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1 119; 59 with ulcerative colitis and 60 with Crohn's disease).
2 RC (222 with ulcerative colitis and 100 with Crohn's disease).
3 ecrease the risk of relapse in patients with Crohn's disease.
4 iation study in two cohorts of patients with Crohn's disease.
5 colitis is an experimental model that mimics Crohn's disease.
6 lth-care costs in paediatric and adult onset Crohn's disease.
7 ry diseases such as rheumatoid arthritis and Crohn's disease.
8 patients with moderately-to-severely active Crohn's disease.
9 19 might be a viable therapeutic approach in Crohn's disease.
10 pulations with moderately to severely active Crohn's disease.
11 erosis, rheumatoid arthritis, psoriasis, and Crohn's disease.
12 the exception of women with active perianal Crohn's disease.
13 re strongly distinguished colonic from ileal Crohn's disease.
14 bnormal biomarkers typically associated with Crohn's disease.
15 y complex perianal fistulas in patients with Crohn's disease.
16 ut microbial Ags in a pattern reminiscent of Crohn's disease.
17 r delay postoperative clinical recurrence of Crohn's disease.
18 owel disease includes ulcerative colitis and Crohn's disease.
19 ation) in patients with treatment-refractory Crohn's disease.
20 c juvenile idiopathic arthritis, leprosy and Crohn's disease.
21 role in the pathogenesis of autoinflammatory Crohn's disease.
22 ntenance of remission in adult patients with Crohn's disease.
23 18 months after resection of all macroscopic Crohn's disease.
24 provide information about the development of Crohn's disease.
25 rovide information about the pathogenesis of Crohn's disease.
26 sen for the treatment of persons with active Crohn's disease.
27 us bacteria, running under healthy mucosa in Crohn's disease.
28 , and provide data on up to 60 patients with Crohn's disease.
29 activation of the PGD2 metabolic pathway in Crohn's disease.
30 ere related to complications and symptoms of Crohn's disease.
31 s in patients with Montreal B2 fibrostenotic Crohn's disease.
32 multiple sclerosis, rheumatoid arthritis and Crohn's disease.
33 etanercept is not effective for treatment of Crohn's disease.
34 or induction and maintenance of remission of Crohn's disease.
35 l bacteria--"dysbiosis"-is characteristic of Crohn's disease.
36 uction are noted in cells from patients with Crohn's disease.
37 of conventional management for treatment of Crohn's disease.
38 receptor A (IL-17RA) inhibition exacerbates Crohn's disease.
39 events in patients with perianal fistulizing Crohn's disease.
40 d and Drug Administration-approved drugs for Crohn's disease.
41 ssociated 4 loci with clinical phenotypes of Crohn's disease.
42 ally and biologically in the pathogenesis of Crohn's disease.
43 us adverse event was worsening of underlying Crohn's disease.
44 tween individuals with ulcerative colitis vs Crohn's disease.
45 e colitis, colonic Crohn's disease and ileal Crohn's disease.
46 intestinal CD4(+) T cells from patients with Crohn's disease.
47 g clinical remission in patients with active Crohn's disease.
