Defecatory disorders in children, including chronic constipation (CC) and fecal incontinence (FI), are common conditions worldwide and have a significant impact on children, their families, and the healthcare system. Anorectal manometry (ARM) and high‐resolution anorectal manometry (HRAM) are relatively novel tools for the assessment of anal sphincter function and rectal sensation and have contributed significantly to improving the understanding of the anorectum as a functional unit. ARM has been recognized as the investigation of choice for adults with symptoms of defecation disorders, including fecal incontinence (FI), evacuation difficulties, and constipation. Although it is the gold standard tool in adults, it has yet to be formally accepted as a standardized diagnostic tool in the pediatric age, with limited knowledge regarding indications, protocol, and normal values. ARM/HRAM is slowly becoming recognized among pediatricians, but given that there are currently no agreed guidelines there is a risk that will lead to diversity in practice. The British Society of Paediatric Gastroenterology, Hepatology and Nutrition (BSPGHAN)—Motility Working Group (MWG) therefore has taken the opportunity to provide guidance on the use of ARM/HRAM in children with CC and/or FI.
Background Antroduodenal manometry (ADM) and histopathology are currently employed to aid the diagnosis of pediatric intestinal pseudo‐obstruction (PIPO). Limited data are available on the reliability of ADM analysis and its correlation with histopathology. We aimed to develop a protocol for enhanced analysis of ADM contractile patterns, including a scoring system, and explore whether this provided better correlation with histopathology. Methods Children referred with suspected PIPO between April 2012‐December 2019 who underwent both ADM and full‐thickness biopsies were included. ADM tracings were analyzed using both standard (conventional ADM) and novel (enhanced ADM) motility parameters. A novel ADM score (GLASS score) was generated based on the enhanced ADM analysis. Conventional and enhanced ADM analyses were then correlated with histopathology. Results Forty patients were included. Using conventional clinical criteria, 29 of these were diagnosed with PIPO and the other 11 with non‐PIPO diagnoses. Twenty‐three of the PIPO patients had abnormal histopathology: 6 myopathy, 4 neuropathy, 3 neuro‐myopathy, and 10 non‐specific changes. No agreement in diagnosis was found between conventional ADM analysis and histopathology (ϰ = 0.068; p = 0.197), whereas the latter significantly correlated with enhanced ADM analysis (ϰ = 0.191; p = 0.003). The enhanced ADM score was significantly higher in PIPO versus non‐PIPO (16.0 vs. 8.0; p < 0.001). Conclusions As opposed to conventional analysis protocols, the newly developed enhanced ADM analysis and associated score is not only able to discriminate between PIPO and non‐PIPO patients, but also between distinct histopathological pathologies. Further studies are required to assess the utility of enhanced ADM analysis in larger populations.
Background: Impaired gut barrier function has been reported in some functional gastrointestinal (GI) disorders. Evidences suggest that gut microbiota affects GI motility in particular Lactobacillus species elicits anti-inflammatory activity and exerts protective effects on damage induced by pathogen Gram negative-derived lipopolysaccharide (LPS). LPS produced an oxidative imbalance in human colonic smooth muscle cells (SMC) that persists after LPS-washout and contributes to SMC morphofunctional alterations. The aim was to evaluate if supernatants harvested from LGG cultures protect SMC from LPS-induced myogenic damage. Methods: L. rhamnosus GG (ATCC 53103 strain) was grown in MRS medium and samples were collected from bacterial cultures in middle exponential phase, in early, in middle and late stationary phase (overnight). Supernatants were recovered, filtered and stored at -20 8C. Highly pure human SMC culture was then exposed for 24 h to highly purified LPS (1 mg/ml) of E. coli (O111:B4) in the absence and presence of the supernatants. Their effects were evaluated on LPS-induced SMC morphofunctional alterations and pro-inflammatory IL-6 production. Data are expressed as mean AE SE (P < 0.05 significant). Results: LPS induced persistent significant 20.7% AE 1.2 cell shortening and 35.2% AE 2.6 decrease in contraction of human colonic SMC. These alterations were paralleled to a 238.5% AE 82.5% increase in IL-6 production. These effects disappeared in the presence of LGG-supernatants, following a progression related to LGG growth curve phases. Supernatants collected in the middle exponential phase already significantly partially restored LPS-induced cell shortening by 43.4% AE 10.2% and IL-6 increase by 47.6% AE 13.1%, but had no effect on LPS-induced inhibition of contraction. Supernatants collected later, in the early and middle stationary phase, further counteract LPS-induced damage, including inhibition of contraction. Maximal protective effects were observed with supernatants of the late stationary phase where LPS-induced cell shortening was reversed by 86% AE 4.7%, inhibition of contraction by 98.2% AE 1.8%, and IL-6 basal production by 91.3% AE 0.6%. Conclusions: LGG-secreted products are substances/byproducts able to directly protect human SMC from LPS-induced myogenic damage. Novel insights are then provided about the possibility that LGG-derived products could reduce the risk of progression to a post-infective motor disorder.
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