Faculty Bibliography

BACKGROUND:Colorectal strictures have been considered independent risk factors for neoplasia in patients with inflammatory bowel disease (IBD). We examined the association between colorectal stricture and subsequent risk of colorectal neoplasia (CRN) in patients with IBD colitis undergoing colonoscopic surveillance. METHODS:We conducted a retrospective cohort analysis of patients with IBD colitis enrolled in colonoscopic surveillance for CRN at an academic medical center between 2005 and 2017. Inclusion criteria were IBD involving the colon for ≥8 years (or any duration with primary sclerosing cholangitis [PSC]) undergoing surveillance. Exclusion criteria were advanced CRN (ACRN; colorectal cancer [CRC] or high-grade dysplasia [HGD]) prior to or at enrollment, prior colectomy, or limited (<30%) disease extent or proctitis. Multivariable logistic and Cox regression analysis estimated the association between colorectal stricture on the index colonoscopy and ACRN, CRN (indefinite dysplasia, low-grade dysplasia, HGD, CRC), or colectomy. RESULTS:Among 789 patients with IBD undergoing CRC surveillance, 72 (9%; 70 with Crohn's colitis) had a colorectal stricture on index colonoscopy. There was no significant difference in the frequency of ACRN or requirement for colectomy between patients with vs without a colorectal stricture (P > .05). Colorectal stricture was not associated with subsequent ACRN (adjusted odds ratio [aOR], 1.41; 95% CI, 0.49-4.07), CRN (aOR, 1.15; 95% CI, 0.51-2.58), or colectomy (aOR, 1.10; 95% CI, 0.65-1.84). CONCLUSIONS:In this analysis of patients with IBD colitis undergoing CRN surveillance, the presence of a colorectal stricture was not independently associated with risk of ACRN or colectomy. Multicenter, prospective studies are needed to confirm these findings, particularly in patients with ulcerative colitis-associated colorectal stricture.

BACKGROUND AND AIMS/OBJECTIVE:Thirty percent of inflammatory bowel disease (IBD) patients hospitalized with flare require salvage therapy or surgery. Additionally, 40% experience length of stay (LOS) > 7 days. No emergency department (ED)-based indices exist to predict these adverse outcomes at admission for IBD flare. We examined whether clinical, laboratory, and endoscopic markers at presentation predicted prolonged LOS, inpatient colectomy, or salvage therapy in IBD patients admitted with flare. METHODS:Patients with ulcerative colitis (UC) or colonic involvement of Crohn's disease (CD) hospitalized with flare and tested for Clostridioides difficile infection (CDI) between 2010 and 2020 at two urban academic centers were studied. The primary outcome was complex hospitalization, defined as: LOS > 7 days, inpatient colectomy, or inpatient infliximab or cyclosporine. A nested k-fold cross-validation identified predictive factors of complex hospitalization. RESULTS:Of 164 IBD admissions, 34% (56) were complex. Predictive factors included: tachycardia in ED triage (odds ratio [OR] 3.35; confidence interval [CI] 1.79-4.91), hypotension in ED triage (3.45; 1.79-5.11), hypoalbuminemia at presentation (2.54; 1.15-3.93), CDI (2.62; 1.02-4.22), and endoscopic colitis (4.75; 1.75-5.15). An ED presentation score utilizing tachycardia and hypoalbuminemia predicted complex hospitalization (area under curve 0.744; CI 0.671-0.816). Forty-four of 48 (91.7%) patients with a presentation score of 0 (heart rate < 99 and albumin ≥ 3.4 g/dL) had noncomplex hospitalization. CONCLUSIONS:Over 90% of IBD patients hospitalized with flare with an ED presentation score of 0 did not require salvage therapy, inpatient colectomy, or experience prolonged LOS. A simple ED-based score may provide prognosis at a juncture of uncertainty in patient care.

