ライフサイエンスコーパス: IBS

1 IBS is not a single disease but rather a symptom cluster

2 IBS patients often are anxious and stressed, and stress

3 IBS status did not alter the association between exposur

4 A total of 193 IBS patients, diagnosed according to Rome II (n = 126) o

5 CC patients (706 F) were enrolled (FC 62.5%, IBS-C 31.3%, NRC 6.2%).

6 Lactobacillus spp. positively affect IBS symptoms, although the mechanisms through which prob

7 ore diagnosis, increased with 486 Euro after IBS was diagnosed, whereas for secondary care patients,

8 ne hundred and one IBS patients covering all IBS subtypes were recruited, and 39 non-IBS subjects wer

9 CgA, and serotonin cells were reduced in all IBS patients and in patients with diarrhea-predominant I

10 iffer between control subjects and IBS-D and IBS-M patients.

11 ps of patients with functional dyspepsia and IBS.

12 ate the association between risk factors and IBS.

13 Questions regarding FD and IBS were extracted from the ROME III adult questionnaire

14 adults meeting the criteria for GERD, FD and IBS, respectively, and in individuals who meet the crite

15 iencing overlapping symptoms of GERD, FD and IBS.

16 patients than in healthy subjects (HS), and IBS patients on a 4-week LFM diet had improved IBS sympt

17 tially increase after a diagnosis of IBS and IBS related costs are significantly higher when patients

18 thereby modulating visceral nociception and IBS symptomatology, and might provide an explanation for

19 The association between OAB and IBS was strong in the control group (OR: 2.42; 95 % CI:

20 PCA and IBS were used in a mixed linear model of capsaicin and d

21 intake on the relationship between SIBO and IBS was the primary endpoint.

22 show an association of waterpipe smoking and IBS.

23 did not differ between control subjects and IBS-D and IBS-M patients.

24 stions following Rome III criteria to assess IBS occurrence.

25 The association between IBS and SIBO was completely independent from PPI intake.

26 ctors partly explain the association between IBS and symptoms of anxiety and depression.

27 ween the IBS group and the no-IBS group, but IBS was not a significant effect modifier for the associ

28 Animals harboring a C-IBS microbiota had reduced DSS colitis with a decreased

29 sp., and mainly Akkermansia muciniphila in C-IBS patients compared to healthy individuals.

30 he crosstalk between the gut microbiota of C-IBS patients and host intestinal homeostasis.

31 flammatory effect of the gut microbiota of C-IBS patients is mediated, in part, by A. muciniphila.

32 e gut microbiota of healthy individuals or C-IBS patients was maintained in corresponding HMAR.

33 ated-predominant irritable bowel syndrome (C-IBS) displays chronic dysbiosis.

34 of 326 primary care and 9274 secondary care IBS patients were included in the analysis.

35 However, methods to combine IBS sharing and pedigree information for genetic predict

36 IBS (IBS-D), mixed-diarrhea-and-constipation IBS (IBS-M), and constipation-predominant (IBS-C) relati

37 irritable bowel syndrome with constipation (IBS-C).

38 patients' levels of anxiety and depression, IBS symptoms, quality of life, and somatization using va

39 f patients with infectious enteritis develop IBS later; risk of IBS was 4-fold higher than in individ

40 used by bacterial infection, 13.8% developed IBS.

41 ed by protozoa or parasites, 41.9% developed IBS, and of patients with enteritis caused by bacterial

42 teritis-are at increased risk for developing IBS, as are individuals with psychological distress and

43 with irritable bowel syndrome with diarrhea (IBS-D) have intestinal hyperpermeability, which contribu

44 the predominant symptom (IBS with diarrhea, IBS with constipation, or mixed IBS) plays an important

45 TR4 to be predominantly present in diarrhoea-IBS patients (IBS-D).

46 clinical presentation and management of FC, IBS-C and NRC in Italy.

47 oenterologists recorded clinical data of FC, IBS-C and NRC patients, using Bristol scale, PAC-SYM and

48 be developed as a new treatment approach for IBS.

49 ty acids (SCFA) as diagnostic biomarkers for IBS.

