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Ann Flynn

Ann Flynn

· Associate Professor (Clinical)

University of Utah · Gastroenterology & Hepatology

Active 1998–2025

h-index8
Citations493
Papers3621 last 5y
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About

Dr. Ann Flynn is a board-certified gastroenterologist specializing in the diagnosis and management of inflammatory diseases of the gastrointestinal (GI) tract, including Crohn's disease, ulcerative colitis, and microscopic colitis. She completed her medical education at New York Medical College, followed by internal medicine residency at the University of Colorado School of Medicine, and gastroenterology fellowship at Indiana University School of Medicine. Additionally, she completed an advanced fellowship in inflammatory bowel disease at Indiana University. Her clinical interests focus on personalized care for patients with inflammatory bowel disease, women's GI health, shared decision-making discussions, patient education, and assisting patients transitioning from pediatric to adult GI clinics. Dr. Flynn is actively involved in the University of Utah Inflammatory Bowel Disease Program, which participates in IBD Qorus, a national collaboration aimed at improving the quality of IBD care. She serves as the IBD Qorus physician leader for the University of Utah and is a member of several professional organizations, including the American College of Gastroenterology, the American Gastroenterological Association, and the Crohn’s and Colitis Foundation. Her dedication to patient care and her leadership in the field underscore her commitment to advancing treatment and outcomes for individuals with inflammatory bowel diseases.

Research topics

  • Internal medicine
  • Medicine
  • Gastroenterology
  • Intensive care medicine
  • Immunology
  • Operations management
  • Nursing
  • Emergency medicine

Selected publications

  • Treat-to-target of endoscopic remission in patients with inflammatory bowel disease in symptomatic remission on advanced therapies (QUOTIENT): rationale, design and protocol for an open-label, multicentre, pragmatic, randomised controlled trial

    BMJ Open Gastroenterology · 2025-03-01 · 1 citations

    articleOpen access

    INTRODUCTION: Targeted immunomodulators (eg, advanced therapies) effectively achieve symptomatic remission in patients with inflammatory bowel disease (IBD). However, ~25%-50% of patients with IBD achieving symptomatic remission with an advanced therapy may have continued endoscopically/radiologically active bowel inflammation, and it is uncertain whether changing alternative advanced therapies in asymptomatic patients with IBD will reduce bowel inflammation and achieve durable deep remission. METHODS AND ANALYSIS: The QUality Outcomes Treating IBD to Target (QUOTIENT) study is an open-label, multicentre, pragmatic, randomised, controlled trial that aims to compare the efficacy and safety of switching to an alternative advanced therapy targeting endoscopic/radiological remission (treat-to-target) versus continuing the initial, or index, advanced therapy, in asymptomatic patients with IBD with moderate-to-severe endoscopic/radiological bowel inflammation. Enrolment is planned for ~250 participants in Canada/USA, randomised 1:1 to switching to alternative advanced therapy or continuing index advanced therapy, and then followed 104 weeks within routine clinical practice. Patient-reported outcomes measure efficacy and quality of life/treatment burden/safety. Primary endpoint is the time from randomisation to treatment failure. ETHICS AND DISSEMINATION: The study is conducted in compliance with the protocol, ICH Good Clinical Practice, applicable regulatory requirements and appropriate review boards/independent ethics committees (approval numbers: Pro00077486; Pro00061437; STUDY00002062; 22-004171; i22-01269; IRB22-0890; IRB_00154397; 2000032384; SHIRB#2022.095-2; STUDY00007146; MMC#2024-18; REB#125290; 17784; Pro00142214; 20240660-01H), with documented written informed consent. Findings will be disseminated through peer-reviewed journals, scientific presentations, and publicly available Patient-Centered Outcomes Research Institute (PCORI) websites, including lay summaries. The Crohn's & Colitis Foundation Education, Support, and Advocacy Department, and our patient advocacy stakeholder, will develop educational and marketing resources to communicate findings to a broad audience (>250 000 patients/caregivers/healthcare professionals). TRIAL REGISTRATION NUMBER: NCT05230173.