Introduction: Patients with inflammatory bowel disease (IBD) have a high degree of sexual dysfunction (SD). Few studies have tracked SD longitudinally or with IBD-specific scales. We aimed to correlate SD with clinical and psychosocial IBD indices and track SD longitudinally using the IBDFemale and Male Sexual Dysfunction Scales (IBD-FSDS and MSDS).
Method(s): We surveyed patients with Crohn's disease (CD) and ulcerative colitis (UC) starting a new biologic or small molecule therapy (anti-TNF, anti-integrin, anti-IL12/23, JAK inhibitor) at start of induction and 2- and 6-months. Surveys also included the PROMIS Brief Sexual Function and Satisfaction Profile, disease activity indices [Harvey-Bradshaw index (HBI), partial Mayo score], and psychosocial scales [Patient Health Questionnaire-9 (PHQ-9), Short IBD Questionnaire (SIBDQ), and IBD-Disability Index (IBDDI)]. Clinical data included endoscopic scores, inflammatory biomarkers (ESR, CRP, calprotectin), and IBD history. Therapy response was defined as a reduction in HBI, pMayo, SCCAI >=3 or total HBI <= 4, pMayo<2, SCCAI <=2 at survey 3.
Result(s): 123 patients (68 males and 53 females) completed survey 1, 89 completed survey 2, and 74 completed survey 3. The median age was 31 years. 58% had CD, 42% had UC, and 31% were nonwhite. At induction, the median MSDS score was 6 out of 40 (IQR 2.5-13.5) and FSDS was 12 out of 60 (3-27.5); (Table 1). SD scores strongly correlated with PROMIS scores (r5-0.75, p<0.001), Mayo endoscopic score (r=0.71, p<0.001), and moderately correlated with HBI (r=0.49, p=0.002) and pMayo scores (0.44, p=0.03), but not with inflammatory biomarkers. SD also correlated with SIBDQ (r=0.55, p<0.001), PHQ-9 (r=0.42, p<0.001), and IBD-DI (r=0.47, p<0.001). MSDS scores significantly improved from survey 1 to survey 3 (p= 0.039). FSDS scores numerically improved but did not reach significance. Over 50% of patients had a significant response to therapy. When stratified by treatment response, MSDS and FSDS scores improved significantly among therapy responders (p=0.006 and p= 0.041, respectively) as did Male-PROMIS scores. This improvement was not observed in non-responders (p=0.27). HBI, SCCAI, pMayo, SIBDQ and IBD-DI also improved among responders.
Conclusion(s): In this longitudinal cohort, there was a strong correlation between SD, disease activity, and psychosocial indices. Among therapy responders, there was a significant improvement in SD. These findings further clarify the relationship between SD and therapeutic response in IBD

Introduction: Inflammatory bowel disease (IBD), psoriasis (PsO), and psoriatic arthritis (PsA) are immune-mediated inflammatory diseases characterized by dysregulation of the immune system. Evidence suggests that they share a common genetic and pathophysiologic pathway and that the presence of one increases the risk of developing others. While rates of PsO and PsA are increased in patients with IBD, data is lacking regarding whether phenotypic differences exist in patients with concurrent disease. In this study, we describe the disease characteristics of patients with IBD and PsO/PsA overlap.
Method(s): We performed a single-center case-control observational study. Eighty-five patients with IBD and PsO and/or PsA were identified and matched with a control group of patients with IBD alone in a 1:2 fashion based on age, sex and IBD type (n=190). Patient demographics, IBD phenotype and history, treatment patterns, and family history were collected.
Result(s): We identified 85 patients with IBD and PsO +/-PsA, matched with 190 controls. IBD 1 PsO/PsA patients were less frequently White (85% vs. 94%) and more frequently Asian (7% vs. 3%), compared with IBD only patients (P, 0.01, Table 1). There were no differences in extent of ulcerative colitis (UC) or distribution of Crohn's disease (CD), but patients with IBD alone were more likely to have penetrating Crohn's disease (48% vs. 7%; P, 0.01), prior hospitalizations (48% vs. 28%; P, 0.01), and prior surgeries (35% vs. 17%; P=0.02), compared to patients with overlap PsO +/-PsA. Rates of exposure to various biologic therapies were similar between the two groups, with the exception of decreased vedolizumab use in the IBD 1 PsO/PsA group (12% vs. 31% respectively; P, 0.01, Table 2). IBD only patients were more likely to have first-degree relatives (FDR) with IBD (35% vs. 23%; P=0.02) and numerically less likely to have a FDR with PsO or PsA (14% vs. 20%; P=0.21) than patients with PsO/PsA overlap (Table 1).
Conclusion(s): In this study, we report for the first time disease characteristics of patients with IBD and overlap PsO or PsA. Our results suggests that patients with IBD and PsO/PsA may have a less severe disease phenotype than patients with IBD alone, and that genetic risks may differ between these two groups. Further prospective studies are needed to confirm these findings

