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Role of Intestinal Microbiota in Ulcerative Colitis

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Table 4: Cl<strong>in</strong>ical trials on the prebiotic effect <strong>in</strong> <strong>in</strong>flammatory bowel disease (<strong>Ulcerative</strong> colitis (UC) and Crohn’s disease (CD))<br />

Reference<br />

Key f<strong>in</strong>d<strong>in</strong>g<br />

Duration time<br />

Test Compound*<br />

Tiral Design*<br />

Subjects<br />

(Casellas et al., 2007)<br />

(Hanai et al., 2004)<br />

Compared with placebo, the prebiotic<br />

Reduced disease activity<br />

Reduced fecal calprotect<strong>in</strong><br />

Compared with control, the prebiotic<br />

Reduced disease activity<br />

2 weeks<br />

12 months<br />

Treatment: OFI (12g/day), n=10<br />

Placebo: Maltodextrose (12 g/day),<br />

n=9<br />

Treatment: GBF (20 g/day), n=22<br />

Control: No additive treatment, n=37<br />

DBRPC<br />

UC (relapse)<br />

Open label<br />

UC (remission)<br />

(Kanauchi et al., 2003)<br />

Compared with control, the prebiotic<br />

Reduced disease activity<br />

24 weeks<br />

Treatment: GBF (20‐30 g/day), n=21<br />

Control: No additive treatment, n=21<br />

Open label<br />

UC (relapse)<br />

(Faghfoori et al., 2011)<br />

Compared with control, the prebiotic<br />

Reduced levels <strong>of</strong> serum pro‐<br />

<strong>in</strong>flammatory cytok<strong>in</strong>es; TNF‐α, IL‐6 and<br />

IL‐8<br />

2 months<br />

Treatment: GBF (30 g/day), n=20<br />

Control: No additive treatment, n=21<br />

Open label<br />

UC (remission)<br />

(Hafer et al., 2007)<br />

Theoretical part<br />

Compared with control, the prebiotic<br />

Did not affect disease activity <strong>in</strong> either UC<br />

or CD<br />

Did not affect immunohistochemical<br />

parameters <strong>in</strong> either UC or CD<br />

Increased quality <strong>of</strong> life <strong>in</strong> UC<br />

4 months<br />

Treatment:<br />

UC, lactulose (10 g/day), n=7<br />

CD, lactulose (10 g/day, n=8<br />

Control:<br />

UC, no additive treatment, n=7<br />

CD, no additive treatment, n=9<br />

RPC<br />

UC (active)<br />

CD (active)<br />

25<br />

(L<strong>in</strong>dsay et al., 2006)<br />

Compared with basel<strong>in</strong>e, the prebiotic<br />

Reduced disease activity<br />

Increased fecal bifidobacteria<br />

Increased dendritic cell IL‐10<br />

Increased dendritic cell TLR‐2 and TLR‐4<br />

expression<br />

3 weeks<br />

Treatment: OFI (15 g/day), n=10<br />

Open label<br />

CD (active)<br />

4. Modulation <strong>of</strong> the gut microbiota<br />

(Benjam<strong>in</strong> et al., 2011)<br />

Compared with placebo, the prebiotic<br />

Did not affect disease activity<br />

Did not affect fecal bifidobacteria<br />

Increased dendritic cell IL‐10<br />

Reduced dendritic cell IL‐6<br />

4 weeks<br />

Treatment: OFI (15 g/day), n=54<br />

Placebo: Maltodextrose (15 g/day),<br />

n=49<br />

DBRPC<br />

CD (active)<br />

*Olig<strong>of</strong>ructose‐enriched <strong>in</strong>ul<strong>in</strong> (OFI), Germ<strong>in</strong>ated barley foodstuff (GBF)<br />

#Doubled‐bl<strong>in</strong>d randomized, placebo controlled (DBRPC), randomized, placebo controlled (RPC)

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