To our knowledge, this study is the first to evaluate the long-term (i.e., 6 months) effects of rifaximin on the gut microbiota of SUDD patients. Here we show that rifaximin significantly reduced the severity of abdominal pain, which is consistent with previous studies. [9,10,11,12]. Treatment with rifaximin over 6 months was not associated with significant changes in the abundance of most major taxa in the fecal microbiome, but the abundance of the fecal microbiome increased. AkkermansiaVerco Colombia, Ruminococcaceae was observed and was inversely associated with abdominal pain severity.
Change in abundance Veillonellaceae, diary starand Anerostipes It was also observed after 6 months of rifaximin administration, but it did not correlate with abdominal pain severity. Therefore, these bacteria may not be involved in the development of abdominal pain in her SUDD.
In our research, Akkermansia These bacteria were identified in the fecal microbiome of 2 patients (16.7%) at the time of treatment and in 9 patients (75.0%) after 6 months of rifaximin treatment, but these bacteria were not identified in another study. was detected in 90.5% of healthy individuals (p < 0.001) (unpublished data from [23]).However, a significantly higher amount of A. muciniphila reported in fecal samples of SUDD patients compared with healthy controls. [7]. However, both our study and the study by Tursi et al. [7] Patients with a recent history of acute diverticulitis were excluded. In patients with diverticulosis, Akkermansia It may increase as a compensatory response. Therefore, patients with a wealth of symptoms may Akkermansia Patients who develop asymptomatic diverticulosis or SUDD but do not have enough diverticulosis Akkermansia This compensatory response leads to the development of acute diverticulitis. Also, in the study of Tursi et al. [7]in SUDD patients; A. muciniphila However, this difference did not reach a significant limit in gut microbiota compared with asymptomatic diverticulosis patients, which may be due to the smaller patient population (15 and 13 patients, respectively). To resolve this issue, new large-scale studies will need to be conducted.
Akkermansia It is the main representative of the phylum Verrucomicrobia in the intestinal microbiota. This bacterium has several beneficial properties, including anti-inflammatory properties. [28,29,30,31,32]. in particular, Akkermansia Increases the thickness of the mucin layer, improves the intestinal epithelial barrier and prevents the transfer of harmful bacteria and their components to the intestinal wall. [31]. This bacterial translocation causes low-level inflammation, which is thought to play an important role in the development of abdominal pain in SUDD. [1]. Furthermore, the intensity of infiltration of the diverticulum mucosa by inflammatory cells is inversely correlated with the abundance of inflammatory cells. Akkermansia Within the mucosal microbiome [5].
positive effect Akkermansia This is thought to be because these bacteria break down mucins into molecules that stimulate their formation by feedback, which are then used by family members of the bacteria. Ruminococcaceae form butyrate [29, 31]known to strengthen the intestinal barrier [33, 34]. In our research, Akkermansia and Ruminococcaceae significantly increased after treatment with rifaximin. However, while the amount increases, Akkermansia significant at both 3rd and 6th month; Ruminococcaceae It was only significant after 6 months of treatment with rifaximin. This result supports the hypothesis of a synergistic effect of these two groups of bacteria on reduced intestinal permeability, bacterial translocation, low-level inflammation, and abdominal pain associated with SUDD patients.
Rifaximin has been reported to increase bacterial abundance in the environment; Ruminococcaceae In the case of a family, its use Akkermansia [13].In previous research [22]rifaximin significantly altered the relative abundance of specific bacteria in SUDD patients, with a significant increase in the abundance of Bacteroidae. Citrobacterand Coprococcusand Mogibacteriaceae, Christensenellaceae, Dehalobacteriaceae, Pasteurellaceae, anaero trunks, Blautia, Egger Terra Renta, Dehalobacterium, SMB53and Haemophilus parainfluenza (p-adj < 0.05) was reported. However, these results may not be representative of the long-term effects of rifaximin on the gut microbiota in patients with SUDD, so they should be taken with caution as patients have only been treated with rifaximin for 7 days. Must see.
Two small studies investigated differences in the gut microbiota between patients with asymptomatic diverticulosis and SUDD [5, 7]. In both studies, Akkermansia In the intestinal microbiota, A. muciniphila The number of species was numerically lower in SUDD patients than in asymptomatic diverticulosis patients (−3.56 ± 1.27 vs − 3.41 ± 1.13, respectively). [7]. However, larger studies are needed to confirm the hypothesis of decreased abundance. Akkermansia In patients with diverticulosis, it is associated with the transition from asymptomatic to symptomatic status. Additionally, cohort studies of asymptomatic diverticulosis patients and regular analysis of gut microbiota may identify predictive factors for SUDD.
All patients in our study received dietary fiber to prevent constipation, a risk factor for complications of diverticular disease. However, this is unlikely to have influenced the results as we selected patients who had consumed dietary fiber for at least 6 months before enrollment. Furthermore, we did not assess the severity of patients’ stool disturbances or bloating, as this may depend on dietary fiber intake.
It must be recognized that this study has several limitations. First, the number of participants was small and a significant proportion of patients were lost to follow-up. Nevertheless, our preliminary results are promising and may support the design of larger controlled studies. The small number of participants could also be explained by the discontinuation of self-administration of rifaximin, as sustained improvement or other differences led to the exclusion of these patients from the study analysis. Another important limitation of our study is the lack of a placebo control group, which is essential to demonstrate a clear symptomatic benefit of rifaximin. Therefore, large-scale randomized controlled trials are needed to confirm our findings.