[4]..Although the name of the disease was later changed, it is certain that it occurs most often in the ileum, especially in the ileocecal region from the terminal ileum to the cecum.


It is often seen in the teens to 10s, and the number of affected people in Japan is about 20 or more.Ulcerative colitisThe number of affected people is smaller than that, and there is almost no onset in middle-aged and elderly people.The most common age of onset is 15 to 19 years for women and 20 to 24 years for men.[2].


Even now, the exact mechanism by which Crohn's disease develops is unknown.Has a genetic predisposition and is an abnormality of the immune system[Note 1]It is thought that environmental factors such as dietary factors may be involved in this.Since the onset is remarkable in young people and the number of patients in developed countries in Europe and the United States is overwhelmingly large, it is said that it is related to the westernization of eating habits, that is, the intake of animal proteins and lipids.

In Europe and the United States, the susceptibility to Crohn's disease is particularly high.Nod2 It is strongly affected by (IBD1) deficient polymorphisms and HLA polymorphisms, but its relationship with Nod2 is not clear in Japanese.In recent years, Japanese Crohn's disease and TNFSF15 (TL1A)CytokineWas reported to be associated with the gene. TL1A is a cytokine associated with inflammation of the intestinal tract and is known to have increased expression in lesions of Crohn's disease, but the association between this and gene polymorphism remains unclear.

In 2005, R Balfour Sartor and others became cattleJone's diseaseIs a bacterium that causes a debilitating disease with diarrhea calledMycobacterium avium subsp. paratuberculosisReported that it may have invaded the human body via milk and other dairy products and caused Crohn's disease.[5]. Also,Mycobacterium There are also reports denying the involvement of[6][7][8]However, as of 2015, there is no evidence that the onset of Crohn's disease is directly related to any bacteria.[8].


Symptoms such as erythema on the legs are seen as skin complications.Since lesions of the disease can occur throughout the gastrointestinal tract, the symptoms are diverse and may be present intermittently.It affects the entire digestive tract from the oral cavity to the anus[4],ManySmall intestine・ Ileocecal part ・anusIt often occurs in the surrounding area.It is divided into "small intestine type" with lesions only in the small intestine, "large intestine type" with lesions only in the large intestine, and "small intestine / large intestine type" with lesions in both, and the small intestine / large intestine type occupies most of them. There is.


Signs and symptoms
Crohn's diseaseUlcerative colitis
DefecationMany are like porridge[9]
..Occasionally steatorrhea
Many are mucous and contain blood[9]
TenesmusUncommon[9]More general[9]
Fevergeneral[9]Severe condition[9]
Weight lossoftenVery rare

As a subjective symptom, in many cases, "stomach ache(Approximately 80%) ""diarrhea(About 80%) ”is the main symptom.Another symptom seen at a high rate is "Fever""Weight loss""anusLesion (anal fistula・ Anal fissure, anal ulcer, etc.) ”“Vomiting, Etc.Ulcerative colitisOften seen in "Bloody stool-Mucous stool"Is not so frequent.

Crohn's disease is a full-thickness inflammatory disease of the gastrointestinal mucosa, so when the inflammation is severe, changes such as "ulcer", "narrowing", "fistula", and "perforation" of the gastrointestinal tract often occur.Bowel obstructionIf gastrointestinal perforation occurs, surgical treatment such as gastrointestinal bowel resection is often required.


In addition to the gastrointestinal tract, Crohn's disease is often accompanied by various clinical features such as the following.


Specimen test

CRP-Erythrocyte sedimentation rateIs used as a test that correlates with activity.In addition, as biomarkers for inflammatory reactions, "fecal calprotectin (FC)", "fecal lactoferrin (FL)", and TCP-353 antibody may be measured and evaluated.[15].