  • <i>TNF</i> promoter hypomethylation is associated with mucosal inflammation in IBD and anti-TNF response

    medRxiv · 2024-02-06

    preprintOpen access

    Abstract Background and aims Inflammatory Bowel Diseases (IBD) are chronic inflammatory conditions influenced heavily by environmental factors. DNA methylation is a form of epigenetic regulation linking environmental stimuli to gene expression changes and inflammation. Here, we investigated how DNA methylation of the TNF promoter differs between inflamed and uninflamed mucosa of IBD patients, including anti-TNF responders and non-responders. Methods We obtained mucosal biopsies from 200 participants (133 IBD and 67 controls) and analyzed TNF promoter methylation using bisulfite sequencing, comparing inflamed with uninflamed segments, in addition to paired inflamed/uninflamed samples from individual patients. We conducted similar analyses on purified intestinal epithelial cells from bowel resections. We also compared TNF methylation levels of inflamed and uninflamed mucosa from a separate cohort of 15 anti-TNF responders and 17 non-responders. Finally, we sequenced DNA methyltransferase genes to identify rare variants in IBD patients and functionally tested them using rescue experiments in a zebrafish genetic model of DNA methylation deficiency. Results TNF promoter methylation levels were decreased in inflamed mucosa of IBD patients and correlated with disease severity. Isolated IECs from inflamed tissue showed proportional decreases in TNF methylation. Anti-TNF non-responders showed lower levels of TNF methylation than responders in uninflamed mucosa. Our sequencing analysis revealed two missense variants in DNMT1 , one of which had reduced function in vivo . Conclusions Our study reveals an association of TNF promoter hypomethylation with mucosal inflammation, suggesting that IBD patients may be particularly sensitive to inflammatory environmental insults affecting DNA methylation. Together, our analyses indicate that TNF promoter methylation analysis may aid in the characterization of IBD status and evaluation of anti-TNF therapy response.

  • TNF Promoter Hypomethylation Is Associated With Mucosal Inflammation in IBD and Anti-TNF Response

    Gastro Hep Advances · 2024-01-01 · 2 citations

    articleOpen access

    Background and Aims: Inflammatory bowel diseases (IBDs) are chronic inflammatory conditions influenced heavily by environmental factors. DNA methylation is a form of epigenetic regulation linking environmental stimuli to gene expression changes and inflammation. Here, we investigated how DNA methylation of the tumor necrosis factor (TNF) promoter differs between inflamed and uninflamed mucosa of IBD patients, including anti-TNF responders and nonresponders. Methods: We obtained mucosal biopsies from 200 participants (133 IBDs and 67 controls) and analyzed TNF promoter methylation using bisulfite sequencing, comparing inflamed with uninflamed segments, in addition to paired inflamed/uninflamed samples from individual patients. We conducted similar analyses on purified intestinal epithelial cells from bowel resections. We also compared TNF methylation levels of inflamed and uninflamed mucosa from a separate cohort of 15 anti-TNF responders and 17 nonresponders. Finally, we sequenced DNA methyltransferase genes to identify rare variants in IBD patients and functionally tested them using rescue experiments in a zebrafish genetic model of DNA methylation deficiency. Results: TNF promoter methylation levels were decreased in inflamed mucosa of IBD patients and correlated with disease severity. Isolated intestinal epithelial cells from inflamed tissue showed proportional decreases in TNF methylation. Anti-TNF nonresponders showed lower levels of TNF methylation than responders in uninflamed mucosa. Our sequencing analysis revealed 2 missense variants in DNA methyltransferase 1, 1 of which had reduced function in vivo. Conclusion: Our study reveals an association of TNF promoter hypomethylation with mucosal inflammation, suggesting that IBD patients may be particularly sensitive to inflammatory environmental insults affecting DNA methylation. Together, our analyses indicate that TNF promoter methylation analysis may aid in the characterization of IBD status and evaluation of anti-TNF therapy response.

