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Background Colon cancer patients often ask how surgery will affect bowel function. Current understanding is informed by conflicting data, making preoperative patient counseling difficult. We aimed to evaluate patient-reported bowel function changes after colectomy for colon malignancy. Material and methods This was a retrospective analysis of a prospectively collected institutional database from July 2015 to June 2019. The included patients underwent colectomy for adenocarcinoma of the colon, and completed the Colorectal Functional Outcome (COREFO) questionnaire at preoperative presentation and postoperative followup. Preoperative and postoperative scores were compared using paired t-tests. Multivariable analysis was performed using domains demonstrating statistical significance on bivariate analysis, assessing the factors that were associated with symptomatic bowel function. Results We identified 117 patients with a mean age of 64 ± 13 y. The median time between preoperative and postoperative questionnaire completion was 52 d (interquartile range 45-70). Bowel movement frequency increased significantly from a mean preoperative score of 9.72 to a mean postoperative score of 14.2 (P = 0.003). There were no significant differences in the remaining four domains of bowel function or global function. Multivariable analysis demonstrated higher likelihood of symptomatic postoperative frequency scores in male patients (OR 3.85, 95% CI 1.44-11.11, P = 0.007) and patients with symptomatic preoperative frequency (OR 5.56, 95% CI 1.62-19.02, P = 0.006). Conclusions Patient-reported bowel movement frequency worsens at postoperative follow-up after colectomy for colon cancer, while overall bowel function does not change. Men and patients with preoperative symptomatic frequency have an increased likelihood of reporting symptomatic postoperative frequency. These findings should guide more personalized and evidence-based preoperative patient counseling.

Background Surgery for anorectal diseases is thought to cause significant pain postoperatively. There is little known regarding standardized opioid-prescribing trends and patient use following surgery for anorectal diseases. We aimed to evaluate and analyze opioid-prescribing trends and patient use for outpatient anorectal operations. Materials and methods All patients who underwent outpatient anorectal surgery performed over a 1-y period at a single institution were eligible. Procedures included hemorrhoidectomy, anal fistula repair/seton, anal fissure treatment with sphincterotomy, and transanal excision of rectal tumors. Demographic, operative, and postoperative data were obtained. Patients were given a survey to determine postoperative pain control with opioid and non-narcotic analgesia use; respondents were included in analysis. Results Forty-two outpatient anorectal surgery patients were included: 13 had hemorrhoidectomy, 22 had anal fistula repair/seton, one had sphincterotomy, and six had transanal excisions. All patients had multimodality treatment with either an anal block and/or postoperative nonopioid analgesics. Ninety percent were prescribed opioids postoperatively with a median of 20 pills (range: 0-120 pills). Forty-three percent (18/42) did not fill their prescription. For those who used opioids, the median number of pills taken was four. Eighty percent of pills prescribed were not used. One patient required a refill. Greater than 60% of respondents reported good to excellent pain control on a five-point scale. Conclusions Most patients had adequate pain control after anorectal surgery with little to no use of opioids and that more than 80% of opioid pills prescribed were not consumed. We intend to standardize our prescribing opioid quantities for outpatient anorectal operations to reflect this reduced use.

Little is known about the pathogenesis of Entamoeba histolytica and how epithelial cells respond to the parasite. Herein, we characterized the interactions between E. histolytica and colonic epithelial cells and the role macrophages play in modulating epithelial cell responses. The human colonic epithelial cell lines Caco-2 and T84 were grown either as monoculture or co-cultured in transwell plates with differentiated human THP-1 macrophages for 24 h before stimulation with soluble amebic proteins (SAP). In naive epithelial cells, prolonged stimulation with SAP reduced the levels of heat shock protein (Hsp) 27 and 72. However in THP-1 conditioned intestinal epithelial cells SAP enhanced Hsp27 and Hsp72, which was dependent on the activation of ERK MAP kinase. Hsp synthesis induced by SAP conferred protection against oxidative and apoptotic injuries. Treatment with SAP inhibited NF-kappaB activation induced by interleukin-1beta; specifically, the NF-kappaB-DNA binding, nuclear translocation of p65 subunit, and phosphorylation of IkappaB-alpha were reduced. Gene silencing by small interfering RNA confirmed the role of Hsp27 in suppressing NF-kappaB activation at IkappaB kinase (IKK) level. By co-immunoprecipitation studies, we found that Hsp27 interacts with IKK-alpha and IKK-beta, and this association was increased in SAP-treated conditioned epithelial cells. Overexpression of wild type Hsp27 amplified the effects of SAP, whereas a phosphorylation-deficient mutant of Hsp27 abrogated SAP-induced NF-kappaB inhibition. In conditioned epithelial cells, Hsp27 was phosphorylated at serine 15 after prolonged exposure to SAP. This mechanism may explain the absence of colonic inflammation seen in the majority of individuals infected with E. histolytica.

Gastrointestinal mucin is a constituent of luminal barrier function and is the first line of host defense against invading pathogens. Mucin carbohydrates and amino acids, as well as trapped soluble host defense molecules, serve as substrates for colonization and control or deter pathogen invasion to the underlying mucosal epithelial cells. Toll-like receptors on the surface of epithelial cells act as sensors for invading pathogens, and the ensuing host response limits parasite invasion and leads to adaptive immunity. The latest work in the field and the use of parasite model systems to illustrate the delicate host-parasite interaction at the mucosal surface of the gut are discussed here.

Hamano et al. have recently reported that in murine models of amebiasis, innate resistance is associated with nonhemopoietic cells and depends on the activity of interleukin-10. This article raises the issue of the importance of predisposition to amebic colitis and discusses which host factors have a role in innate resistance to invasive disease. Resistance studies that elucidate the mechanisms involved in parasite clearance or parasite invasion are essential to understanding the incidence of amebiasis in humans.