Crohn's disease is characterized by the following endoscopic findings:fundamentallyColonoscopyOthersUpper gastrointestinal endoscopyA full gastrointestinal examination, including an examination, is performed.For detailed examination of lesions in the small intestineEnteroscopyInspection and againCapsule endoscopeExamination is also performed, but it should be performed with caution as capsule stagnation may occur if there is a stenotic lesion.

  • Discontinuous lesions
  • Paving stone statue
  • Longitudinal ulcer
  • Multiple aphthous ulna: Oral aphthous ulcer is often seen as a subjective symptom
  • Stenosis lesions, fissures, fistula lesions
  • Bamboo segmental changes: often seen in gastric lesions

Contrast examination

X-ray inspectionThe above-mentioned endoscopic findings are also observed in the gastrointestinal angiography.Since there are many lesions in the small intestine, gastrointestinal angiography is often used and useful in searching for lesions in the small intestine, not endoscopy.

CT / MRI examination

Since it is easily performed, it is often used for screening for gross changes and the like.In recent years, "CT MRI-Colonography" examination by 3D reconstruction is also performed.


The pathological findings of Crohn's disease are characterized as follows.

  • Noncaseous epithelioid cell granulomas: microscopicGranulomas(However, the detection rate in histological examination is about 50% at most)
  • Full-thickness inflammation of the gastrointestinal mucosa Findings:lymphocytesInflammation image with many infiltrations
  • Fissure formation: tissue defect associated with lymphatic vessels
  • Ulcer lesions: Mucosal ulcers are found longitudinally[Note 2].
  • Stepping stone lesions: Unlike ulcerative colitis, lesions are discontinuous.


Basically, it is diagnosed by clinical images, gastrointestinal images (endoscopic findings, gastrointestinal angiography findings), and pathological findings.

Specific diseaseTherefore, the former Ministry of Health and Welfare Crohn's disease diagnostic criteria are generally widely used because of the application for public funding.

Diagnostic criteria

Diagnostic criteria[1]Is quoted from the materials of the Intractable Disease Information Center and modified.[2].

  • Definite (confirmed cases) and Probable (suspicious cases) are targeted.
  1. Major findings
    A. Longitudinal ulcer
    In the case of the small intestine, it often occurs on the mesenteric attachment side.
    B. Paving stone statue
    C. Noncaseous epithelioid cell granuloma
    The diagnostic rate is improved by making continuous sections.Judgment by a pathologist familiar with the gastrointestinal tract is desirable
  2. Secondary findings
    Extensive irregularities of the gastrointestinal tract-round ulcer or aphthous ulcer
    It is typically parallel, but may not be parallel.
    In addition, it is necessary to stay for at least 3 months.
    It is also necessary to exclude intestinal tuberculosis, intestinal Behcet's disease, simple ulcers, NSAIDs ulcers, and infectious enteritis.
    b. Characteristic anal lesions
    Anal fissure, cavitating ulcer, anal fistula, perianal abscess, edematous dermatitis, etc. Crohn's disease Anal lesions Gross findings Refer to the atlas and make a diagnosis by an anal disease specialist familiar with Crohn's disease.
    c. Characteristic gastric • duodenal lesions
    Bamboo nodal appearance, notch-like depression, etc.Diagnosis by a specialist familiar with Crohn's disease is desirable.
Diagnostic category[2]
  • Definite (confirmed case):
    1. Those with major findings A or B.
      For longitudinal ulcers only, it is necessary to rule out ischemic bowel lesions and ulcerative colitis.For paving stones only, it is necessary to rule out ischemic bowel lesions.
    2. Those with a major finding C and a secondary finding a or b.
    3. Those with all of the secondary findings a, b, and c.
  • Probable (suspicious case):
    1. Those with a major finding C and a secondary finding c.
    2. Those with major findings A or B but indistinguishable from ulcerative colitis, intestinal Behcet's disease, simple ulcers, and ischemic intestinal lesions.
    3. Those with only the main finding C.
      It is necessary to rule out inflammatory diseases with granulomas such as intestinal tuberculosis.
    4. Those with only one or one of the secondary findings.
Severity classification
Crohn's disease IOIBD score[2]
  • One item is one point, and two or more points are eligible for medical expenses subsidy.
    1. stomach ache
    2. Diarrhea or mucous stools more than 1 times a day
    3. Anal lesions
    4. Fistula
    5. Other complications (uveitis, irisitis, aphthous ulcer, arthritis, skin symptoms (erythema nodosum, pyoderma gangrenosum), deep venous thrombosis, etc.)
    6. Abdominal mass
    7. Weight loss
    8. Fever of 38 ℃ or higher
    9. Abdominal pain
    10. Hemoglobin 10g / dL or less