  • Surgery for Crohn’s Disease Is Associated With a Dysbiotic Microbiome and Metabolome: Results From Two Prospective Cohorts

    Cellular and Molecular Gastroenterology and Hepatology · 2024-01-01 · 14 citations

    articleOpen access

    BACKGROUND & AIMS: Crohn's disease is associated with alterations in the gut microbiome and metabolome described as dysbiosis. We characterized the microbial and metabolic consequences of ileal resection, the most common Crohn's disease surgery. METHODS: H nuclear magnetic resonance spectroscopy. Fecal bile acids and plasma 7α-hydroxy-4-cholesten-3-one (C4) was measured with mass spectrometry. RESULTS: Intestinal resection was associated with reduced alpha diversity and altered beta diversity with increased Proteobacteria and reduced Bacteroidetes and Firmicutes. Surgery was associated with higher representation of genes in the KEGG pathway for ABC transporters and reduction in genes related to bacterial metabolism. Surgery was associated with reduced concentration of the But gene but this did not translate to reduced fecal butyrate concentration. Surgery was associated with decreased abundance of bai operon genes, with increased plasma C4 concentration, increased primary bile acids and reduced secondary bile acids, including isoLCA. Additionally, Egerthella lenta, Adlercreutzia equalofaciens, and Gordonibacter pamelaeae were lower in abundance among patients with prior surgery in both cohorts. CONCLUSIONS: In 2 different populations, prior surgery in Crohn's disease is associated with altered fecal microbiome. Patients who had undergone ileal resection had reduction in the potentially beneficial bacteria E lenta and related actinobacteria and secondary bile acids, including isoLCA, suggesting that these could be biomarkers of patients at higher risk for disease progression.

  • Family Planning for Patients With Inflammatory Bowel Disease in the Post-Dobbs Era.

    PubMed · 2024-08-01

    articleOpen access

    Federal protections for abortion care in the United States ended in June 2022. For people with inflammatory bowel disease (IBD) who are capable of pregnancy, the implications of an unwanted or mistimed conception, particularly in the setting of active disease flares or teratogenic treatment, are precarious and geographically variable. Prioritizing evidence-based and person-centered counseling for preconception health and contraceptive care needs is important during health care visits and not limited to reproductive health providers. Development of multidisciplinary clinics or complex contraception clinics in high-volume IBD centers can support time-sensitive counseling and services for patients. This article reviews reproductive considerations for people with IBD, particularly in the setting of legislative restrictions in the post-Dobbs landscape.

  • Postvaccination Symptoms After a Fourth Dose of mRNA SARS-CoV-2 Vaccination in Patients With Inflammatory Bowel Disease

    Inflammatory Bowel Diseases · 2023-09-29 · 1 citations

    articleOpen access

    Journal Article Corrected proof Postvaccination Symptoms After a Fourth Dose of mRNA SARS-CoV-2 Vaccination in Patients With Inflammatory Bowel Disease Get access Yoo Jin Lee, MD, Yoo Jin Lee, MD F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USADepartment of Internal Medicine, Keimyung University School of Medicine, Daegu, Republic of Korea https://orcid.org/0000-0003-1799-0146 Search for other works by this author on: Oxford Academic PubMed Google Scholar Dalin Li, PhD, Dalin Li, PhD F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Angela Mujukian, MD, Angela Mujukian, MD F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Philip Debbas, BS, Philip Debbas, BS F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Melissa Hampton, BS, Melissa Hampton, BS F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Emebet Mengesha, BS, Emebet Mengesha, BS F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Susan Cheng, MD, MMSc, MPH, Susan Cheng, MD, MMSc, MPH Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Joseph E Ebinger, MD, Joseph E Ebinger, MD Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Michael Chiorean, MD, Michael Chiorean, MD Swedish Medical Group, Seattle, Washington, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Donald Lum, MD, Donald Lum, MD The Oregon Clinic, Portland, Oregon, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar ... Show more Oriana M Damas, MD, Oriana M Damas, MD Division of Gastroenterology, Miller School of Medicine, University of Miami, Miami, Florida, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Jonathan Braun, MD, PhD, Jonathan Braun, MD, PhD F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA https://orcid.org/0000-0003-1646-2974 Search for other works by this author on: Oxford Academic PubMed Google Scholar Dermot P B McGovern, MB, DPhil, Dermot P B McGovern, MB, DPhil F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Gil Y Melmed, MD, MS, Gil Y Melmed, MD, MS F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA Address correspondence to: Gil Y. Melmed, F. Widjaja Inflammatory Bowel Disease Institute, Karsh Division of Gastroenterology and Hepatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA (gil.melmed@cshs.org). https://orcid.org/0000-0002-2591-5165 Search for other works by this author on: Oxford Academic PubMed Google Scholar CORALE-IBD Study Group CORALE-IBD Study Group Search for other works by this author on: Oxford Academic PubMed Google Scholar Inflammatory Bowel Diseases, izad198, https://doi.org/10.1093/ibd/izad198 Published: 29 September 2023 Article history Received: 06 February 2023 Editorial decision: 29 July 2023 Published: 29 September 2023