48 RISK study, an inception cohort of pediatric Crohn's disease.
49 and South America, including Brazil (APC for Crohn's disease +11.1% [95% CI 4.8-17.8] and APC for ulc
51 ubphenotypes to 34,819 patients (19,713 with Crohn's disease, 14,683 with ulcerative colitis) genotyp
52 00 person-years (10/100,000 person-years for Crohn's disease, 19/100,000 person-years for ulcerative
54 lcerative colitis 505 per 100 000 in Norway; Crohn's disease 322 per 100 000 in Germany) and North Am
55 ]) in the tight control group, and worsening Crohn's disease (35 [29%] of 122 patients), arthralgia (
56 ture loci were mapped for 1088 patients with Crohn's disease, 361 with ulcerative colitis, 62 with IB
57 itis +14.9% [10.4-19.6]) and Taiwan (APC for Crohn's disease +4.0% [1.0-7.1] and APC for ulcerative c
59 e aged 18 years or older; documented to have Crohn's disease; able to speak or understand English, Fr
60 was clinical recurrence of Crohn's disease (Crohn's Disease Activity Index >150 plus 100-point incre
61 sess Regional Homogeneity (ReHo) levels, and Crohn's Disease Activity Index (CDAI) and Inflammatory B
62 f >6 in one or more segments with ulcers), a Crohn's Disease Activity Index (CDAI) of 150-450 dependi
63 e Crohn's disease at screening, defined as a Crohn's Disease Activity Index (CDAI) of 220-450, with m
64 erum levels of C-reactive protein (CRP), and Crohn's disease activity index (CDAI) scores were measur
66 (defined as a decrease from baseline in the Crohn's Disease Activity Index [CDAI] score of >/=100 po
68 dices, such as the Mayo Clinic Score and the Crohn's Disease Activity Index; these indices incorporat
69 ystemic lupus erythematosus, celiac disease, Crohn's disease, Addison's disease, primary biliary cirr
70 he autophagy gene ATG16L1 is associated with Crohn's disease, an inflammatory bowel disease (IBD), an
71 8% and 0.3% (odds ratio 2.04; 1.59-2.62) for Crohn's disease and 1.3% and 0.7% (odds ratio 1.75; 1.44
73 o analyzed sera from 29 patients with active Crohn's disease and 33 patients with active ulcerative c
74 imens from inflamed colon of 8 patients with Crohn's disease and 8 patients with ulcerative colitis,
75 milarity between plasma palmitoleic acid and Crohn's disease and find that specific fatty acids exace
76 and Wales) who had a confirmed diagnosis of Crohn's disease and had undergone intestinal resection.
77 ons (P < 4.2 x 10(-5)) were observed between Crohn's disease and IBD and African-specific SNPs in STA
79 immune cells among associations stronger in Crohn's disease and in gut mucosa among associations str
80 6L1 (rs2241880; T300A) increases the risk of Crohn's disease and it has been shown to enhance suscept
81 the list of susceptibility genes shared with Crohn's disease and leprosy and implicate mucosal factor
82 e placebo group had a clinical recurrence of Crohn's disease and needed anti-inflammatory rescue trea
83 opment of IBD as a time-dependent covariate, Crohn's disease and no IBD (both vs ulcerative colitis)
84 mean levels of disease activity (P = .18 for Crohn's disease and P = .14 for ulcerative colitis).
86 h defined formula diets, helps children with Crohn's disease and reduces inflammation and dysbiosis.
88 is demonstrated through its applications to Crohn's disease and schizophrenia using the largest stud
89 es cerevisiae antibody levels is observed in Crohn's disease and this deficiency is frequently associ
92 ope and Israel, comprising 212 patients with Crohn's disease and treatment-refractory, draining, comp
96 n's disease, and ulcerative colitis) than by Crohn's disease and ulcerative colitis as currently defi
97 ng and the need for surgery in patients with Crohn's disease and ulcerative colitis have reached inco
98 c inflammatory bowel diseases (IBD) known as Crohn's disease and ulcerative colitis have shown strong
104 cancer (15 with ulcerative colitis, 14 with Crohn's disease, and 2 with indeterminate colitis) and p
105 that are traditional for clinical trials in Crohn's disease, and identify factors that predict benef
107 s including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models.
108 ously develop chronic ileitis that resembles Crohn's disease, and that DC migration is severely impai
109 pothesis that colonic Crohn's disease, ileal Crohn's disease, and ulcerative colitis are all genetica
110 three groups (ileal Crohn's disease, colonic Crohn's disease, and ulcerative colitis) than by Crohn's
113 apies for perianal fistulas in patients with Crohn's disease are often ineffective in producing long-
115 hma, atherosclerosis, pulmonary diseases and Crohn's disease as hubs and thus pointing to common infl
116 ease conditions, like Alzheimer's Disease or Crohn's Disease, associated with altered autophagy.