Introduction: Postoperative prophylaxis with biologics following ileocecal resection (ICR) for Crohn's disease (CD) reduces endoscopic postoperative recurrence (POR) rates. However, there is limited data regarding optimal treatment strategies of endoscopic POR. We aimed to assess the outcomes of various therapeutic regimens to treat endoscopic POR despite biologic prophylaxis.
Method(s): Retrospective cohort study of adult CD patients who underwent ICR between 2009-2020 at single referral institution. Patients with bowel continuity restoration, first detection of endoscopic POR whilst on a biologic, and >=1 postoperative colonoscopy were included. Modified Rutgeerts' score assessed disease activity and endoscopic POR was defined as Rutgeerts' >=i2b. Treatment changes after POR detection were categorized as therapy optimization (steroids, immunomodulators, dose intensification of biologic, new biologic within class) or new biologic class. The primary outcome of the study was treatment failure defined as endoscopic POR at immediate follow up colonoscopy or surgical POR prior to subsequent colonoscopy. Secondary outcome was endoscopic healing at follow up endoscopy.
Result(s): 81 CD patients with endoscopic POR (54.6% i2b, 22.2% i3, and 22.2% i4) despite biologic prophylaxis were included. A majority (85.4%) were on anti-TNF, 8.6% vedolizumab, and 4.9% were on ustekinumab at time of POR. The predominant intervention was therapy optimization (76.3%, n=61) while 24.7% (n=20) were started on a new biologic class. 60 patients, comprised of 48 (78.7%) therapy optimization and 12 (60.0%) new biologic class, experienced treatment failure (84.6% endoscopic, 15.4% surgical) (P=0.08). On multivariable modeling, initiation of new biologic class was associated with reduced risk for treatment failure compared to therapy optimization (aOR: 0.26 [0.07-0.93]; p=0.04) (Table 1). In patients without surgical POR (n=68), 28 patients, comprised of 18 (35.3%) therapy optimization and 10 (58.9%) of new biologic class, had endoscopic healing at time of follow up endoscopy. On modeling adjusting for endoscopic severity, initiation of new biologic class was associated with endoscopic healing relative to therapy optimization (aOR: 3.3 [1.0-11.92]; p=0.05).
Conclusion(s): In CD patients who experience POR despite biologic prophylaxis, changing mechanism of action may promote greater endoscopic healing than therapy optimization. Larger studies assessing factors associated with response and prospective trials are needed to confirm results