50 t patients who met the Rome III criteria for IBS at a secondary/tertiary care outpatient clinics in S

51 y monozygotic (MZ) twin pairs discordant for IBS (95 pairs) in birth weight group < 2500 g and >/= 25

52 Future research on risk factors for IBS among giardiasis patients and the pathophysiology of

53 ke (n = 713) showed that odds ratio (OR) for IBS in the event of SIBO was 5.63 (3.73-8.51, p < 0.0001

54 is intestinal microbiota signature, we found IBS symptom severity to be associated negatively with mi

55 PUFA metabolites extracted from IBS biopsies or colons of mice with visceral hypersensit

56 Intracolonic administration of FS from IBS patients, but not FS from HS or LFM-treated IBS pati

57 sensory neurons exposed to supernatants from IBS biopsies produced 5,6-EET via a mechanism that invol

58 hypersensitivity caused by supernatants from IBS biopsies.

59 Mean scores for GSRS-IBS bloating were 9.3 +/- 3.5, 11.6 +/- 3.5, and 10.1 +/

60 There was no difference in GSRS-IBS scores between gluten and placebo groups.

61 cipants completed the German version of GSRS-IBS (called Reizdarm-Fragebogen, RDF), as well as the Gi

62 en participants had the highest overall GSRS-IBS score after consuming gluten, 24 had the highest sco

63 The overall GSRS-IBS score for participants consuming fructans was signif

64 Overall GSRS-IBS scores differed significantly during gluten, fructan

65 Rating Scale-Irritable Bowel Syndrome (GSRS-IBS) and Hospital Anxiety and Depression scale were fulf

66 ing Scale for Irritable Bowel Syndrome (GSRS-IBS) into German and to evaluate its psychometric qualit

67 Rating Scale Irritable Bowel Syndrome (GSRS-IBS) version.

68 The German version of the GSRS-IBS RDF proves to be an effective, reliable, and valid q

69 ans to induce symptoms, measured by the GSRS-IBS.

70 on tended to have lower scores on total GSRS-IBS score (6 vs 10.5; p = 0.062) and lower or equal scor

71 ods We randomly assigned 2427 adults who had IBS with diarrhea to eluxadoline (at a dose of 75 mg or

72 females were 1.67 times more likely to have IBS than males (P< 0.05).

73 lcohol drinkers were twice as likely to have IBS than never-drinkers (P< 0.01).

74 aterpipe were 1.63 times more likely to have IBS than those who never smoked waterpipe (P< 0.05).

75 30 years old were at a higher risk of having IBS (P< 0.01).

76 IBS-D), mixed-diarrhea-and-constipation IBS (IBS-M), and constipation-predominant (IBS-C) relative to

77 d in patients with diarrhea-predominant IBS (IBS-D), mixed-diarrhea-and-constipation IBS (IBS-M), and

78 on biopsy samples from 40 patients with IBS (IBS biopsies) and 11 healthy individuals undergoing colo

79 S patients on a 4-week LFM diet had improved IBS symptoms and reduced fecal LPS levels.

80 5-HT4 receptors are promising candidates in IBS pathophysiology since they regulate gut motor functi

81 n explanation for the success of LFM diet in IBS patients.

82 The difference in IBS prevalence by socio-demographic characteristics, smo

83 s a precipitating and perpetuating factor in IBS has gained recent interest, but food intolerance fol

84 n was requested in 31.6%, more frequently in IBS-C than in NRC.

85 Fecal LPS was higher in IBS patients than in healthy subjects (HS), and IBS pati

86 PAC-SYM and PAC-QoL scores were higher in IBS-C than in FC and NRC.

87 f TRPV1 or TRPA1 agonists, were increased in IBS biopsies compared with controls; increases correlate

88 While the PYY cell density was increased in IBS-C relative to controls, it did not differ between co

89 at EGC-enteric nerve unit may be involved in IBS-like visceral hypersensitivity, and this process is

90 diated sensitization of TRPV1 is involved in IBS.

91 teroglial cells (EGCs) and enteric nerves in IBS-like visceral hypersensitivity.

92 hotherapy were more frequently prescribed in IBS-C, prucalopride and pelvic floor rehabilitation in F

93 eks 1 through 26, the corresponding rates in IBS-3001 were 23.4% and 29.3% versus 19.0% (P=0.11 and P

94 espectively), and the corresponding rates in IBS-3002 were 30.4% and 32.7% versus 20.2% (P=0.001 and

95 %) in the low-FODMAP group had reductions in IBS severity scores >/=50 compared with baseline vs 17 p

96 l polypeptide (VIP) in barrier regulation in IBS and healthy individuals.

97 re for the assessment of symptom severity in IBS, which can be used in clinical practice as well as i

98 eath tests were more frequently suggested in IBS-C and anorectal manometry in FC.