  • Postvaccination Symptoms After SARS-CoV-2 mRNA Vaccination Among Patients With Inflammatory Bowel Disease: A Prospective, Comparative Study

    Inflammatory Bowel Diseases · 2023-08-09 · 5 citations

    articleOpen access

    BACKGROUND: Vaccine hesitancy is prevalent among people with IBD, in part due to insufficient evidence regarding comparative safety of vaccines in this population. METHODS: We conducted a nationwide comparative study of postvaccination symptoms among those with IBD and health care workers (HCWs) without IBD. Symptom frequency, severity, and duration were measured. Continuous and categorical data were analyzed using Wilcoxon rank-sum and Fisher's exact test. Regression analysis was used to adjust for confounding variables. RESULTS: We had 2910 and 2746 subjects who completed a survey after dose 1 (D1) and dose 2 (D2) respectively (D1: HCW = 933, IBD = 1977; D2: HCW = 884, IBD = 1862). Mean age was 43 years, 67% were female, and 23% were nonwhite; 73% received BNT162b2 (Pfizer) including almost all HCWs and 60% of IBD patients. Most postvaccine symptoms were mild and lasted ≤2 days after both doses in both groups. Health care workers experienced more postvaccination symptoms overall than IBD patients after each dose (D1: 57% vs 35%, P < .001; D2: 73% vs 50%, P < .001). Gastrointestinal symptoms were noted in IBD more frequently after D1 (5.5% vs 3%, P = .003) but not after D2 (10% vs 13%, P = .07). Inflammatory bowel disease subjects who received mRNA-1273 (Moderna) reported more overall symptoms compared with BNT162b2 (57% vs 46%, P < .001) including gastrointestinal symptoms (12% vs 8%, P = .002) after D2. CONCLUSIONS: People with IBD had fewer postvaccination symptoms following the first 2 doses of SARS-CoV-2 mRNA vaccines than HCWs. Among those with symptoms, most symptoms were mild and of short duration.

  • S1202 Reversal of Anti-Tumor Necrosis Factor Drug Antibodies in Response to Drug Escalation and/or Immunomodulator Addition Is More Successful with Infliximab Than Adalimumab

