Clostridium difficile and Pediatric Inflammatory Bowel Disease

Martinelli, Massimo; Strisciuglio, Caterina; Veres, Gábor; Pærregaard, Anders; Pavić, Ana Močić; Aloi, Marina; Martín-de-Carpi, Javier; Levine, Arie; Turner, Dan; Pezzo, Mariassunta Del; Staiano, Annamaria; Miele, Erasmo

doi:10.1097/mib.0000000000000219

Cited by 56 publications

(39 citation statements)

References 29 publications

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“…In adult outpatients with ileal-anal pouch anastomosis (IPAA) for IBD, incidence of CDI is 10.7%-18.3%[33,34]. The incidence of CDI in IBD among pediatric patients is 7.8%-69%, similarly with a higher incidence among patients with UC as opposed to CD[35-40]. …”

Section: Discussionmentioning

confidence: 99%

Management of inflammatory bowel disease withClostridium difficileinfection

D’Aoust

Battat

Bessissow

2017

WJG

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AIMTo address the management of Clostridium difficile (C. difficile) infection (CDI) in the setting of suspected inflammatory bowel disease (IBD)-flare.METHODSA systematic search of the Ovid MEDLINE and EMBASE databases by independent reviewers identified 70 articles including a total of 932141 IBD patients or IBD-related hospitalizations.RESULTSIn those with IBD, CDI is associated with increased morbidity, including subsequent escalation in IBD medical therapy, urgent colectomy and increased hospitalization, as well as excess mortality. Vancomycin-containing regimens are effective first-line therapies for CDI in IBD inpatients. No prospective data exists with regards to the safety or efficacy of initiating or maintaining corticosteroid, immunomodulator, or biologic therapy to treat IBD in the setting of CDI. Corticosteroid use is a risk factor for the development of CDI, while immunomodulators and biologics are not.CONCLUSIONStrong recommendations regarding when to initiate IBD specific therapy in those with CDI are precluded by a lack of evidence. However, based on expert opinion and observational data, initiation or resumption of immunosuppressive therapy after 48-72 h of targeted antibiotic treatment for CDI may be considered.

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Section: Discussionmentioning

confidence: 99%

Management of inflammatory bowel disease withClostridium difficileinfection

D’Aoust

Battat

Bessissow

2017

WJG

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“…This finding contrasts with data in patients with IBD, who are less likely to have been exposed to antibiotics than controls with C. difficile infection. 11,27 Gut microbiota composition differs in patients with CeD compared with healthy controls, with an increase of certain Clostridia species. 16,28,29 One possible explanation for the increased risk of C. difficile infection among patients with CeD relates to the treatment with a gluten-free diet.…”

Section: Discussionmentioning

confidence: 99%

“…31 One previous study found that children with inflammatory bowel disease had carriage rates of C. difficile nearly 10 times greater than those of children with CeD, though in that study those with inflammatory bowel disease included inpatients (which likely included patients in the midst of a disease flare) while those with CeD were restricted to outpatients. 11 …”

Section: Discussionmentioning

confidence: 99%

Risk of Clostridium difficile Infection in Patients With Celiac Disease: A Population-Based Study

Lebwohl

Nobel

Green

et al. 2017

American Journal of Gastroenterology

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Background & Aims Patients with celiac disease are at increased risk for infections such as tuberculosis, influenza, and pneumococcal pneumonia. However, little is known about the incidence of Clostridium difficile infection (CDI) in patients with celiac disease. Methods We identified patients with celiac disease based on intestinal biopsies submitted to all pathology departments in Sweden over a 39-year period (from July 1969 through February 2008). We compared risk of CDI (based on stratified Cox proportional hazards models) among patients with celiac disease vs without celiac disease (controls) matched by age, sex, and calendar period. Results We identified 28,339 patients with celiac disease and 141,588 controls; neither group had a history of CDI. The incidence of CDI was 56/100,000 person-years among patients with celiac disease and 26/100,000 person-years among controls, yielding an overall hazard ratio (HR) of 2.01 (95% CI, 1.64–2.47; P<.0001). The risk of CDI was highest in the first 12 months after diagnosis of celiac disease (HR, 5.20; 95% CI, 2.81–9.62; P<.0001), but remained high, compared to that of controls, 1–5 years after diagnosis (HR, 1.85; 95% CI, 1.22–2.81; P=.004). Among 493 patients with CDI, antibiotic data were available for 251; there were no significant differences in prior exposures to antibiotics between patients with celiac disease and controls. Conclusions In a large population-based cohort study, patients with celiac disease had significantly higher incidence of CDI than controls. This finding is consistent with prior findings of higher rates of other infections in patients with celiac disease, and suggests the possibility of altered gut immunity and/or microbial composition in patients with celiac disease.

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“… 22 Similar results were also seen in children in a prospective multicenter study with detection of C. difficile toxins A and B by enzyme immunoassay giving a 10-fold higher detection in children with IBD compared with children with celiac disease (7.5% versus 0.8%; P = 0.008); this study however included both symptomatic and asymptomatic subjects. 23 Interestingly, a further study did not find a significant difference in the prevalence of toxigenic C. difficile between pediatric patients with IBD and controls using PCR to detect the toxin B gene (C. difficile detection of 11.6% in patients with Crohn's disease, 18.4% in patients with ulcerative colitis [UC], and 11.8% in controls [ P = 0.25]); however, this study looked at both inpatients and outpatients, and also likely symptomatic and asymptomatic colonization because some patients who tested positive also had diarrhea. 24 Furthermore, as compared with enzyme-linked immunoassay testing, PCR testing for detection of the toxin B gene of C. difficile is significantly more sensitive.…”

Section: Colonizationmentioning

confidence: 99%

“… 30 In pediatric IBD, antibiotic exposure has not been found to be the major risk factor for CDAD or C. difficile colonization. 18 , 23 Instead, it is proposed that the underlying dysbiosis with decreased diversity of species that is found in IBD, in both Crohn's disease and UC, predisposes to the loss of colonization resistance to C. difficile in IBD, leading to increased rates of CDI in this population. 31 , 32 Moreover, increased Proteobacteria and decreased Bacteroidetes have also been reported in those with IBD compared with non-IBD controls, 32 similar to some reports of microbiome changes in recurrent CDI.…”

Section: Pathogenesismentioning

confidence: 99%