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BACKGROUND & AIMS Cirrhosis disrupts the hypothalamic-pituitary-gonadal axis causing low testosterone. Testosterone deficiency is associated with sarcopenia and osteopenia, leading to a state of frailty and worse clinical outcomes, morbidity and mortality. We aimed to conduct a systematic review on the relationship between serum testosterone and laboratory, anthropometric and clinical outcomes in observational and interventional studies in cirrhosis. METHODS PubMed and EMBASE were searched from inception through 27 August 2020 and reviewed independently by two investigators; a third reviewer solved disagreement. A qualitative summary of relevant findings was done. Methodological quality was assessed using the Newcastle Ottawa Scale for non-interventional studies and the Cochrane Risk of Bias for interventional studies. RESULTS Out of 3569 articles, 15 met inclusion criteria with six observational studies of 1267 patients and nine interventional studies of 580 patients. In observational studies, low serum testosterone level was associated with sarcopenia, shorter median time to hepatic decompensation, transplant requirement, higher model for end-stage liver disease (MELD) scores, and death in cirrhotic patients. Nine interventional studies (361 treated with testosterone vs 219 placebo, 1-36 months) showed that testosterone supplementation improved serum testosterone, appendicular mass and bone mineral density. However, no trial reported improvement in liver-related scores, complications, readmission rates or death. CONCLUSIONS Low serum testosterone is associated with increased morbidity and mortality in cirrhosis patients. Testosterone supplementation improved intermediate endpoints, but there was no conclusive data on clinical outcomes. Testosterone supplementation may be a promising strategy to improve frailty and decrease significant clinical complications in cirrhosis.

The Houston Consensus Conference and American College of Gastroenterology (ACG) have recommended Helicobacter pylori screening in United States populations with specific risk factors. However, the performance of these guidelines in clinical practice is not known.We identified consecutive patients undergoing upper endoscopy with gastric biopsies for any indication in a safety-net hospital in Houston, TX during January 2015-December 2016. We tested the association between the presence of H pylori (histopathology, stool antigen, urea breath test, immunoglobulin G serology, or prior treatment) and H pylori risk factors using logistic regression models, reported as odds ratios and 95% confidence intervals (CIs). We evaluated the area under the receiver operating characteristic (AUROC) curve for predictive ability of individual risk factors identified by the Houston Consensus Conference and ACG.Of 942 patients, the prevalence of H pylori infection was 51.5%. The risk factors with the highest predictive performance included first-generation immigrant (AUROC, 0.59) and Hispanic or black race/ethnicity (AUROC, 0.57), whereas the remaining 7 risk factors/statements had low predictive value. A model that combined first-generation immigrant status, black or Hispanic race/ethnicity, dyspepsia, and reflux had higher predictive ability for H pylori infection (AUROC, 0.64; 95% CI, 0.61-0.68) than any individual risk factor.In this contemporary U.S. cohort, the performance of individual risk factors identified by the Houston Consensus Conference and ACG was generally low for predicting H pylori infection except for black or Hispanic race/ethnicity and first-generation immigrant status. A risk prediction model combining several risk factors had improved diagnostic performance and should be validated in future studies.

