Evidence map›Paper›PMID 29436337›Full record

Trial reportThe American journal of tropical medicine and hygiene2018

Rifaximin Reduces Markers of Inflammation and Bacterial 16S rRNA in Zambian Adults with Hepatosplenic Schistosomiasis: A Randomized Control Trial.

Edford Sinkala, Kanekwa Zyambo, Ellen Besa, Patrick Kaonga, Bright Nsokolo, Violet Kayamba, Michael Vinikoor, Rabison Zulu, Martin Bwalya, Graham R Foster and 1 more

Open access · bronzeAbstract readClinical Trial, Phase IIRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The American journal of tropical medicine and hygiene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 43% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 3 countries.

Edford SinkalaDepartment of Internal Medicine, Tropical Gastroenterology & Nutritional Group, University of Zambia, Lusaka, Zambia.
Kanekwa ZyamboDepartment of Internal Medicine, Tropical Gastroenterology & Nutritional Group, University of Zambia, Lusaka, Zambia.
Ellen BesaDepartment of Internal Medicine, Tropical Gastroenterology & Nutritional Group, University of Zambia, Lusaka, Zambia.
Patrick KaongaDepartment of Internal Medicine, Tropical Gastroenterology & Nutritional Group, University of Zambia, Lusaka, Zambia.
Bright NsokoloDepartment of Internal Medicine, Tropical Gastroenterology & Nutritional Group, University of Zambia, Lusaka, Zambia.
Violet KayambaDepartment of Internal Medicine, Tropical Gastroenterology & Nutritional Group, University of Zambia, Lusaka, Zambia.
Michael VinikoorCentre for Infectious Disease Research in Zambia, Lusaka, Zambia.
Rabison ZuluPaediatric Centre of Excellence Laboratory, University Teaching Hospital, Lusaka, Zambia.
Martin BwalyaPaediatric Centre of Excellence Laboratory, University Teaching Hospital, Lusaka, Zambia.
Graham R FosterBlizard Institute, Barts & The London School of Medicine, Queen Mary University of London, London, United Kingdom.
Paul KellyPaediatric Centre of Excellence Laboratory, University Teaching Hospital, Lusaka, Zambia.
Tropical Gastroenterology & Nutrition group · ZMUniversity of Zambia · ZMUniversity Teaching Hospital · ZMCentre for Infectious Disease Research in Zambia · ZMQueen Mary University of London · GB

Funding

Medical Research Council MR/K007394/1Wellcome TrustWellcome Trust WT087537MA
6 · The paper itself

Abstract

Cirrhosis is the dominant cause of portal hypertension globally but may be overshadowed by hepatosplenic schistosomiasis (HSS) in the tropics. In Zambia, schistosomiasis seroprevalence can reach 88% in endemic areas. Bacterial translocation (BT) drives portal hypertension in cirrhosis contributing to mortality but remains unexplored in HSS. Rifaximin, a non-absorbable antibiotic may reduce BT. We aimed to explore the influence of rifaximin on BT, inflammation, and fibrosis in HSS. In this phase II open-label trial (ISRCTN67590499), 186 patients with HSS in Zambia were evaluated and 85 were randomized to standard care with or without rifaximin for 42 days. Changes in markers of inflammation, BT, and fibrosis were the primary outcomes. BT was measured using plasma 16S rRNA, lipopolysaccharide-binding protein, and lipopolysaccharide, whereas hyaluronan was used to measure fibrosis. Tumor necrosis factor receptor 1 (TNFR1) and soluble cluster of differentiation 14 (sCD14) assessed inflammation. 16S rRNA reduced from baseline (median 146 copies/µL, interquartile range [IQR] 9, 537) to day 42 in the rifaximin group (median 63 copies/µL, IQR 12, 196),

Indexed as

AdultAnti-Bacterial AgentsBacterial TranslocationBiomarkersFemaleHumansInflammationLipopolysaccharide ReceptorsLiver Diseases, ParasiticMaleMiddle AgedReceptors, Tumor Necrosis Factor, Type IRifaximinRNA, BacterialRNA, Ribosomal, 16SSchistosomiasisAnti-Bacterial AgentsBiomarkersLipopolysaccharide ReceptorsReceptors, Tumor Necrosis Factor, Type IRifaximinRNA, BacterialRNA, Ribosomal, 16S

Identifiers

PMID29436337
PMCPMC5928821
OpenAlexW2791551873

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.