99 list of 31 illnesses and symptoms, including IBS and symptoms of anxiety and depression.

100 th a cut-off value > 0.015 mmol/l indicating IBS, the sensitivity, specificity, positive and negative

101 creased risk of OAB, whereas post-infectious IBS was not.

102 Total mean IBS-Severity Scoring System score was significantly lowe

103 ) to exclude organic diseases that can mimic IBS.

104 th diarrhea, IBS with constipation, or mixed IBS) plays an important role in selection of diagnostic

105 ng disease and in remission do not have more IBS symptoms than controls.

106 ce differed between the IBS group and the no-IBS group, but IBS was not a significant effect modifier

107 all IBS subtypes were recruited, and 39 non-IBS subjects were included as a control group.

108 al tissues from patients with IBS-D (but not IBS with constipation or controls) had increased levels

109 Factors important to the development of IBS include alterations in the gut microbiome, intestina

110 weight increased the risk for development of IBS, with environmental influences in utero as the most

111 HTR4 might be involved in the development of IBS-D.

112 the fungal microbiome) in the development of IBS.

113 for 3 months to 10 years for development of IBS.

114 substantially increase after a diagnosis of IBS and IBS related costs are significantly higher when

115 The diagnosis of IBS relies on symptom-based criteria, exclusion of conce

116 17.5% of the participants had a diagnosis of IBS, 19.9% were receiving treatment for chronic inflamma

117 ture (stability selection) of both groups of IBS patients differed from healthy volunteers, and the m

118 One-year incidence of IBS was higher in persons with giardiasis (IR = 37.7/100

119 tion of miR-16 and miR-103 in the jejunum of IBS-D patients correlating with symptoms.

120 ificantly increased in the colonic mucosa of IBS patients.

121 netic factors influence the co-occurrence of IBS and symptoms of anxiety and depression.

122 d risk of, risk factors for, and outcomes of IBS after infectious enteritis.

123 equal to 22 kg/m(2) (OR: 0.60), presence of IBS (OR: 6.29), type 2 diabetes mellitus (OR: 1.59) and

124 identify cohort studies of the prevalence of IBS 3 months or more after infectious enteritis.

125 to calculate the summary point prevalence of IBS after infectious enteritis, as well as relative risk

126 The pooled prevalence of IBS at 12 months after infectious enteritis was 10.1% (9

127 New data on the high prevalence of IBS in an adult population in Lebanon has been reported.

128 The prevalence of IBS in patients with UC with longstanding disease is not

129 The prevalence of IBS in the study population according to Rome III criter

130 We investigated the prevalence of IBS-like symptoms in patients with UC in remission and l

131 antly associated with a higher prevalence of IBS.

132 those who had not (95% CI, 3.1-5.7); risk of IBS was 2.3-fold higher in individuals who had infectiou

133 ectious enteritis develop IBS later; risk of IBS was 4-fold higher than in individuals who did not ha

134 Risk of IBS was 4.2-fold higher in patients who had infectious e

135 Risk of IBS was significantly increased in women (odds ratio [OR

136 The severity of IBS symptoms was reduced in both groups during the inter

137 file that is associated with the severity of IBS symptoms.

138 ed with intestinal dysbiosis and symptoms of IBS develop following gastroenteritis.

139 w therapeutic agent that reduced symptoms of IBS with diarrhea in men and women, with sustained effic

140 study of patients with relapsing symptoms of IBS-D, repeat rifaximin treatment was efficacious and we

141 ht therefore be manipulated for treatment of IBS-related visceral hypersensitivity.

142 One hundred and one IBS patients covering all IBS subtypes were recruited, a

143 BL had no significant effect on anxiety or IBS symptoms.

144 meeting the criteria for either GERD, FD or IBS have significantly higher odds of reporting poor sel

145 viduals experiencing symptoms of GERD, FD or IBS report poor self-rated health as well as impaired fu

146 The performance of the SPC analysis (OS: IBS, 0.149; C index, 0.654; PFS: IBS, 0.138; C index, 0.

147 proved when combined with clinical data (OS: IBS, 0.142; C index, 0.696; PFS: IBS, 0.132; C index, 0.

148 index, 0.554) and clinical risk models (OS: IBS, 0.161, C index, 0.640; PFS: IBS, 0.139; C index, 0.

149 er compared with that of the radiologic (OS: IBS, 0.175; C index, 0.603; PFS: IBS, 0.149; C index, 0.