Introduction: Previous clinical trials and societal guidelines have established preoperative risk factors for postoperative recurrence (POR) of Crohn's disease (CD). However, in patients who are in endoscopic remission at time of their index postoperative ileocolonoscopy, risk factors for later development of POR is unknown. This study aimed to assess the relative risk of POR after initial endoscopic remission.
Method(s): Retrospective cohort study of adult CD patients who underwent ileocolonic resection (ICR) between the years of 2009-2020. Patients with bowel continuity restoration and index postoperative ileocolonoscopy with modified Rutgeerts' score of <= i2a disease were included. Postoperative ileocolonoscopies were assessed by retrospective application of Rutgeerts' score. The primary outcome was a composite outcome of objective recurrence including radiologic (active disease on cross-sectional enterography), endoscopic (Rutgeerts score >= i2b), and surgical (repeat ICR) POR after initial endoscopic remission.
Result(s): 232 CD patients (median age 35 years, 45.2% stricturing, 15.5% >=2 prior ICR) with initial endoscopic remission (98 i0, 49 i1, 85 i2a disease) were included in the study. The median time to index postoperative colonoscopy was 334 days. 131 (56.5%; 46.9% i0, 53.1% i1,69.4% i2a) patients went on to develop composite POR at median interval of 2.84 years. Risk of composite POR was associated with index Rutgeerts' score (p=0.008; 41.4% endoscopic POR, 38.3% radiologic POR, 14.2% surgical POR). On multivariable Cox proportional hazard regression, patients with i1 disease (aHR: 1.76 95% CI [1.04-2.99]; p=0.036) or i2a disease (aHR; 2.24 [1.49-3.36]; p<0.001) at initial postoperative colonoscopy were at increased risk for composite POR relative to patients with i0 disease (Figure 1; Table 1). Additionally, patients that were exposed to biologics prior to ICR were at increased risk for late POR relative to biologic-naive patients (aHR: 1.84 [1.15-2.95]; p=0.012). Patients with i2a disease was independently associated with decreased time to radiologic (aHR: 1.66 [1.04-2.65]; p=0.033), endoscopic (aHR:2.85 [1.76-4.59]; p<0.001 ), and surgical (aHR: 2.42 [1.11-5.29]; p=0.027) POR (Table 1).
Conclusion(s): Postoperative CD recurrence following early endoscopic remission is common. Early mild ileal or anastomotic inflammation confers increased risk for late recurrence. Future studies to determine surveillance strategies for patients in initial endoscopic remission are needed

Introduction: Traveler's diarrhea is the most common travel related illness and is often encountered in the outpatient setting. Most pathogens that cause traveler's diarrhea are poorly characterized by conventional stool testing such as stool culture and ova and parasite exam. Multiplex polymerase chainreaction based gastrointestinal pathogen panels (GI PCR) offer advantages in sensitivity and turnaround time, however their impact on clinical management is unclear. Our aim was to evaluate the clinical impact of GI PCR testing in outpatients presenting with traveler's diarrhea.
Method(s): We performed a retrospective study comparing outpatients presenting with acute gastrointestinal symptoms at an academic medical center who received stool testing with GI PCR from September 2015 to April 2019, to patients who presented with similar symptoms from February 2009 to April 2012, when GI PCR was unavailable, and received stool culture and ova and parasite exam ("conventional testing"). Patients who received GI PCR were matched by age and sex to patients who received conventional testing. We recorded pathogens isolated, demographic data, history of travel within 30 days of presentation, presenting symptoms and rates of antibiotic therapy.
Result(s): We identified 1,018 outpatients who received GI PCR or conventional stool testing. (n5509 each). There were 70 patients in the conventional cohort and 78 in the GI PCR cohort, respectively, with traveler's diarrhea. In patients who received GI PCR, we observed higher diagnostic yield in patients with traveler's diarrhea who received GI PCR, compared to patients without a history of recent travel (54 vs. 39%, p50.01, Table 1). There was no difference in diagnostic yield in patients who received conventional stool testing (9 vs 10%, p50.74). Patients with travelers' diarrhea were more likely to have pathogenic species of Escherichia coli (E. coli) identified on testing (45 vs. 22%, p, 0.01, Table 2), particularly Enteroaggregative E. coli (23 vs. 6%, p, 0.01). Patients with traveler's diarrhea were more likely to receive antibiotics whether they received GI PCR (38 vs. 27%, p50.04) or conventional testing (35 vs. 25%, p50.06).
Conclusion(s): GI PCR was associated with a higher diagnostic yield in patients presenting with travelers' diarrhea. Patients with travelers' diarrhea were significantly more likely to have pathogenic E. coli species identified on PCR testing, with up to 45% of patients testing positive