There is no cure by 2019, so the goal is to manage the activity of the disease, introduce it into remission (symptom-free or very weak), and maintain it.Treatment is nutrition therapy as a medical treatment (diet remedy) AndDrug therapyIf you have strong symptoms such as tumor or stenosis, surgical treatment is also considered.In children, it is necessary to consider the adverse effects on the growth of drugs, and in principle nutrition therapy is used.[16].

Nutrition therapy

Nutrition therapy has fewer side effects than drug therapy[16]..Resting the intestinal tract induces remission, suppresses inflammation and improves symptoms.

In enteral nutrition therapy, nutritional supplements may be administered to the intestine using a nasal tube or taken by mouth.[16]..Nutritional supplements are nutritional supplements containing carbohydrates, proteins, fats, vitamins and minerals.If the patient is severely ill and cannot receive nutrition from the gastrointestinal tract, fast and receive complete parenteral nutrition therapy.[16]..It is a nutritional supplement by high-calorie infusion.

In severe cases, fasting may continue, so while continuing dietary restrictions to maintain remission,Elemental dietIt is also necessary to take.Specifically, they are instructed to limit the intake of lipids while using nutritional supplements, to limit meat, and to avoid fibrous foods.That is, foods mainly composed of amino acids that do not show antigenicity and foods with reduced fat mass are mainly used.Generally, a "low-fat" and "low-residue" diet is recommended as a diet that is less prone to inflammation.However, in recent years, fiber may not be restricted only when there is no stenosis.

Patients with Crohn's disease are in the bloodErgothioneineIt has been reported that the concentration of ergothioneine is low, suggesting a relationship between intestinal inflammation suppression and ergothioneine.[17].

Systematic review

From very low quality studies, corticosteroids are better at inducing remission than enteral nutrition in adults and vice versa in children, requiring further study confirmation (2017, 27).[18]..For maintenance by enteral nutrition therapyRandomized controlled trial (RCT) No firm conclusions from 4 studies, and 4 ongoing trials will be reviewed again when completed (2018)[19].

Omega-3 fatty acidsResults are inconsistent with supplements (2013)[20].ProbioticsThen there is only one study and an appropriate RCT is needed (1)[21].glutamineTwo small RCTs are not enough, but the results show that they are not useful.[22].

Drug treatment

It is used properly during the active period as described below.Mesalazine and salazosulfapyridine are used to maintain remission, and these are used to maintain remission when biopharmaceuticals (molecular-targeted therapies) are used.[16].