    The American Journal of Gastroenterology · 2023-10-01

    article

    Introduction: Formation of antidrug antibodies (ADA) against anti-tumor necrosis factor α (TNF) drugs is a major cause of loss of response in inflammatory bowel disease (IBD) treatment. Salvage strategies to continue the same anti-TNF drug after development of ADA include dose escalation, addition of an immunomodulator (IMM, e.g., methotrexate or azathioprine), or both (a dual strategy). IMM addition has been found to successfully reverse ADAs in small studies. This study compares the efficacy of these ADA reversal strategies when used in patients treated with infliximab vs adalimumab. Methods: We reviewed the case records of our IBD patients who had developed ADAs to infliximab or adalimumab and were subsequently treated with different salvage strategies, including anti-TNF escalation (increase in either dose, frequency, or both), immunomodulator addition, or both. The primary outcome was ADA reversal (undetectable ADA). A secondary outcome was the change in anti-TNF drug level. Both the patient’s original anti-TNF drug and the salvage strategy used were then correlated to the primary and secondary outcomes. Results: 20 patients were identified. 15 patients had Crohn’s disease and 5 had ulcerative colitis. The median duration of anti-TNF therapy before ADA discovery was 10 months. At the time of ADA discovery, 12 patients were on infliximab; 3 patients underwent anti-TNF dose escalation, 2 had an IMM added, and 7 had both anti-TNF escalation and IMM addition. 8 patients were on adalimumab; 2 patients had anti-TNF therapy escalated, 1 had an IMM added, and 5 had a dual strategy. The overall ADA reversal rate was 80% (Table 1). Overall, antibody reversal was higher for patients on infliximab compared to adalimumab (100% vs 50%, respectively; P= 0.014). Sensitivity analysis comparing patients who received the dual strategy showed greater antibody reversal for patients on infliximab compared to adalimumab (100% vs 20%, P= 0.010). Anti-TNF drug levels increased significantly for patients treated with the dual salvage strategy and trended towards higher levels for patients treated with anti-TNF drug escalation or IMM addition alone (Figure 1). Conclusion: Salvage strategies including anti-TNF dose escalation, immunomodulator addition, or a dual strategy, are effective in ADA reversal. A dual strategy significantly increases anti-TNF drug level. Fewer patients on adalimumab had successful ADA reversal compared to patients on infliximab, suggesting ADA reversal is more successful with infliximab.Figure 1.: Drug levels of (A) infliximab and (B) adalimumab before and after salvage therapy by anti-TNF drug escalation, immunomodulator (IMM) addition, or a dual strategy of both anti-TNF drug escalation and IMM addition. Both infliximab and adalimumab levels increased significantly with the dual strategy and trended towards a significant increase with anti-TNF drug escalation or IMM addition. Table 1. - Patient characteristics at time of development of antibodies to anti-tumor necrosis factor drugs and subsequent anti-drug antibody (ADA) resolution to various salvage strategies including dose escalation and/or immunomodulator (IMM) addition Infliximab escalation alone (n=3) IMM addition while on stable infliximab (n=2) Infliximab escalation + IMM addition (n=7) Adalimumab escalation (n=2) IMM addition while on stable adalimumab (n=1) Adalimumab escalation + IMM addition (n=5) Crohn's disease (n) 3 1 4 2 0 5 Duration of current anti-TNF therapy before ADA discovery (months, mean±s.d.) 43.3 (47.3) 33.5 (28.5) 20.7 (40.7) 50.5 (4.5) 4 (n/a) 12.6 (7.1) Antibody reversal (n, %) 3 (100) 2 (100) 7 (100) 2 (100) 1 (100) 1 (20)

  • S725 linical Utility of Precision-Guided Dosing Tool for Infliximab During Maintenance Therapy of Inflammatory Bowel Disease