117 but is conserved in the sequence of deafness/Crohn's disease-associated homopolymeric glycoproteins a
118 ontrast to the dogma, we find that the major Crohn's disease-associated NOD2 mutations could cause a
119 binding oligomerization domain 2 (NOD2), the Crohn's disease-associated sensor of bacterial peptidogl
121 k stratification of paediatric patients with Crohn's disease at diagnosis, and selection of anti-TNFa
122 ast 3 months, assessed as moderate-to-severe Crohn's disease at screening, defined as a Crohn's Disea
123 ssed their association with 17 phenotypes of Crohn's disease (based on disease location, disease beha
124 nd maintenance of remission in patients with Crohn's disease, based on direct and indirect evidence.
125 garding the best treatment for patients with Crohn's disease because of the lack of direct comparativ
126 non progressed to phase 3 clinical trials in Crohn's disease but efficacy was limited, with the need
127 is an effective treatment for patients with Crohn's disease, but has never been adequately evaluated
128 composition of the intestinal microbiota in Crohn's disease, but its role on skin microbiota is unkn
129 venting postoperative clinical recurrence of Crohn's disease, but only in patients who are smokers.
130 een recommended for monitoring patients with Crohn's disease, but whether their use in treatment deci
131 ur understanding of the microbiome's role in Crohn's disease by studying a unique, well-suited cohort
133 nificantly greater than that between PSC and Crohn's disease (CD) (rG = 0.04) (P = 2.55 x 10(-15)).
135 s that might decrease the risk of relapse of Crohn's disease (CD) after surgery, but it is unclear wh
137 distal ileum tissues from 6-8 patients with Crohn's disease (CD) and 6-8 individuals without CD (con
138 is strongly associated with the aetiology of Crohn's Disease (CD) and exclusive enteral nutrition (EE
139 e been proposed for patients with refractory Crohn's disease (CD) and fistulizing CD, respectively.
140 ducted for 20 SNPs in 10 genes of paediatric Crohn's disease (CD) and for 8 SNPs in 5 genes of paedia
141 pression of PGD2 metabolic pathway actors in Crohn's disease (CD) and the ability of the enteric nerv
142 paediatric inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC) and to
143 e-smoking interactions) that affect risk for Crohn's disease (CD) and ulcerative colitis (UC) in a ca
144 Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are co
145 (IBD) consists of two main disease-subtypes, Crohn's disease (CD) and ulcerative colitis (UC); these
146 (IBD) loci, but the genetic architecture of Crohn's disease (CD) and ulcerative colitis remain incom
147 nign neoplasms, ulcerative colitis (UC), and Crohn's disease (CD) between 2005 and 2011 was obtained.
148 l diseases (IBD) ulcerative colitis (UC) and Crohn's disease (CD) cause significant morbidity and are
149 l diseases (IBD) ulcerative colitis (UC) and Crohn's disease (CD) cause significant morbidity and are
158 erapy, we conducted a prospective study with Crohn's disease (CD) or ulcerative colitis (UC) patients
160 in resting state brain activity in remissive Crohn's Disease (CD) patients after electro-acupuncture
162 ced by the dramatic therapeutic responses in Crohn's disease (CD) patients induced by chimeric anti-T
165 ced by EGCs from rats and from patients with Crohn's disease (CD), compared with controls, along with
167 AGI2, MAGI3, PARD3, PTEN, and TJP1) and IBD, Crohn's disease (CD), or ulcerative colitis (UC) were in
168 ith a greater disease activity (p = 0.05 for Crohn's disease (CD), p = 0.03 for Ulcerative Colitis (U
169 nflammatory bowel disease (PIBD), comprising Crohn's disease (CD), ulcerative colitis (UC) and inflam
170 patients with UC compared with patients with Crohn's disease (CD)-associated colitis or without infla
184 13 years) newly diagnosed with IBD (43 with Crohn's disease [CD], 23 with ulcerative colitis [UC]),
185 ts (31 with ulcerative colitis [UC], 57 with Crohn's disease [CD], and 22 healthy individuals [contro
186 (211 with ulcerative colitis [UC], 234 with Crohn's disease [CD]; 236 male), enrolled in Germany fro
