Introduction

Chronic anal fissure is a frequent cause of referral to the proctology clinic and is associated with significant morbidity. In cases refractory to conservative measures, botulinum toxin (BT) is an alternative to a surgical approach, without the risk of permanent damage to the internal anal sphincter.

Aims & Methods

The aim of this study was to assess the efficacy of BT in anal fissure healing and to identify predictors of non-response. This was a retrospective, single-centre, observational study. Patients with chronic anal fissure who underwent TB between 2019 and 2023. Patients with a follow-up of less than 3 months or inflammatory bowel disease were excluded. On clinical reassessment, patients were categorised as complete, partial or refractory.

Results

Of the 118 patients selected, 80 were included. The average age was 49.1 ± 14.9 years, with 73.8% (n=59) of the patients female. The overall TB response rate was 62.0%. More than one TB session was carried out on 40.0% (n=32) of the patients, with an average of 1.5±0.6 per patient, with an interval between sessions of 3.4 ± 5.8 months. On reassessment after the first application, 30.0% (n=24) showed a complete response, 56.3% (n=45) a partial response and 13.8% (n=11) were refractory. Of the partial or refractory responders, after completing the treatment cycle, 56.5% (n=13) showed a complete response, 26.1 (n=6) a partial response and 17.4% (n=4) were refractory. During a median follow-up of 10.0 [3-48] months, 7 patients became asymptomatic and 2 patients had a recurrence of the cleft. 21 patients (26.3%) were referred for surgery. The duration of symptoms was an independent predictor of TB treatment failure and the need for surgery (OR 4.895; p=0.049).

Conclusion

TB has a satisfactory response rate in the treatment of patients with chronic anal fissure, making it possible to avoid surgery in patients, specially with a short duration of symptoms.

Introduction

Crohn's disease (CD) is a complex chronic intestinal inflammatory disease with unknown etiology¹. Gut microbiota is involved in the bile acid metabolism in the intestine and the regulation of intestinal mucosal immunization to maintain intestinal homeostasis². The histological changes in the intestinal mucosa of CD are closely related to impaired intestinal barrier function^3-5. Abnormal gut microbiota and metabolic disorders can destroy the normal intestinal barrier function and intestinal homeostasis, thereby continuously aggravating the inflammatory reactions^6,7.

Aims & Methods

To further explore the related factors affecting the incidence and provide essential guidelines for clinical prevention and treatment of CD, the prospective case-control study conducted a multi-omics analysis of gut microbiota, fecal bile acid profiles, serum cytokines and intestinal barrier function in patients with active CD, patients in remission and normal controls.

Results

The study found that CD patients had unique gut microbiota and fecal bile acid profiles compared with normal controls, which were related to the disease activity. The beneficial bacteria represented by Romboutsia were positively correlated with the concentrations of fecal secondary bile acids, while negatively correlated with the concentrations of primary bile acids. When patients were active, their gut-beneficial bacteria decreased, affecting the bile acid metabolism. The variation of CD patients' bile acid profile was increased. The production of secondary bile acids was decreased. The levels of proinflammatory cytokines in peripheral blood were increased, such as FC, ESR, CRP and HBP, with P values all below 0.001. And the CD active group had significantly higher levels of IL-6, IL-8, IL-10 and IL-1β than those in remission, with P values of <0.001, 0.005, 0.04 and 0.044, respectively. The intestinal physical barrier and mucosal barrier were damaged with disease activity of CD.

Conclusion

The study suggested that the occurrence and development of CD might be caused by the interaction between gut microbiota and the metabolic product bile acid, which leads to the consequence of immune response in the body and the damage to the intestinal barrier.

References

1. Suau R, Pardina E, Domènech E, Lorén V, Manyé J. The Complex Relationship Between Microbiota, Immune Response and Creeping Fat in Crohn's Disease. J Crohns Colitis. 2022;16(3):472-89.
2. Leonardi I, Gao IH, Lin WY, et al. Mucosal fungi promote gut barrier function and social behavior via Type 17 immunity. Cell. 2022;185(5):831-46.e14.
3. Leibovitzh H, Lee SH, Raygoza Garay JA, et al. Immune response and barrier dysfunction-related proteomic signatures in preclinical phase of Crohn's disease highlight earliest events of pathogenesis. Gut. 2023;72(8):1462-71.
4. Rath T, Atreya R, Bodenschatz J, et al. Intestinal Barrier Healing Is Superior to Endoscopic and Histologic Remission for Predicting Major Adverse Outcomes in Inflammatory Bowel Disease: The Prospective ERIca Trial. Gastroenterology. 2023;164(2):241-55.
5. Maddipatla SC, Kolachala VL, Venkateswaran S, et al. Assessing Cellular and Transcriptional Diversity of Ileal Mucosa Among Treatment-Naïve and Treated Crohn's Disease. Inflamm Bowel Dis. 2023;29(2):274-85.
6. Caparrós E, Wiest R, Scharl M, et al. Dysbiotic microbiota interactions in Crohn's disease. Gut Microbes. 2021;13(1):1949096.
7. Leibovitzh H, Lee SH, Xue M, et al. Altered Gut Microbiome Composition and Function Are Associated With Gut Barrier Dysfunction in Healthy Relatives of Patients With Crohn's Disease. Gastroenterology. 2022;163(5):1364-76.e10.

Disclosure

All authors declared no potential conflicts of interest with respect to the study.

Clinical Case Summary

Introduction: With an incidence of 0.5-1%, jejunal diverticulosis is a rare gastrointestinal pathology, which remains mostly asymptomatic. However 18% of patients present with life-threatening complications like bleeding or perforation.
Case report: We present the case of a 75-year-old patient admitted to the intensive care unit (ICU) with suspected middle gastrointestinal bleeding. The patient presented to the emergency unit with symptoms including recurrent syncope, hematemesis and hematochezia. Additionally, vital signs such as arterial hypotonia and tachycardia were noted, along with the initial hemoglobin value of 5.5 g/dl, which indicated significant blood loss.Because of the unstable hemodynamic situation the patient was transferred to the ICU. For airway protection endotracheal intubation was performed. An enteroscopy detected blood in the stomach, duodenum and jejunum and revealed multiple jejunal diverticula, however without active bleeding. After transfusion of multiple erythrocyte concentrates and administration of cathecolamines, the patient could be stabilized. Despite initial interventions, a recurrence of decreased hemoglobin levels was observed. Computed tomography failed to localize the bleeding. Emergency laparotomy revealed jejunal diverticulosis, necessitating resection of 40 cm of the jejunum. Intraoperative, resection borders could be endoscopically guided. Postoperatively, the patient was successfully extubated and discharged days later.
Conclusion: Localization of small bowel diverticula bleeding can be endoscopically or radiologically achieved, however is often difficult and problematic. Jejunal diverticular bleeding must be suspected in cases of obscure bleeding and therapeutic strategies must be interdisciplinary discussed. Surgical laparotomy represents ultima ratio in these pathology. A precise surgical resection can be achieved using intraoperative endoscopy in such cases.