150 Overlap IBS was present in 33 % of the FD patients.

151 ominantly present in diarrhoea-IBS patients (IBS-D).

152 to iHT performed by therapists in pediatric IBS or FAP(S).

153 ologic (OS: IBS, 0.175; C index, 0.603; PFS: IBS, 0.149; C index, 0.554) and clinical risk models (OS

154 models (OS: IBS, 0.161, C index, 0.640; PFS: IBS, 0.139; C index, 0.599).

155 alysis (OS: IBS, 0.149; C index, 0.654; PFS: IBS, 0.138; C index, 0.611) was higher compared with tha

156 l data (OS: IBS, 0.142; C index, 0.696; PFS: IBS, 0.132; C index, 0.637).

157 tures of ileal and colonic mucosa from 10 PI-IBS, diarrhea predominant subtype (D) patients, and 10 h

158 nique cohort of individuals who developed PI-IBS following exposure to contaminated drinking water 7

159 her while IL-10 mRNA levels were lower in PI-IBS D than in HC in both ileum and colon.

160 ating the inflammatory/immune-response in PI-IBS in an ex-vivo organ culture model.

161 onse in an ex-vivo organ culture model of PI-IBS D.

162 at neuronal signaling within the bowel of PI-IBS patients is sensitized 2 years after the initial inf

163 Post-infectious irritable bowel syndrome (PI-IBS) is a common gastrointestinal disorder characterized

164 post-infectious irritable bowel syndrome (PI-IBS) is convincing.

165 rated from tissue biopsy of patients with PI-IBS.

166 l signaling in the bowel of patients with PI-IBS.

167 placebo group reached the primary end point (IBS-3001 trial, 23.9% with the 75-mg dose and 25.1% with

168 ts and the pathophysiology of postinfectious IBS is needed.

169 ts and in patients with diarrhea-predominant IBS (IBS-D), mixed-diarrhea-and-constipation IBS (IBS-M)

170 n IBS (IBS-M), and constipation-predominant (IBS-C) relative to the control subjects.

171 A diet low in FODMAPs reduces IBS symptoms as well as traditional IBS dietary advice.

172 h placebo; P=0.01 and P=0.004, respectively; IBS-3002 trial, 28.9% and 29.6%, respectively, vs. 16.2%

173 ed with C index and integrated Brier scores (IBS, lower scores indicating higher accuracy) and compar

174 he intestinal microbial signature for severe IBS in the validation set.

175 lexity into a microbial signature for severe IBS, consisting of 90 bacterial operational taxonomic un

176 2) and lower or equal scores on all specific IBS symptoms in comparison to controls.

177 Sporadic IBS was associated with increased risk of OAB, whereas p

178 idean tree built based on identity by state (IBS) indices revealed that the clustering pattern of div

179 rediction based on either identity by state (IBS) sharing or pedigree information has been investigat

180 diasis were more likely to have a subsequent IBS diagnosis, despite accounting for confounders.

181 Determining the predominant symptom (IBS with diarrhea, IBS with constipation, or mixed IBS)

182 atients with CD or irritable bowel syndrome (IBS) (controls).

183 a of patients with irritable bowel syndrome (IBS) affect the function of enteric and extrinsic sensor

184 ased prevalence of irritable bowel syndrome (IBS) after acute gastroenteritis.

185 vious diagnosis of irritable bowel syndrome (IBS) and 23 (28.8%) had one of functional dyspepsia.

186 ctal cancer (CRC), irritable bowel syndrome (IBS) and controls to be run through the machine.

187 e role of TRPV1 in irritable bowel syndrome (IBS) and evaluated if an antagonist of histamine recepto

188 ctive in pediatric irritable bowel syndrome (IBS) and functional abdominal pain or functional abdomin

189 the prevalence of irritable bowel syndrome (IBS) and its correlates in the Middle East.

190 dyspepsia (FD) and irritable bowel syndrome (IBS) are common functional gastrointestinal conditions w

191 asis diagnosis and irritable bowel syndrome (IBS) diagnosis.