187 ed studies on the use of CE in patients with Crohn's disease, celiac disease, gastrointestinal bleedi
188 barrier are associated with diseases such as Crohn's disease, colitis, and colon cancer, but mechanis
189 much better explained by three groups (ileal Crohn's disease, colonic Crohn's disease, and ulcerative
191 uggest that the inflammatory milieu found in Crohn's disease could lead to or result from deregulatio
192 primary endpoint was clinical recurrence of Crohn's disease (Crohn's Disease Activity Index >150 plu
193 ts (aged 18-75 years) with active endoscopic Crohn's disease (Crohn's Disease Endoscopic Index of Sev
194 ulcers in the ileum or colon, or both, and a Crohn's Disease Endoscopic Index of Severity (CDEIS) of
195 ars) with active endoscopic Crohn's disease (Crohn's Disease Endoscopic Index of Severity [CDEIS] >6;
196 This study supports the hypothesis that in Crohn's disease, enteric neurons and glial cells form a
198 s were aged 18-75 years, with a diagnosis of Crohn's disease for at least 3 months, assessed as moder
199 genetic risk scores (GRSs) in distinguishing Crohn's disease from healthy samples, but also serve to
200 points for trials in ulcerative colitis and Crohn's disease have been based on composite indices, su
202 0.99) and a nonsignificant decreased risk of Crohn's disease (hazard ratio = 0.38, 95% confidence int
203 ease progression compared with patients with Crohn's disease (HR, 1.56; P < .001) or no IBD (HR, 1.15
204 r clinical trials of conventional therapy in Crohn's disease, HSCT resulted in clinical and endoscopi
205 k scores to test the hypothesis that colonic Crohn's disease, ileal Crohn's disease, and ulcerative c
206 n subjects with active ulcerative colitis or Crohn's disease, implicating the loss of this barrier-pr
207 we provide a physician-oriented overview of Crohn's disease in adults, ranging from epidemiology and
209 l ileum <40 cm), non-stricturing, ileocaecal Crohn's disease in whom conventional therapy has failed
210 ence of inflammatory bowel diseases, such as Crohn's disease, in developed nations is associated with
211 UK, adults with non-stricturing, ileocaecal Crohn's disease, in whom conventional therapy has failed
214 n 401 colon specimens from patients with UC, Crohn's disease, irritable bowel syndrome, sporadic colo
218 ophagy in intestinal defense and suggest why Crohn's disease is associated with genetic mutations tha
221 hat the genetic contribution to prognosis in Crohn's disease is largely independent of the contributi
222 resident intestinal E. coli associated with Crohn's disease, is characterized by enhanced epithelial
224 r1 displayed mucosal dysfunction and induced Crohn's disease-like ileitis following transfer into Rag
226 analyses of colon tissues from patients with Crohn's disease (n = 61) or ulcerative colitis (UC, n =
227 vity (based on the Harvey-Bradshaw Index for Crohn's disease [n = 356] or the partial Mayo score for
231 e patients were aged 18-80 years, had active Crohn's disease of the terminal ileum, and had not respo
232 with high rates of relapse in patients with Crohn's disease or ulcerative colitis (approximately 75%
233 ies reporting the incidence or prevalence of Crohn's disease or ulcerative colitis from 1990 or later
234 ge psychological conditions in patients with Crohn's disease or ulcerative colitis is necessary for t
235 n with inflammatory bowel disease (IBD; i.e. Crohn's disease or ulcerative colitis) and typically dev
236 in patients with gastrointestinal bleeding, Crohn's disease, or celiac disease, who have had negativ
237 (S727) response in patients with Montreal B2 Crohn's disease, particularly in response to IL-6 leadin
238 genes that are likely to be associated with Crohn's disease pathogenesis, and our rank of candidate
239 ytometry in blood and intestinal tissue from Crohn's disease patients (CD patients) and healthy contr
240 and clinical Crohn's disease phenotype in 69 Crohn's disease patients and 30 age- and sex-matched hea
241 ApoA1 expression, which is downregulated in Crohn's disease patients and causally linked to colitis
242 ccording to the Montreal classification: 4/6 Crohn's disease patients are B1, 2/6 Crohn's disease pat