BACKGROUND: Helicobacter pylori infection is an established causal factor for non-cardia gastric cancer. H. pylori negative gastric cancer prevalence among U.S. patients is unclear. METHODS: This retrospective cohort study examined H. pylori prevalence among consecutive patients with incident non-cardia gastric adenocarcinoma at the Houston VA Hospital (11/2007–10/2018). H. pylori positivity was defined by H. pylori on histopathology, positive antibody serology, stool antigen, or urea breath testing. We examined for trends in H. pylori negative gastric cancer based on year of diagnosis. Associations between histopathologic and cancer-related outcomes with H. pylori positivity were determined using regression models. RESULTS: Of 91 patients with gastric adenocarcinoma, most were men (N=87, 95.6%), black (N=47, 51.6%), with mean age at diagnosis of 68.0 years (SD 10.8). In addition to gastric cancer biopsy histopathology, 74 patients (81.3%) had ≥1 testing for H. pylori, including antibody serology (n=34), non-cancer gastric biopsy histopathology (n=63), or stool antigen (n=1). The overall prevalence of H. pylori infection was 38.5% and 45.9% among patients with ≥2 H. pylori tests. The proportions of H. pylori positive gastric cancer decreased from 50.0% (2007–2010) to 43.4% (2011–2014) and 29.3% (2015–2018) (p=0.096). Active/acute gastritis (adjOR 3.74), atrophic gastritis (adjOR 15.30), and gastric intestinal metaplasia (adjOR 3.65) were associated with H. pylori positive gastric cancer. DISCUSSION: The prevalence of H. pylori infection among patients with non-cardia gastric adenocarcinoma is relatively low (38.5–45.9%) and decreasing over time. This finding suggests there may be other important causal factors apart from H. pylori for gastric adenocarcinoma.

BACKGROUND: Despite tremendous interest in modulating the microbiome to improve health, the association between diet and the colonic mucosa–associated gut microbiome in healthy individuals has not been examined. OBJECTIVE: To investigate the associations between Healthy Eating Index (HEI)–2005 and the colonic mucosa–associated microbiota. METHODS: In this cross-sectional observational study, we analyzed bacterial community composition and structure using 16S rRNA gene (V4 region) sequencing of 97 colonic mucosal biopsies obtained endoscopically from different colon segments of 34 polyp-free participants. Dietary consumption was ascertained using an FFQ. Differences in α- and β-diversity and taxonomic relative abundances between the higher and lower score of total HEI and its components were compared, followed by multivariable analyses. RESULTS: The structure of the microbiota significantly differed by the scores for total HEI, total and whole fruits (HEI 1 and HEI 2), whole grains (HEI 6), milk products and soy beverages (HEI 7), and solid fat, alcohol, and added sugar (HEI 12). A lower score for total HEI and HEIs 2, 7, and 12 was associated with significantly lower richness. A lower score for total HEI was associated with significantly reduced relative abundance of Parabacteroides, Roseburia, and Subdoligranulum but higher Fusobacterium. A lower score for HEI 2 was associated with lower Roseburia but higher Bacteroides. A lower score for HEI 7 was associated with lower Faecalibacterium and Fusobacterium but higher Bacteroides. A lower score for HEI 12 was associated with lower Subdoligranulum but higher Escherichia and Fusobacterium (false discovery rate–adjusted P values

OBJECTIVES The risk of noncardia gastric cancer is increased in the presence of gastric intestinal metaplasia. We aimed to identify demographic and lifestyle factors independently associated with the risk of gastric intestinal metaplasia. METHODS We used data from a cross-sectional study of patients attending primary care and endoscopy clinics at the Michael E. DeBakey VA Medical Center in Houston, Texas, between February 2008 and August 2013. All patients completed standardized questionnaires and underwent endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included patients with intestinal metaplasia on any noncardia gastric biopsy; we defined extensive gastric intestinal metaplasia as antrum and corpus involvement. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic regression models. RESULTS We identified 423 cases with gastric intestinal metaplasia and 1,796 controls without gastric intestinal metaplasia. Older age (vs