192 Patients with irritable bowel syndrome (IBS) have increased postprandial symptom responses and m

193 nts diagnosed with Irritable Bowel Syndrome (IBS) in primary and secondary care, compare these costs

194 Irritable Bowel Syndrome (IBS) is a functional somatic syndrome characterized by p

195 Irritable bowel syndrome (IBS) is a gut-brain disorder involving alterations in in

196 BACKGROUND & AIMS: Irritable bowel syndrome (IBS) is associated with intestinal dysbiosis and symptom

197 Irritable bowel syndrome (IBS) is more common in patients with ulcerative colitis

198 Irritable bowel syndrome (IBS) is one of the most common functional gastrointestin

199 study investigated Irritable Bowel Syndrome (IBS) prevalence in a sample of Lebanese adult individual

200 The diagnosis of irritable bowel syndrome (IBS) relies on symptom-based criteria.

201 drates can provoke irritable bowel syndrome (IBS) symptoms by escaping absorption in the small bowel

202 induce symptoms of irritable bowel syndrome (IBS) via unclear mechanisms.

203 induce symptoms of irritable bowel syndrome (IBS) via unclear mechanisms.

204 patients who have irritable bowel syndrome (IBS) with diarrhea.

205 m of patients with irritable bowel syndrome (IBS), and whether any abnormalities in ileal enteroendoc

206 reduce symptoms of irritable bowel syndrome (IBS), but little is known about their effects on psychia

207 ctional disorders; irritable bowel syndrome (IBS), functional dyspepsia (FD) and chronic fatigue (CF)

208 erlap frequency of irritable bowel syndrome (IBS), gastroesophageal reflux disease (GERD), and overac

209 is one feature of irritable bowel syndrome (IBS).

210 a risk factor for irritable bowel syndrome (IBS).

211 some patients with irritable bowel syndrome (IBS).

212 n in patients with irritable bowel syndrome (IBS).

213 inical features of irritable bowel syndrome (IBS).

214 t of patients with irritable bowel syndrome (IBS).

215 t of patients with irritable bowel syndrome (IBS).

216 te the severity of irritable bowel syndrome (IBS).

217 inical features of irritable bowel syndrome (IBS).

218 stinct categories: irritable bowel syndrome (IBS); functional constipation (FC); functional diarrhea

219 erbate symptoms of irritable bowel syndrome (IBS); however, their mechanism of action is unknown.

220 arrhea-predominant irritable bowel syndrome (IBS-D).

221 GIDs, including globus, rumination syndrome, IBS, bloating, constipation, functional abdominal pain,

222 he analysis of the full sample revealed that IBS was significantly associated with symptoms of anxiet

223 diagnostic properties were shown for all the IBS subgroups.

224 ceived food intolerance differed between the IBS group and the no-IBS group, but IBS was not a signif

225 In the IBS and control group, the mean age was 46.2 (SD 12.9) a

226 Symptom severity was assessed using the IBS Symptom Severity Scale, and patients completed a 4-d

227 reduces IBS symptoms as well as traditional IBS dietary advice.

228 line vs 17 patients (46%) in the traditional IBS diet group (P = .72).

229 low in FODMAPs, 34 completed the traditional IBS diet).

230 nteers and 9 patients with minor, transient, IBS-like symptoms but no sign of constipation.

231 patients, but not FS from HS or LFM-treated IBS patients, induced VH in rats, which was ameliorated

232 100 mg) or placebo twice daily for 26 weeks (IBS-3002 trial) or 52 weeks (IBS-3001 trial).

233 y for 26 weeks (IBS-3002 trial) or 52 weeks (IBS-3001 trial).

234 oratory set comprised 149 subjects (110 with IBS and 39 healthy subjects); 232 fecal samples and 59 m

235 alidation set comprised 46 subjects (29 with IBS and 17 healthy subjects); 46 fecal samples, but no m

236 , placebo-controlled study of 44 adults with IBS and diarrhea or a mixed-stool pattern (based on Rome

237 The trial included adults with IBS-D, mean abdominal pain and bloating scores of 3 or m

238 rcise were not significantly associated with IBS occurrence.

239 Persons diagnosed with IBS before the date of study entry were excluded.

240 ontrols, we associated fungal dysbiosis with IBS.

241 ad been previously diagnosed most often with IBS (p = 0.13) or dyspepsia (p = .036).

242 The frequency of overlap with IBS, GERD, and OBS were determined for the whole group a

243 d a 2x2 factorial trial of 104 patients with IBS (18-65 years old), based on the Rome III criteria, a

244 , cross-over study of 29 adult patients with IBS (based on Rome III criteria, with symptoms of abdomi

245 d colon biopsy samples from 40 patients with IBS (IBS biopsies) and 11 healthy individuals undergoing

246 iet frequently recommended for patients with IBS (ie, a regular meal pattern; avoidance of large meal

247 formed a double-blind trial of patients with IBS (mean age, 31 y; range, 18-65 y; 34 female).