243 on: 4/6 Crohn's disease patients are B1, 2/6 Crohn's disease patients are B2, 2/2 ulcerative colitis
244 sis finds that gut microbiota collected from Crohn's disease patients are functionally distinct from
245 ebsiella strains isolated from the saliva of Crohn's disease patients can induce Th1 cell responses t
249 up of isolates from the intestinal mucosa of Crohn's disease patients that can invade intestinal epit
250 fully improved anemia in clinical responsive Crohn's disease patients, and DMT1 was found to be marke
254 i-S. cerevisiae antibody levels and clinical Crohn's disease phenotype in 69 Crohn's disease patients
256 al of 57 markers with strong associations to Crohn's disease phenotypes (P < 2 x 10(-4)) were subsequ
259 genetic landscape of ankylosing spondylitis, Crohn's disease, psoriasis, primary sclerosing cholangit
262 bined with biomarkers in patients with early Crohn's disease results in better clinical and endoscopi
263 th inflammatory autoimmune disorders such as Crohn's disease, rheumatoid arthritis, and ankylosing sp
264 ve variably beneficial effects in psoriasis, Crohn's disease, rheumatoid arthritis, psoriatic arthrit
265 ry rare, damaging missense variants in known Crohn's disease risk genes, suggesting that more compreh
266 tive to LACC1 Ile254, cells transfected with Crohn's disease-risk LACC1 Val254 or LACC1 with mutation
267 APCs in intestinal tissue from patients with Crohn's disease show selective failure in PD-L1 expressi
269 nth infection protects mice deficient in the Crohn's disease susceptibility gene Nod2 from intestinal
270 be critical for signaling downstream of the Crohn's disease susceptibility protein nucleotide-bindin
271 than conventional management for controlling Crohn's disease symptoms, the risk of major adverse outc
272 tissues from patients with UC, but not ileal Crohn's disease, than control tissues; levels of GATA3 c
273 patients with moderately to severely active Crohn's disease, those receiving intravenous ustekinumab
274 iduals with select nonpsychiatric disorders (Crohn's disease, type 1 and type 2 diabetes mellitus, mu
276 crobiota are involved in the pathogenesis of Crohn's disease, ulcerative colitis, and pouchitis.
277 atients were 17 years old or younger and had Crohn's disease, ulcerative colitis, or IBD-unclassified
279 Granulomatous inflammation consistent with Crohn's disease was found on histopathological examinati
281 , which is associated with susceptibility to Crohn's disease, was significantly correlated with an im
282 "The Treatment-Naive Microbiome in New-Onset Crohn's Disease," was designed to improve our understand
283 matory bowel diseases ulcerative colitis and Crohn's disease, we sequenced the whole genomes of 4,280
284 ent of certain inflammatory diseases such as Crohn's disease, Wegener's granulomatosis, or sarcoidosi
285 3 or 4 neutropenia, candida infections, and Crohn's disease were 0.7, 0.9, and 0.7 cases per 100 pat
287 atients with refractory perianal fistulizing Crohn's disease were randomly assigned to groups given i
288 2008, and April 23, 2012, 240 patients with Crohn's disease were randomly assigned: 128 to mercaptop
289 groups (198 blood donors, 151 patients with Crohn's disease) were analyzed using the assay, as well
290 t into mechanisms underlying exacerbation of Crohn's disease when IL-17A or IL-17RA is inhibited.
291 patients with suspected, known, or relapsed Crohn's disease when ileocolonoscopy and imaging studies
292 s, IL-12 and IL-23 p40 inhibition attenuates Crohn's disease, whereas IL-17A or IL-17 receptor A (IL-
293 r complex perianal fistulas in patients with Crohn's disease who did not respond to conventional or b
295 2a trial of patients with moderate to severe Crohn's disease who had failed treatment with tumor necr
297 ected from patients with treatment-resistant Crohn's disease who participated in a trial of ustekinum
299 outcomes in patients with moderate to severe Crohn's disease who were managed with a tight control al
300 oing intestinal resection of all macroscopic Crohn's disease, with an endoscopically accessible anast
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