Thomas A Ullman

Icahn School of Medicine at Mount Sinai, Borough of Manhattan, New York, United States

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Publications (97)877.71 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Serrated colorectal polyps, which, besides hyperplastic polyps, comprise sessile serrated adenomas/polyps and traditional serrated adenomas, are presumptive precursors of at least 20% of sporadic colorectal carcinomas; however, their significance in patients with inflammatory bowel disease is unclear. We retrospectively evaluated 78 serrated polyps, removed over a 14-year period from 6602 inflammatory bowel disease patients undergoing endoscopic surveillance, with respect to morphologic, clinicopathologic, and molecular features, and compared rates of advanced neoplasia (high-grade dysplasia and carcinoma) development following the index serrated polyp diagnosis to reference inflammatory bowel disease cohorts without serrated polyps. Serrated polyps negative for dysplasia, which morphologically resembled sporadic sessile serrated adenoma/polyps, occurred mainly in females, in the proximal colon, and contained BRAF mutations. Serrated polyps with low-grade dysplasia resembled sporadic traditional serrated adenomas and occurred mainly in males, in the distal colon, and contained KRAS mutations. Serrated polyps indefinite for dysplasia were morphologically heterogeneous, but similar to serrated polyps positive for low-grade dysplasia with respect to male predominance, left-sided location, and KRAS mutation rates. Rates of prevalent neoplasia associated with serrated polyps positive for low-grade dysplasia, indefinite for dysplasia, and negative for dysplasia were 76, 39, and 11%, respectively (P<0.001). Actuarial 10-year rates of incident advanced neoplasia after an initial diagnosis of serrated polyp positive for low-grade dysplasia, indefinite for dysplasia, and negative for dysplasia were 17, 8, and 0%, respectively, the first and last being significantly different (P=0.02) and comparable to those of corresponding reference populations of inflammatory bowel disease patients with and without low-grade dysplasia at baseline, respectively. We conclude that in serrated polyps from inflammatory bowel disease patients, dysplasia grade correlates with morphology, sex, anatomic location, BRAF and KRAS mutation status, prevalent conventional neoplasia, and rates of advanced neoplasia development.Modern Pathology advance online publication, 25 September 2015; doi:10.1038/modpathol.2015.111.
    Modern Pathology 09/2015; DOI:10.1038/modpathol.2015.111 · 6.19 Impact Factor
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    ABSTRACT: Early readmission rates are becoming an integral measure of the quality of care for hospitalized patients with chronic diseases. The incidence and predictors of early readmission in patients with inflammatory bowel disease (IBD) are uncertain. Risk factors for readmission over the first few weeks may differ from those that influence re-hospitalization at later time points. We examined the incidence and predictors of both 30-day and 90-day readmissions among ulcerative colitis (UC) patients. A retrospective, cohort study was performed including all severe UC patients admitted to a tertiary-care hospital between January 2007 and December 2011. All-cause readmissions to the medical or surgical service within 30 and 90 days were recorded to allow the calculation of early readmission rates. We used multiple logistic regression to analyze demographic, hospital-related, general medical and IBD-specific factors as potential risk factors for readmission. There were a total of 229 patients discharged following hospitalization for severe UC. The 30- and 90-day readmission rates were 11.7% and 20.5%, respectively. Forty-seven percent of early readmissions were for colectomy. In the 30-day analysis, only the presence of extensive colitis (odds ratio 3.59; 95% confidence interval [CI] 1.41-9.13) compared with left-sided disease was independently associated with readmission. Extensive colitis (3.09, 95% CI 1.33-7.08), albumin on admission (0.56, 0.31-0.99) and being admitted to a housestaff service (2.87, 95% CI 1.14-6.54), were independent predictors of readmission at 90 days. Early readmission is common in IBD. Independent risk factors for early readmission included extensive colitis, admission albumin, and being admitted to a housestaff service.