Salicylic acidFormulation
The most basic and common drug used for both maintenance and induction of remission.
  • Mesalazine(Abbreviation 5-ASA: Also known as Mesalazine / 5-aminosalicylic acid, trade name Pentasa)
  • Sulfasalazine (Abbreviation SASP, also known as sulfasalazine, trade name salazopyrin, azulfidine) For large intestine type[16].
Corticosteroids ・Steroidal anti-inflammatory drug
  • Budesonide Effective for local lesions, mainly from the ileum to the ascending colon[16]..If the effect is insufficient so far, go to the following (to treat moderate or higher)[16].
  • Prednisolone Although it has a strong effect, it causes side effects after long-term use, so it should be gradually reduced for the purpose of inducing remission.[16]..Weight lossWithdrawalMay be difficult[16]..Attention should be paid to infectious diseases caused by the side effects of weakened immunity.[16]..In severe cases, it may be injected intravenously.[16].
  • Azathioprine It can also be used in combination when the raw material for steroids is difficult.[16]..It may take 3-4 months to be effective[16].
  • Mercaptopurine(6-MP) Instead of the above azathioprine[16].
Molecular target drug
If the effect is insufficient, including nutritional therapy, the use of biopharmaceuticals (molecular-targeted therapies) is considered.[16].
All are indicated except for marked stenosis, internal fistula and abscess formation.
Unapproved molecular targeted therapy in Japan
  • Certolizumab(Simdia): Anti-TNF drug.Not approved in Japan.米 国Then there is approval for Crohn's disease.in JapanRheumatoid arthritisOnly adapted.
  • Tofacitinib(Zeljanz): Not approved in Japan. JAK inhibitor.Not approved in Japan. (Ulcerative colitis is approved)
It is mainly used to relieve symptoms such as pain relief and anti-inflammatory action.
Systematic review

With aminosalicylic acid preparations for induction of remission up to moderate disease,SulfasalazineIs less effective than steroids but slightly more effective than placebo, mesalazine is as effective as placebo, and there is moderate quality evidence that mesalazine plus budesonide results are inconsistent (2016, 20 studies)[23]..Mesalazine is not more effective than placebo in maintaining introduced remission and no additional studies are recommended (2016, 12 placebo-controlled studies)[24].AntibioticsHas high-quality evidence that it has no clinical effect during the active phase, and the effect on the maintenance phase of remission is unclear (2019, 13 RCTs of various antibiotics).[25]..Although the immunosuppressive drugs azathioprine and mercaptopurine are not as effective as placebo in inducing remission and clinical improvement during the active phase, they are superior to infliximab (molecular-targeted therapeutic agent) in remission induction than placebo alone. 2016, 13 RCTs)[26].

Of steroidsBudesonideIs more effective than placebo in inducing remission (2015, 14 studies)[27]..After introduction, the use of budezonide for more than 3 months is not effective due to the increased side effects of suppression of corticosteroids (2014, 12 studies).[28]..Corticosteroids are superior to enteral nutrition therapy in induction of remission in adults and vice versa in children due to very low quality studies and require further study confirmation (2017, 27).[18].

For biopharmacy, there is high-quality evidence that ustekinumab is effective in inducing moderate to severe remissions for up to 9 weeks of use and requires testing for long-term use (2016, 6 RCTs). )[29]..It is effective for maintenance from induction of remission with each drug of infliximab and adalimumab, and the side effects are similar, and there is no study comparing their relative efficacy (2008, 3 cases of infuri and 2 cases of adalim).[30].. From a total of 4 patients in 342 studies, the rate of induction and maintenance of remission was higher with oral nutrition therapy than with infliximab alone.[31]..The use of anti-TNF drugs increases the risk of postoperative complications, especially due to infections (2016, 14 studies)[32].

Of newly available biopharmacyUstekinumab,(English editionNatalizumab (anti-α4β7 drug) is superior to placebo for induction of remission, but none of them is superior (2018, 9 studies)[33].NatalizumabIn rare casesProgressive multifocal leukoencephalopathy There are other drugs that are at risk of developing (PML) and dying and do not (2018)[34].

surgical treatment

Basically no surgical treatment, but severe stenosis for which medical treatment is not effectiveBowel obstructionIf you have a perforation, fistula or abscess, surgery is indicated.Even in that case, excision is minimized to avoid short bowel syndrome as much as possible, and strictureplasty is performed.Even if the lesion is removed by surgery, the recurrence rate is extremely high, and it often relapses especially at the rejoint site after surgery.

Blood cell component removal therapy

Along with ulcerative colitis, it becomes a key point of the mechanism of inflammation developmentWhite blood cell or White blood cellWithinGranulocytesA cure to get rid of.