248 ollected during endoscopy from patients with IBS (n = 183) and without IBS (controls) (n = 36).

249 psy specimens collected from 9 patients with IBS (ROME 3 criteria) and 15 healthy subjects.

250 hy volunteers with those of 39 patients with IBS (with visceral hypersensitivity or normal levels of

251 psy samples collected from 101 patients with IBS and 23 asymptomatic healthy individuals (controls).

252 Biopsies from an additional 5 patients with IBS and 4 controls were mounted in chambers and Salmonel

253 lyzed intestinal mycobiomes of patients with IBS and a rat model of visceral hypersensitivity.

254 present in colon tissues from patients with IBS and act as endogenous agonists to induce hypersensit

255 e was reduced in biopsies from patients with IBS and controls after addition of antibodies against VP

256 In an analysis of patients with IBS and controls, we associated fungal dysbiosis with IB

257 ucosa-associated microbiota of patients with IBS and evaluated whether these were associated with sym

258 Patients with IBS and healthy individuals without IBS (controls) have

259 al and mucosal microbiota from patients with IBS and healthy individuals, we identified an intestinal

260 ssues of controls, mucosa from patients with IBS had a significant increase in the area of lamina pro

261 Biopsies from patients with IBS had higher levels of tryptase, larger numbers of MCs

262 Plasma samples from patients with IBS had higher levels of VIP than plasma samples from co

263 Colon tissues from patients with IBS have increased levels of specific PUFA metabolites.

264 olonic epithelium tissues from patients with IBS have increased translocation of commensal and pathog

265 key to successful treatment of patients with IBS is a good physician-patient relationship and use of

266 tprandial symptom responses in patients with IBS is unclear.

267 More patients with IBS reached the predefined symptom threshold after intak

268 also increased in tissues from patients with IBS vs controls (18% increase; P = .16) along with level

269 undance or composition between patients with IBS vs healthy patients.

270 ses of submucosal neurons from patients with IBS were potentiated compared with those of healthy volu

271 pioid receptor antagonist), in patients with IBS with diarrhea.

272 a placebo-controlled study of patients with IBS, a low FODMAP diet associates with adequate symptom

273 In biopsies from patients with IBS, addition of Salmonella significantly reduced levels

274 m rectal biopsy specimens from patients with IBS, but not from the healthy volunteers, sensitized TRP

275 d after drink consumption than patients with IBS, despite similar MRI parameters and breath hydrogen

276 In colon biopsies from patients with IBS, larger numbers of E coli HS and S typhimurium passe

277 ased on a prospective study of patients with IBS, psychosocial morbidities are associated with increa

278 Patients with IBS-C reported more severe symptoms and worse quality of

279 Intestinal tissues from patients with IBS-D (but not IBS with constipation or controls) had in

280 intestinal tissue samples from patients with IBS-D, MIR29 targets and reduces expression of CLDN1 and

281 ore intestinal permeability in patients with IBS-D.

282 rbohydrate-related symptoms in patients with IBS.

283 d increases quality of life in patients with IBS.

284 ship in a prospective study of patients with IBS.

285 ymptoms, and abdominal pain in patients with IBS.

286 ncreased in mucosal tissues of patients with IBS.

287 2/DQ8 haplotypes compared with patients with IBS.

288 ment approach is advocated for patients with IBS.

289 ms and the fecal microbiota in patients with IBS.

290 ) on anxiety and depression in patients with IBS.

291 roup; secondly, to explore the relation with IBS status; and thirdly, to investigate associations wit

292 d with a smaller proportion of subjects with IBS (4%) (P < .001).

293 Twenty-five subjects with IBS and 25 controls were included in this explanatory ca

294 of subjects with CD, and 2% of subjects with IBS developed ADs (P < .001).

295 ation of healthy subjects from subjects with IBS.

296 Colon biopsies from 32 women with IBS and 15 age-matched healthy women (controls) were mou

297 f those, 260 children (aged 8-18 years) with IBS or FAP(S) were included in this study.

298 from patients with IBS (n = 183) and without IBS (controls) (n = 36).

299 istinguish between subjects with and without IBS, the total amount and the amount of each of the SCFA

300 nts with IBS and healthy individuals without IBS (controls) have similar physiological responses afte

301 health care expenditure for patients without IBS and describe these costs in further detail.