Rituximab is effective in treating several cancers. Little is known about gastrointestinal adverse events associated with rituximab. We describe the clinical, endoscopic, and histologic features of rituximab-associated colitis (RC) at a tertiary care cancer center.We conducted a retrospective study of cancer patients who had received rituximab and had undergone a colonoscopy between 2000 and 2018. Patients with competing etiologies for colitis were excluded.Of the 13,717 patients who had received rituximab during the study period, 1660 had undergone colonoscopy. Among them, 70 (4%) had RC. Median time from rituximab treatment to RC onset was 181 days. Fifty-three patients had clinical gastrointestinal symptoms: 39 had diarrhea, 19 had abdominal pain, 11 had blood per rectum, and 5 had a concurrent fever. The median duration of symptoms was 21 days. Fifty patients (71%) received treatment for RC: immunosuppressive therapy in 12, antimicrobial agents in 21, antimotility agents in 42, and supportive care in 42. Nine patients had mucosal ulceration on endoscopy, and 52 had features of active inflammation on histology. Thirty-nine patients needed hospital admission, and 2 needed intensive care unit admission. One patient had colonic perforation that required surgical intervention. Patients who had abnormal endoscopic findings needed more frequent hospitalization (P=0.024) and more treatment for RC (P=0.001).RC is usually a mild disease requiring supportive care only. Nonetheless, on rare occasions, it can be severe enough to lead to colonic perforation and intensive care unit admission. Steroids used with the chemotherapeutic regimen can hamper RC severity.

Background Current treatment guidelines for immune-mediated colitis (IMC) recommend 4 to 6 weeks of steroids as first-line therapy, followed by selective immunosuppressive therapy (SIT) (infliximab or vedolizumab) in patients who do not respond to steroids. We assessed the effect of early SIT introduction and number of SIT infusions on clinical outcomes. Methods We performed a retrospective review of patients with IMC who received SIT at The University of Texas MD Anderson Cancer Center between January and December 2018. Logistic regression analyses were used to assess associations between clinical outcomes and features of IMC. Results Of the 1459 patients who received immune checkpoint inhibitors, 179 developed IMC of any grade; 84 of these 179 patients received SIT. Of the 84 patients who received SIT, 79% were males, and the mean age was 60 years (standard deviation, 14). Compared with patients who received SIT > 10 days after IMC onset, patients who received early SIT (≤10 days) required fewer hospitalizations (P = 0.03), experienced steroid taper failure less frequently (P = 0.03), had fewer steroid tapering attempts (P

Patients with non-Hodgkin’s lymphoma (NHL) are frequently referred for colonoscopy to evaluate gastrointestinal symptoms during their treatment course. Here, we described the rate of colonic adenomas in patients with NHL. This was a retrospective study of patients with NHL who underwent colonoscopy after being diagnosed with NHL between January 2000 and December 2017. Of the 17,938 patients who had been diagnosed with NHL in the study period, 2176 met the inclusion criteria. The mean age at the time of colonoscopy was 61 years. Most patients were male (61%). Overall, 1273 polyps were detected in 811 patients (37%). Sessile serrated adenomas were detected in 102 (5%) patients. The overall ADR was 12% in patients younger than 40 years of age (n = 103), 26% in patients aged 40–50 (n = 251), 34% in patients aged 51–60 (n = 630), and 43% in patients older than 60 (n = 1212). Most polyps were located in the right colon (63%), and 101 (8%) were larger than 1 cm. Villous adenomatous features were present in 1% of polyps, while high-grade dysplasia was detected in 22%. Invasive adenocarcinoma was identified in 4%. The median interval from lymphoma diagnosis to adenoma detection was 1.4 years (interquartile range 0.5–3.8 years). A repeat colonoscopy was performed in 343 patients. The overall ADR on repeat colonoscopy was 30%. Cox regression analysis revealed that age (hazards ratio 1.04; 95% confidence interval 1.03–1.05; P