    Scandinavian Journal of Gastroenterology 04/2015; 50(9). DOI:10.3109/00365521.2015.1020862 · 2.36 Impact Factor
  • Gastroenterology 04/2015; 148(4):S-184. DOI:10.1016/S0016-5085(15)30613-2 · 16.72 Impact Factor
  • Gastroenterology 04/2015; 148(4):S-449. DOI:10.1016/S0016-5085(15)31511-0 · 16.72 Impact Factor
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    ABSTRACT: Inflammatory bowel disease (IBD) is a chronic condition of the bowel that affects over 1 million people in the United States. The recurring nature of disease makes IBD patients ideal candidates for patient-engaged care that is centered on enhanced self-management and improved doctor-patient communication. In IBD, optimal approaches to management vary for patients with different phenotypes and extent of disease and past surgical history. Hence, a single quality metric cannot define a heterogeneous disease such as IBD, unlike hypertension and diabetes. A more comprehensive assessment may be provided by complementing traditional quality metrics with measures of the patient's quality of life (QOL) through an application like HealthPROMISE. The objective of this pragmatic randomized controlled trial is to determine the impact of the HealthPROMISE app in improving outcomes (quality of care [QOC], QOL, patient adherence, disease control, and resource utilization) as compared to a patient education app. Our hypothesis is that a patient-centric self-monitoring and collaborative decision support platform will lead to sustainable improvement in overall QOL for IBD patients. Participants will be recruited during face-to-face visits and randomized to either an interventional (ie, HealthPROMISE) or control (ie, education app). Patients in the HealthPROMISE arm will be able to update their information and receive disease summary, quality metrics, and a graph showing the trend of QOL (SIBDQ) scores and resource utilization over time. Providers will use the data for collaborative decision making and quality improvement interventions at the point of care. Patients in the control arm will enter data at baseline, during office visits, and at the end of the study but will not receive any decision support (trend of QOL, alert, or dashboard views). Enrollment in the trial will be starting in first quarter of 2015. It is intended that up to 300 patients with IBD will be recruited into the study (with 1:1 allocation ratio). The primary endpoint is number of quality indicators met in HealthPROMISE versus control arm. Secondary endpoints include decrease in number of emergency visits due to IBD, decrease in number of hospitalization due to IBD, change in generic QOL score from baseline, proportion of patients in each group who meet all eligible outpatient quality metrics, and proportion of patients in disease control in each group. In addition, we plan to conduct protocol analysis of intervention patients with adequate HealthPROMISE utilization (more than 6 log-ins with data entry from week 0 through week 52) achieving above mentioned primary and secondary endpoints. HealthPROMISE is a unique cloud-based patient-reported outcome (PRO) and decision support tool that empowers both patients and providers. Patients track their QOL and symptoms, and providers can use the visual data in real time (integrated with electronic health records [EHRs]) to provide better care to their entire patient population. Using pragmatic trial design, we hope to show that IBD patients who participate in their own care and share in decision making have appreciably improved outcomes when compared to patients who do not. NCT02322307; (Archived by WebCite at
    02/2015; 4(1):e23. DOI:10.2196/resprot.4042
  • Gastroenterology 12/2014; 147(6):1189-90. DOI:10.1053/j.gastro.2014.10.030 · 16.72 Impact Factor
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    ABSTRACT: Inflammation during inflammatory bowel disease may alter nutrient availability to adherent mucosal bacteria and impact their metabolic function. Microbial metabolites may regulate intestinal CD4 T-cell homeostasis. We investigated the relationship between inflammation and microbial function by inferred metagenomics of the mucosal microbiota from colonic pinch biopsies of patients with inflammatory bowel disease. Paired pinch biopsy samples of known inflammation states were analyzed from ulcerative colitis (UC) (23), Crohn's disease (CD) (21), and control (24) subjects by 16S ribosomal sequencing, histopathologic assessment, and flow cytometry. PICRUSt was used to generate metagenomic data and derive relative Kyoto Encyclopedia of Genes and Genomes Pathway abundance information. Leukocytes were isolated from paired biopsy samples and analyzed by multicolor flow cytometry. Active inflammation was defined by neutrophil infiltration into the epithelium. Carriage of metabolic pathways in the mucosal microbiota was relatively stable among patients with inflammatory bowel disease, despite large variations in individual bacterial community structures. However, microbial function was significantly altered in inflamed tissue of UC patients, with a reduction in carbohydrate and nucleotide metabolism in favor of increased lipid and amino acid metabolism. These differences were not observed in samples from CD patients. In CD, microbial lipid, carbohydrate, and amino acid metabolism tightly correlated with the frequency of CD4Foxp3 Tregs, whereas in UC, these pathways correlated with the frequency of CD4IL-22 (TH22) cells. Metabolic pathways of the mucosal microbiota in CD do not vary as much as UC with inflammation state, indicating a more systemic perturbation of host-bacteria interactions in CD compared with more localized dysfunction in UC.