This disease is a chronic disease that repeats remission and activity, and although it is currently impossible to cure it completely, it is rarely directly life-threatening.However, the surgery rate is as high as 5% 33.3 years after the onset and 10% in 70.8 years, and the re-surgery rate after surgery is as high as 5% in 28 years, so it is important to prevent relapse and recurrence. ..The cumulative survival rate 10 years after diagnosis is 96.9%.


Because of the chronic illness, it becomes a fight against illness while living a daily life.In addition, since it is not generally well known, activities to raise awareness and understanding of illness have been required.In recent years, mental support such as TOKYO IBD, an organization where patients and supporters gather to exchange information on Crohn's disease and colorectal diseases, and NPOs that support intractable diseases are gradually increasing.


注 釈

  1. ^ mainlyMacrophage Tumor necrosis factor αTo sayCytokineTo secrete and damage normal cells of the intestinal wall
  2. ^ On the other handIntestinal tuberculosisWill cause a ring-shaped ulcerative lesion


  1. ^ a b Crohn's disease diagnostic criteria (revised January 2018)
  2. ^ a b c d e Crohn's disease Intractable Diseases Medical Research Foundation / Intractable Diseases Information Center Retrieved November 2016, 11
  3. ^ Final warning!Takeshi's Really Scary Home Medical Examination Room | "Truly Scary Cold-like Symptoms-Diarrhea-" Asahi Broadcasting Homepage
  4. ^ a b Kibun Hibi, Yasushi Iwao, Yasuo Hosoda and others, "Crohn's diseaseJournal of the Japanese Society of Internal Medicine 1993 Vol. 82, No. 5, p.663-668, two:10.2169 / naika.82.663
  5. ^ Sartor RB: Does Mycobacterium avium subspecies paratuberculosis cause Crohn's disease? Gut 54; 896-898: 2005, two:10.1136 / gut.2004.055889
  6. ^ Kensuke Kobayashia, William R. Brown, Patrick J. Brennana, Martin J. Blaser,Serum antibodies to mycobacterial antigens in active Crohn's disease. Gastroenterology. Volume 94, Issue 6, June 1988, Pages 1404–1411
  7. ^ Yasunobu Fifty, Shoichi Iriguchi, Shuko Kadota, Yumiko Okada, etc.Verification of HTST sterilization conditions in a milk plant of Mycobacterium avium subtilis Report of National Institute of Health Sciences 2010 No. 128, Part XNUMX
  8. ^ a b Kosaku Minamiki, Shindai Mizuno, Makoto Naganuma and others,Inflammatory bowel disease and gut bacteria Journal of the Japanese Society of Gastroenterology, 2015, Vol. 112, No. 11, p.1947-1955, two:10.11405 / nisshoshi.112.1947
  9. ^ a b c d e f internetmedicin.se> Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.
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  11. ^ Takehiko Kaneko,Digestive disorders and skinThe Japanese Journal of Dermatology, 2010, Vol. 120, No. 7, p.1465-1471, two:10.14924 / dermatol.120.1465 (With certification)
  12. ^ Pyoderma gangrenosum-- 14. Skin disorders MSD Manual Professional Edition
  13. ^ Tsunekazu Mizushima, Riichiro Nezu, Toshiki Ito, etc.3 cases of colorectal cancer associated with Crohn's disease Journal of the Japanese Society of Gastroenterology, 2005, Vol. 102, No. 7, p.912-917, two:10.11405 / nisshoshi.102.912
  14. ^ Minoru Fujita, Hideki Koga, Mitsuo Iida et al., "A case of ileal cancer that was associated with small intestinal Crohn's disease and could be preoperatively diagnosed by biopsy from a sigmoid fistula of the ileum," "Stomach and Intestine," Vol. 1, No. 37 (8). July, 2002) p.7-1067, two:10.11477 / mf.1403104510 (Paid browsing)