Background Limited data are available concerning the clinical features of toxic gastrointestinal (GI) effects of taxane-based therapy. We describe the clinical, endoscopic and histologic features of taxane-induced colitis. Methods This retrospective study included cancer patients who received taxane therapy and underwent colonoscopy for GI symptoms from 2000-2018. Results Of the 45,527 patients who received taxane therapy during the study period, 76 (0.2%) met the inclusion criteria. Most patients (54%) received paclitaxel, 37% docetaxel, and 9% nab-paclitaxel. The median time from taxane therapy initiation to colitis symptom onset was 31 days. The median duration of colitis symptoms was 30 days. Colitis treatment comprised immunosuppressive therapy in 8 patients (11%), antibiotics in 17 (22%), antimotility agents in 18 (24%), and octreotide or somatostatin in 2 (3%). Thirty-five patients (46%) required hospitalization and seven (9%) required admission to the intensive care unit (ICU). Endoscopy revealed mucosal ulceration in 19 patients (25%), nonulcerative inflammation in 32 (42%), and normal findings in 25 (33%). Seventeen patients (22%) had features of lymphocytic colitis. One patient had spontaneous colonic perforation that required surgical intervention. Colitis symptoms recurred in 7 patients (9%) after initial improvement. Patients who received nab-paclitaxel developed GI toxicity earlier (P=0.003), required colitis-related hospitalization more frequently (P=0.005), and received intravenous fluids more frequently (P=0.025), compared with patients who received other taxanes. Conclusions Taxane-related colitis can present with significant inflammation on colonoscopy, and in a minority of patients as microscopic colitis. Taxane-induced colitis, although uncommon, can lead to ICU admission and colonic perforation.

Table S1. Effect of steroid treatment duration and timing to SIT initiation after IMC onset. Figure S1. Recurrence of IMC after ICI resumption. Figure S2. Kaplan-Meier curve showing overall survival duration of patients who received vedolizumab only compared with that of patients who received infliximab with or without vedolizumab. Figure S3. Kaplan-Meier curve showing overall survival duration of patients who developed IMC after more than three infusions of ICI compared with those who developed IMC after three or fewer infusions. (DOCX 61 kb)

Introduction Proton pump inhibitors (PPIs) are one of the most commonly prescribed medications in the United States. Some recent studies have suggested that PPIs may have a negative effect on the gut microbiome. Dysbiosis of the gut microbiome has been linked with inflammatory bowel disease (IBD). We hypothesized that PPI use is associated with increased IBD flares and activity. This study was aimed to assess the effect of PPIs on IBD flares and activity. Methods We conducted a prospective longitudinal study of Veterans from the IBD clinic at the Michael E. DeBakey VA Medical Center from 2014 to 2018. Our eligibility criteria included patients who were at least 18 years of age, who were diagnosed with Crohn’s Disease (CD) or Ulcerative Colitis (UC), and who had at least 2 clinic visits. IBD flare was defined by patient self-report of IBD flare between clinical encounters. IBD activity was quantified using the partial Mayo Score (pMayo) for UC, and the Harvey Bradshaw Index (HBI) for CD. Remission was defined by pMayo< 2 for UC and HBI< 5 for CD. The exposure of PPI was confirmed by chart review. Associations of PPI use with IBD flare and activity were assessed using T-tests and Chi-squared tests. Results A total of 132 patients were included in the analysis of which 74 had CD and 58 had UC. 40 patients were PPI users, and IBD flares occurred in 60 patients. No significant association between PPI usage and IBD flares were observed: 42.5% of PPI users developed flares compared to 46.7% of non-PPI users who developed flares, p-value=0.658. In patients with CD, PPI use was associated with non-remission status (RR 2.53; 95% CI 1.04–6.15). In UC patients, PPI use was not associated with non-remission status (RR 1.10; 95% CI 0.67 - 1.79). 13 CD patients on PPIs discontinued the PPI between encounters, which was associated with a statistically significant decrease in HBI (3.62 to 2.54, p-value= 0.005). Among UC patients who discontinued PPIs, there was a non-significant trend towards decreased pMayo (2.26 to 1.59, p-value= 0.069). Discussion Amongst CD patients, PPI use was not associated with interval flare however it was associated with non-remission status. Cessation of PPIs was associated with a statistically significant decrease in HBI in CD patients. Amongst UC patients, no significant associations between PPI use and flare or activity were observed. Decreasing unnecessary PPI use in patients with CD may decrease disease severity.