    The American Journal of Gastroenterology · 2022-10-01

    article

    Introduction: A precision-guided dosing tool that uses Bayesian data assimilation was developed to forecast Infliximab (IFX) exposure. Our objective was to establish the utility of the tool in clinical decision making during IFX maintenance therapy when used reactively, to address inadequate disease control that results from suboptimal exposure, and proactively, to sustain exposure commensurate with disease remission in inflammatory bowel disease (IBD). Methods: Blood specimens were collected, anytime beyond 20 days after a prior infusion in a prospective study (EMPOWER). Pharmacokinetic (PK) testing was conducted at Prometheus Laboratories (San Diego, CA). Serum IFX, antibodies to IFX (ATI) and albumin concentrations were all imputed with dosing regimen and weight in a Bayesian data assimilation tool to produce individualized PK profiles that forecasted IFX concentration and time to trough concentration below pre-specified thresholds (e.g., < 10 µg/mL). Forecasted exposure at various dosing regimens was also provided. Physician’s global assessment of disease activity was collected with the decision to change IFX dosing that resulted from PK test results. Statistical analysis consisted of Mann-Whitney and Fisher Exact test as appropriate. Results: A total of 111 patients were assessed by 21 physicians. A change in IFX dose regimen was initiated in 51 patients (46%). Inadequate exposure and forecasted IFX levels below 10 µg/mL associated with dose intensification (76%, median IFX 6.3 µg/mL) (p< 0.01), with lower remission rate (23.5%) achieved in that group as compared to two other groups having better disease control and PK profiles (p< 0.001) (Table). Forecasted IFX levels below 10 µg/mL were associated with 4-fold higher likelihood of active disease (OR=4.1; 95%CI: 1.7-9.4) as compared to IFX levels above 10 µg/mL (p< 0.01). Time to trough below 10µg/mL was shorter in active disease (median: 46 days, IQR: 32-59) than in remission (median 57 days, IQR: 48-69) (p< 0.001). As presented in Figure, dose intensification using a 5 mg/kg every 4 weeks dosing regimen forecasted 2.3-fold higher IFX levels as compared to a 10 mg/kg every 8 weeks dosing regimen (median of 17.1 vs 7.4 µg/mL, respectively) (p< 0.001). Similar results were observed among patients presenting with disease remission. Conclusion: Our study suggests that the precision-guided dosing tool provides clinical utility and helps with dose adjustments in both interval changes as well as dose intensification.Figure 1.: Forecasted IFX Exposure at various dose and interdose intervals, given the individual PK parameters Table 1. - Patient Characteristics (n=111), by treatment intervention based on test results Variable IFX Dose RegimenReductionN=17 IFX Dose RegimenContinuationN=60 IFX Dose RegimenIntensificationN=34 OverallPopulationN=111 Patient Characteristics Age (years) 16 (14-19) 32 (18-45) 32 (17-46) 26 (16-44) Female (%, n/N) 44.1% (7/17) 43.3% (26/60) 44.1% (15/34) 43.2% (48/111) CD/UC/Indeterminate 13/3/1 36/15/8 22/9/3 71/27/12 Weight (Kg) 64 (43-76) 71 (61-92) 69 (61-92) 70 (60-84) Dose mg/Kg 10.0 (9.0-10.4) 8.2 (5.0-10.0) 5.5 (5.0-10.0) 8.0 (5.1-10.0) Interdose interval (weeks) 6 (5-8) 8 (6-8) 8 (6-8) 8 (6-8) PGA Remission Status, remission (%, n/N) 70.6% (12/17) 41.7% (25/60) 23.5% (8/34) 40.5% (45/111) Clinical PK Measurements Measured IFX levels (µg/mL) 23.3 (17.2-28.5) 12.9 (7.2-20.6) 8.0 (5.2-14.7) 12.5 (7.2-20.9) ATI status (%, n/N) 0% (0/17) 10.0% (6/60) 11.8% (4/34) 9.0% (10/111) Albumin (g/dL) 4.1 (4.0-4.3) 4.0 (3.6-4.2) 3.9 (3.7-4.2) 4.0 (3.7-4.2) Clearance (L/day) 0.19 (0.15-0.22) 0.27 (0.20-0.33) 0.28 (0.22-0.35) 0.25 (0.19-0.31) Time to Trough < 10 µg/mL (weeks) 11 (10-12) 7 (6-9) 6 (4-7) 7 (6-9) Forecasted Trough (µg/mL) 26.2 (20.1-34.5) 12.7 (8.6-17.6) 6.3 (3.1-9.4) 11.6 (6.5-19.5) Forecasted Trough < 10 µg/mL 0% (0/17) 31.7% (19/60) 76.5% (26/34) 40.5% (45/111)

  • 656: POST-VACCINATION SYMPTOMS AFTER A THIRD DOSE OF SARS-COV-2 MRNA VACCINATION IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE

    Gastroenterology · 2022-05-01

    articleOpen access

Frequent coauthors

  • David Hudesman

    36 shared
  • Sumona Saha

    UW Health University Hospital

    32 shared
  • Meenakshi Bewtra

    University of Pennsylvania

    32 shared
  • Matthew Bohm

    Indiana University School of Medicine

    16 shared
  • Kirk Russ

    University of Alabama at Birmingham

    16 shared
  • Elizabeth Scoville

    Vanderbilt University Medical Center

    16 shared
  • Laura E. Raffals

    Mayo Clinic in Arizona

    16 shared
  • Themistocles Dassopoulos

    Wockhardt (United States)

    16 shared

Education

  • M.D.

    New York Medical College

  • Other, Internal Medicine

    University of Colorado School of Medicine

  • Other, Gastroenterology

    Indiana University School of Medicine

  • Other, Inflammatory Bowel Disease

    Indiana University

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