Diagnosis and management of intestinal Behçet’s disease

Hisamatsu, Tadakazu; Naganuma, Makoto; Matsuoka, Katsuyoshi; Kanai, Takanori

doi:10.1007/s12328-014-0488-0

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Diagnosis and management of intestinal Behçet’s disease

review-article

Author(s): Tadakazu Hisamatsu , Makoto Naganuma , Katsuyoshi Matsuoka , Takanori Kanai

Publication date (Electronic): 20 April 2014

Journal: Clinical Journal of Gastroenterology

Publisher: Springer Japan

Keywords: Intestinal Behçet’s disease, Anti-TNFα mAb, Trisomy 8, Adalimumab

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Abstract

Behçet’s disease (BD) is a chronic relapsing disease with multiple organ system involvement characterized clinically by oral and genital aphthae, cutaneous lesions, and ophthalmological, neurological, and/or gastrointestinal manifestations. Little clinical evidence is available regarding the management of patients with intestinal BD, despite recognition that the presence of intestinal lesions is a poor prognostic factor, causing perforation and massive bleeding. Many recent case reports have suggested that anti-tumor necrosis factor alpha (TNF)α monoclonal antibodies (mAbs) are effective in patients with intestinal BD. Adalimumab, a fully human anti-TNFα mAb, has been approved in Japan for the treatment of intestinal BD. Here, we review the pathogenesis, diagnosis and management of intestinal BD, including evidence of the efficacy of anti-TNFα mAbs.

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Most cited references 73

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A chromosome 8 gene-cluster polymorphism with low human beta-defensin 2 gene copy number predisposes to Crohn disease of the colon.

Klaus Fellermann, Daniel E. Stange, Elke Schaeffeler … (2006)

Defensins are endogenous antimicrobial peptides that protect the intestinal mucosa against bacterial invasion. It has been suggested that deficient defensin expression may underlie the chronic inflammation of Crohn disease (CD). The DNA copy number of the beta-defensin gene cluster on chromosome 8p23.1 is highly polymorphic within the healthy population, which suggests that the defective beta-defensin induction in colonic CD could be due to low beta-defensin-gene copy number. Here, we tested this hypothesis, using genomewide DNA copy number profiling by array-based comparative genomic hybridization and quantitative polymerase-chain-reaction analysis of the human beta-defensin 2 (HBD-2) gene. We showed that healthy individuals, as well as patients with ulcerative colitis, have a median of 4 (range 2-10) HBD-2 gene copies per genome. In a surgical cohort with ileal or colonic CD and in a second large cohort with inflammatory bowel diseases, those with ileal resections/disease exhibited a normal median HBD-2 copy number of 4, whereas those with colonic CD had a median of only 3 copies per genome (P=.008 for the surgical cohort; P=.032 for the second cohort). Overall, the copy number distribution in colonic CD was shifted to lower numbers compared with controls (P=.002 for both the surgical cohort and the cohort with inflammatory bowel diseases). Individuals with or = 4 copies (odds ratio 3.06; 95% confidence interval 1.46-6.45). An HBD-2 gene copy number of < 4 was associated with diminished mucosal HBD-2 mRNA expression (P=.033). In conclusion, a lower HBD-2 gene copy number in the beta-defensin locus predisposes to colonic CD, most likely through diminished beta-defensin expression.

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Long-term outcome of treatment with infliximab in 614 patients with Crohn's disease: results from a single-centre cohort.

F Schnitzler, Anna M Ferrante, M Ferrante … (2009)

This observational study assessed the long-term clinical benefit of infliximab (IFX) in 614 consecutive patients with Crohn's disease (CD) from a single centre during a median follow-up of 55 months (interquartile range (IQR) 27-83). The primary analysis looked at the proportion of patients with initial response to IFX who had sustained clinical benefit at the end of follow-up. The long-term effects of IFX on the course of CD as reflected by the rate of surgery and hospitalisations and need for corticosteroids were also analysed. 10.9% of patients were primary non-responders to IFX. Sustained benefit was observed in 347 of the 547 patients (63.4%) receiving long-term treatment. In 68.3% of these, treatment with IFX was ongoing and in 31.7% IFX was stopped, with the patient being in remission. Seventy patients (12.8%) had to stop IFX due to side effects and 118 (21.6%) due to loss of response. Although the yearly drop-out rates of IFX in patients with episodic (10.7%) and scheduled treatment (7.1%) were similar, the need for hospitalisations and surgery decreased less in the episodic than in the scheduled group. Steroid discontinuation also occurred in a higher proportion of patients in the scheduled group than in the episodic group. In this large real-life cohort of patients with CD, long-term treatment with IFX was very efficacious to maintain improvement during a median follow-up of almost 5 years and changed disease outcome by decreasing the rate of hospitalisations and surgery.

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Author and article information

Contributors

Tadakazu Hisamatsu: +81-3-33531211 , +81-3-33572778 , hisamachi@a7.keio.jp

Journal

Journal ID (nlm-ta): Clin J Gastroenterol

Journal ID (iso-abbrev): Clin J Gastroenterol

Title: Clinical Journal of Gastroenterology

Publisher: Springer Japan (Tokyo )

ISSN (Print): 1865-7257

ISSN (Electronic): 1865-7265

Publication date (Electronic): 20 April 2014

Publication date PMC-release: 20 April 2014

Publication date (Print): 2014

Volume: 7

Pages: 205-212

Affiliations

[ ]Division of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582 Japan

[ ]Center for Diagnostic and Therapeutic Endoscopy, School of Medicine, Keio University, Tokyo, Japan

Article

Publisher ID: 488

DOI: 10.1007/s12328-014-0488-0

PMC ID: 4037558

PubMed ID: 24883128

SO-VID: 8b66c488-7d91-449c-b9a3-de2d9094b204

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.