Imperial College London
Alternate

ProfessorMarkThursz

Faculty of Medicine, Department of Metabolism, Digestion and Reproduction

Professor of Hepatology. Head of Department
 
 
 
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Contact

 

+44 (0)20 3312 1903m.thursz

 
 
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Assistant

 

Ms Dawn Campbell +44 (0)20 3312 6454

 
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Location

 

Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Cobbold:2018:10.1111/hepr.12904,
author = {Cobbold, JFL and Atkinson, S and Marchesi, JR and Smith, A and Wai, SN and Stove, J and Shojaee-Moradie, F and Jackson, N and Umpleby, AM and Fitzpatrick, J and Thomas, EL and Bell, JD and Holmes, E and Taylor-Robinson, SD and Goldin, RD and Yee, MS and Anstee, QM and Thursz, MR},
doi = {10.1111/hepr.12904},
journal = {HEPATOLOGY RESEARCH},
pages = {69--77},
title = {Rifaximin in non-alcoholic steatohepatitis: An open-label pilot study},
url = {http://dx.doi.org/10.1111/hepr.12904},
volume = {48},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - AimGut microbial dysbiosis is implicated in the pathogenesis of nonalcoholic steatohepatitis (NASH). We investigated downstream effects of gut microbiota modulation on markers of hepatic inflammation, steatosis, and hepatic and peripheral insulin sensitivity in patients with NASH using rifaximin therapy.MethodsPatients with biopsyproven NASH and elevated aminotransferase values were included in this openlabel pilot study, all receiving 6 weeks rifaximin 400 mg twice daily, followed by a 6week observation period. The primary endpoint was change in alanine aminotransferase (ALT) after 6 weeks of rifaximin. Secondary endpoints were change in hepatic lipid content and insulin sensitivity measured with a hyperinsulinemic–euglycemic clamp.ResultsFifteen patients (13 men and 2 women) with a median (range) age of 46 (32–63) years were included. Seven had diabetes on oral hypoglycemic medications and 8 had no diabetes. After 6 weeks of therapy, no differences were seen in ALT (55 [33–191] vs. 63 [41–218] IU/L, P = 0.41), peripheral glucose uptake (28.9 [19.4–48.3] to 25.5 [17.7–47.9] μmol/kg/min, P = 0.30), hepatic insulin sensitivity (35.2 [15.3–51.7]% vs. 30.0 [10.8–50.5]%, P = 0.47), or hepatic lipid content (21.6 [2.2–46.2]% vs. 24.8 [1.7–59.3]%, P = 0.59) before and after rifaximin treatment. After 12 weeks from baseline, serum ALT increased to 83 (30–217) IU/L, P = 0.02. There was a significant increase in the homeostasis model assessment–estimated insulin resistance index (P = 0.05). The urinary metabolic profile indicated a significant reduction in urinary hippurate with treatment, which reverted to baseline after cessation of rifaximin, although there was no consistent difference in relative abundance of fecal microbiota with treatment.ConclusionThese data do not indicate a beneficial effect of rifaximin i
AU  - Cobbold,JFL
AU  - Atkinson,S
AU  - Marchesi,JR
AU  - Smith,A
AU  - Wai,SN
AU  - Stove,J
AU  - Shojaee-Moradie,F
AU  - Jackson,N
AU  - Umpleby,AM
AU  - Fitzpatrick,J
AU  - Thomas,EL
AU  - Bell,JD
AU  - Holmes,E
AU  - Taylor-Robinson,SD
AU  - Goldin,RD
AU  - Yee,MS
AU  - Anstee,QM
AU  - Thursz,MR
DO  - 10.1111/hepr.12904
EP  - 77
PY  - 2018///
SN  - 1386-6346
SP  - 69
TI  - Rifaximin in non-alcoholic steatohepatitis: An open-label pilot study
T2  - HEPATOLOGY RESEARCH
UR  - http://dx.doi.org/10.1111/hepr.12904
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000419347800009&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/61812
VL  - 48
ER  -
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