Introduction: Health disparities in health care utilization and clinical outcomes are strongly linked to race, ethnicity, socioeconomic, and insurance status in many diseases. We aimed to measure racial and socioeconomic disparities in inflammatory bowel disease (IBD) care including disease characteristics, treatment, health care utilization, and clinical outcomes.
Method(s): We performed a retrospective chart review of patients 18 years and older with established IBD care at a private or public hospital in New York City. Established care was defined as having at least 1 colonoscopy and 1 clinic visit within the same hospital. Patient demographics, disease characteristics, and outcomes were collected. Multivariate logistic regression was performed and reported as odds ratios (OR) with 95% confidence intervals (CI).
Result(s): A total of 322 patients, 50% from each hospital, were included in the analysis. Public hospital IBD patients were more likely to have Medicaid and visit the ED (17% vs 6%, OR 5.3, CI 2.1-14, and 41% vs. 11%, OR 4.0, 1.5-11,) compared to private hospital patients. Focusing on race, Black IBD patients were more likely to be hospitalized (36%, OR 7.6 CI 1.0-161) compared to other races. In terms of insurance, Medicare patients were more likely to be hospitalized and require surgery (28%, OR 4.9 CI 1.1-22 and 16%, OR 14, CI 1.7-120) compared to uninsured patients or those with Medicaid or private insurance. Unemployed IBD patients had higher rates of surgery (18% vs. 9%, OR 3.6, CI 1.2-10). CD patients who were unemployed had higher rates of prolonged steroid use, ED visits, and hospitalizations (OR 8.5, CI 1.2-79, OR 14, CI 1.7-173, OR 15, 1.9-191) compared to employed CD patients. UC patients with Medicaid were more likely to be hospitalized (OR 3.6, 1.0-14) compared to uninsured patients or those with Medicaid or private insurance. UC patients with private insurance were more likely to achieve mucosal healing (OR 5.3, 1.1-31) compared to uninsured patients or those with Medicaid or Medicare.
Conclusion(s): Race, employment, and insurance status were linked with disparities in IBD care. Public hospital use, Black race, unemployment, and non-private insurance were associated with various adverse IBD outcomes including increased ED visits, hospitalizations, requirement for surgery, prolonged steroid use, and decreased rates of mucosal healing. Future work should focus on identifying interventions to resolve disparities for these patient populations

Introduction: Postoperative recurrence (POR) of Crohn's disease (CD) following ileocecal resection (ICR) is common. Endoscopic CD activity guides postoperative management. Histologic activity precedes endoscopic activity. In patients in endoscopic remission, the influence of histologic activity on risk of subsequent POR is unknown. We aimed to assess the impact of histologic activity on subsequent endoscopic POR in CD individuals in endoscopic remission following ICR.
Method(s): Adult CD patients who underwent ICR between the years 2009 to 2020 with no active disease (Rutgeerts' i0) on index colonoscopy with biopsies of the neoterminal ileum or anastomosis were included. Those without a follow up after the first endoscopy were excluded. The rate of composite POR, including endoscopic (>=i2b disease), radiologic, surgical, and pharmacologic recurrence (i.e. change in treatment), was compared between patients with histologic activity versus quiescence using chi-square and Kaplan-Meier survival analysis curves. Cox proportional hazard modeling was used to compare histologic activity to high-risk features of surgical recurrence and use of postoperative biologic prophylaxis.
Result(s): There were 79 CD patients (Mean age 34 years, 49.4% ileocolonic disease, 71.2% stricturing, 34.5% >=1 prior ICR, 27.8% active smoking, and 25.3% treated with postoperative biologic prophylaxis) with i0 disease and random endoscopic biopsies after ICR that were included. Overall composite recurrence rate was 58.2% over median follow up of 1242 days. Histologic activity was not associated with composite POR (P=0.49) including endoscopic (P=0.50), radiologic (0.99), surgical (0.78), or pharmacologic recurrences (Biologic: P=0.59; Immunomodulator: P=0.99; Steroid POR: P=0.54). Composite POR was not significantly different by histologic activity group (P=0.29) (Figure 1). Adjusting for high risk predictive factors of POR, histologic activity was not associated with composite POR (HR 1.71 (0.92-3.21); P=0.09). While active smoking was significantly associated (HR 2.29 (1.11-4.72); P=0.025) with composite POR, postoperative biologic prophylaxis was protective (HR 0.41 (0.20-0.81); P=0.01) (Table 1).
Conclusion(s): Histologic activity in endoscopically normal exam is not associated with endoscopic, radiologic, surgical, and pharmacologic postoperative recurrences. Future studies are required to assess the utility of endoscopic biopsies in CD patients with i0 disease to better guide the management of postoperative CD