ArticleOncotarget2018
Specific alterations in gut microbiota are associated with prognosis of Budd-Chiari syndrome.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Associations between changes in the gut microbiota and liver cirrhosis: a systematic review and meta-analysis.BMC gastroenterology · 2025Pooled it
- Budd-Chiari syndrome in a 33-year-old woman with hypercoagulable state: A case report.Radiology case reports · 2025Article
- Gut dysbiosis contributes to the development of Budd-Chiari syndrome through immune imbalance.mSystems · 2024Article
- Association between monosodium glutamate consumption with changes in gut microbiota and related metabolic dysbiosis-A systematic review.Food science & nutrition · 2024Review
- Alterations in Faecal Metagenomics and Serum Metabolomics Indicate Management Strategies for Patients With Budd-Chiari Syndrome.Frontiers in cellular and infection microbiology · 2021Article
- Effects of protease and phytase supplements on small intestinal microbiota and amino acid digestibility in broiler chickens.Poultry science · 2019Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gut microbiota is associated with liver diseases. However, gut microbial characteristics of Budd-Chiari syndrome (B-CS) have not been reported. Here, by MiSeq sequencing, gut microbial alterations were characterized among 37 health controls, 20 liver cirrhosis (LC) patients, 31 initial B-CS patients (B-CS group), 33 stability patients after BCS treatment (stability group) and 23 recurrent patients after BCS treatment (recurrence group). Gut microbial diversity was increased in B-CS versus LC. Bacterial community of B-CS clustered with controls but separated from LC. Operational taxonomic units (OTUs) 421, 502 (Clostridium IV) and 141 (Megasphaera) were unique to B-CS. Genera Escherichia/Shigella and Clostridium XI were decreased in B-CS versus controls. Moreover, nine genera, mainly including Bacteroides and Megamonas, were enriched in B-CS versus LC. Notably, Megamonas could distinguish B-CS from LC with areas under the curve (AUCs) of 0.7904. Microbial function prediction revealed that L-amino acid transport system activity was decreased in B-CS versus both LC and controls. Furthermore, OTUs 27 (Clostridium XI), 137 (Clostridium XIVb) and 40 (Bacteroides) were associated with B-CS stability. Importantly, genus Clostridium XI was enriched in stability group versus both recurrence group and B-CS group. Also, PRPP glutamine biosynthesis was reduced in stability group versus recurrence group, but was enriched in stability group versus B-CS group. In conclusion, specific microbial alterations associated with diagnosis and prognosis were detected in B-CS patients. Correction of gut microbial alterations may be a potential strategy for B-CS prevention and treatment.
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