  15. ^ Treatment Strategy for Crohn's Disease-Ask Now for Biopharmacy-2011 JDDW2011 Fukuoka
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  17. ^ Serum Metabolomics Identifies Altered Bioenergetics, Signaling Cascades in Parallel with Exposome Markers in Crohn's Disease. two:10.3390 / molecules24030449.. PMID 30691236. 
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  19. ^ Akobeng AK, Zhang D, Gordon M, MacDonald JK (August 2018). “Enteral nutrition for maintenance of remission in Crohn's disease”. Cochrane Database System Rev 8: CD005984. two:10.1002 / 14651858.CD005984.pub3. PMID 30098021. 
  20. ^ Swan K, Allen PJ (May 2013). “Omega-3 fatty acid for the treatment and remission of Crohn's disease”. J Complement Integr Med 10. two:10.1515 / jcim-2012-0010. PMID 23652637. 
  21. ^ Butterworth AD, Thomas AG, Akobeng AK (July 2008). “Probiotics for induction of remission in Crohn's disease”. Cochrane Database System Rev (3): CD006634. two:10.1002 / 14651858.CD006634.pub2. PMID 18646162. 
  22. ^ Akobeng AK, Elawad M, Gordon M (February 2016). “Glutamine for induction of remission in Crohn's disease”. Cochrane Database System Rev 2: CD007348. two:10.1002 / 14651858.CD007348.pub2. PMID 26853855. 
  23. ^ Lim WC, Wang Y, MacDonald JK, Hanauer S (July 2016). “Aminosalicylates for induction of remission or response in Crohn's disease”. Cochrane Database System Rev 7: CD008870. two:10.1002 / 14651858.CD008870.pub2. PMC 6457996. PMID 27372735. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457996/. 
  24. ^ Akobeng AK, Zhang D, Gordon M, MacDonald JK (September 2016). “Oral 5-aminosalicylic acid for maintenance of medically-induced remission in Crohn's disease”. Cochrane Database System Rev 9: CD003715. two:10.1002 / 14651858.CD003715.pub3. PMC 6457838. PMID 27681657. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457838/. 
  25. ^ Townsend CM, Parker CE, MacDonald JK, Nguyen TM, Jairath V, Feagan BG, Khanna R (February 2019). “Antibiotics for induction and maintenance of remission in Crohn's disease”. Cochrane Database System Rev 2: CD012730. two:10.1002 / 14651858.CD012730.pub2. PMID 30731030. 
  26. ^ Chande N, Townsend CM, Parker CE, MacDonald JK (October 2016). “Azathioprine or 6-mercaptopurine for induction of remission in Crohn's disease”. Cochrane Database System Rev 10: CD000545. two:10.1002 / 14651858.CD000545.pub5. PMC 6464152. PMID 27783843. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6464152/. 
  27. ^ Rezaie A, Kuenzig ME, Benchimol EI, Griffiths AM, Otley AR, Steinhart AH, Kaplan GG, Seow CH (June 2015). “Budesonide for induction of remission in Crohn's disease”. Cochrane Database System Rev (6): CD000296. two:10.1002 / 14651858.CD000296.pub4. PMID 26039678. 
  28. ^ Kuenzig ME, Rezaie A, Seow CH, Otley AR, Steinhart AH, Griffiths AM, Kaplan GG, Benchimol EI (August 2014). “Budesonide for maintenance of remission in Crohn's disease”. Cochrane Database System Rev (8): CD002913. two:10.1002 / 14651858.CD002913.pub3. PMID 25141071. 
  29. ^ MacDonald JK, Nguyen TM, Khanna R, Timmer A (November 2016). “Anti-IL-12 / 23p40 antibodies for induction of remission in Crohn's disease”. Cochrane Database System Rev 11: CD007572. two:10.1002 / 14651858.CD007572.pub3. PMC 6464484. PMID 27885650. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6464484/. 
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