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.
Highlights
Budd–Chiari syndrome (B-CS) is characterized by hepatic venous outflow tract obstruction at various levels from the small hepatic veins to the inferior vena cava (IVC), resulting from thrombosis or its fibrous sequelae [1, 2]
Aspartate aminotransferase and glutamyl transpeptidase levels were significantly increased in liver cirrhosis (LC) group and B-CS group versus healthy controls; no obvious differences were detected between LC group and B-CS group
We identified gut microbial diversity and species richness in B-CS patients versus LC patients
Summary
Budd–Chiari syndrome (B-CS) is characterized by hepatic venous outflow tract obstruction at various levels from the small hepatic veins to the inferior vena cava (IVC), resulting from thrombosis or its fibrous sequelae [1, 2]. Increasing www.impactjournals.com/oncotarget evidence indicates that there are distinct variations in the B-CS prevalence, aetiological distribution, clinical characteristics, and occlusion sites between Asian and western countries, necessitating the use of different treatment modalities [3, 4]. In Western countries, B-CS is mainly caused by blood system disorders, and patients present with hepatic vein thrombosis [2, 5, 6]. IVC obstruction is more common in Asian B-CS patients [7]. Few risk factors for this disease have been identified, and the pathogenesis remains unclear
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