    Inflammatory Bowel Diseases 02/2014; 20(4). DOI:10.1097/MIB.0000000000000011 · 4.46 Impact Factor
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    ABSTRACT: Giant inflammatory polyposis (GIP), characterized by mass-like agglomerations of inflammatory polyps, is a rare complication of inflammatory bowel disease (IBD). We reviewed a series of cases of GIP to determine its diagnostic impact on the clinical and pathologic distinction between ulcerative colitis (UC) and colonic Crohn's disease (CD). All colons with GIP resected over a 13-year period were identified prospectively and the corresponding clinical and pathologic records were reviewed. Twelve cases of GIP were identified, accounting for 0.8% of colectomies for IBD during the same time interval. Preoperatively, 6 (50%) patients were diagnosed with UC, 2 (17%) with CD and 4 (33%) with indeterminate colitis (IC). Postoperatively, 6 of the diagnoses (50%) were revised based on strict histopathologic criteria: all 4 diagnoses of IC to UC, one diagnosis of CD to UC, and one diagnosis of UC to CD, for a total of 10 diagnoses of UC (83%) and two of CD (17%). Significantly, 7 of 10 cases with postoperative diagnoses of UC (70%) had Crohn's-like transmural inflammation exclusively within the polyposis segments attributed to fecal entrapment and stasis and accounting for the Crohn's-like clinical complications in these cases. This case series of GIP, the largest reported from a single center, highlights the high rate of Crohn's-like clinical and pathological manifestations of GIP and their potential to confound the accurate classification of patients with IBD. A diagnosis of UC should not be amended to CD based on the findings of the polyposis segment alone.
    Journal of Crohn s and Colitis 12/2013; 8(7). DOI:10.1016/j.crohns.2013.11.027 · 6.23 Impact Factor
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    ABSTRACT: BACKGROUND: The pathogenesis of inflammatory bowel disease (IBD) may be caused by abnormal interactions between the immune system and microbiome. Recent studies using 16S ribosomal sequencing have shown that IBD is associated with dysbiosis of the microbiota. Inflammation may alter nutrient availability to adherent mucosal bacteria and impact their metabolic function. Microbial metabolites may also regulate intestinal CD4+ T cell homeostasis. We investigated the relationship between inflammation and microbial function by inferred metagenomics of the mucosal microbiota from colonic pinch biopsies of IBD patients to characterize differences in microbial metabolic pathways between inflamed and non-inflamed biopsy sites.METHODS: Institutional review board approval was obtained before involving patients in the study. Paired pinch biopsy samples of known inflammation states were analyzed from UC (23), CD (21) and controls (24) by 16S ribosomal sequencing and inferred metagenomics with comparison to pathology results and flow cytometry data. The V4 region of the 16S rRNA gene was amplified and sequenced on a MiSeq sequencer. Sequences were assigned to operational taxonomic units (OTUs) and classified taxonomically according to the Ribosomal Database Project (RDP) for use in taxonomic analysis. PICRUSt was then used with the Greengenes OTU database to generate metagenomic data, and derive relative Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway abundance information. Leukocytes were isolated from paired biopsy samples and activated with PMA/Ionomycin for intracellular cytokine (IL-22, IL-17, IFN-g, IL-4 and TNFa) as well as nuclear antigen (Foxp3) analysis by multi-color flow cytometry on a BD LSRII. Active inflammation was defined by neutrophil infiltration into the epithelium, in the setting of epithelial cell damage.RESULTS: Carriage of metabolic pathways in the mucosal microbiota was relatively stable among IBD patients despite large variations in individual bacterial community structures (Fig. 1). However, microbial function was significantly altered in inflamed tissue of UC patients, with a reduction in carbohydrate and nucleotide metabolism in favor of increased lipid and amino acid metabolism (Fig. 2). These differences were not observed in samples from CD patients. In CD patients, microbial lipid and carbohydrate metabolism was tightly correlated with frequency of CD4+Foxp3+ Tregs, whereas in UC patients lipid and carbohydrate metabolism was correlated with frequency of CD4+IL-22+ (TH22) cells (Fig. 3).CONCLUSIONS: Metabolic pathways of the mucosal microbiota in CD do not vary as much as UC with inflammation state, indicating a more systemic perturbation of host-bacteria interactions in CD compared to more localized dysfunction in UC. The alterations in metabolic pathways correlate specifically with frequency of Tregs during CD, but with TH22 cells during UC. Alterations to metabolic pathways of the mucosal microbiota may affect the production of metabolites that can regulate intestinal CD4+ T cell populations and inflammatory responses of the gut.(C) Crohn's & Colitis Foundation of America, Inc.
    Inflammatory Bowel Diseases 12/2013; 19:S9-S12. DOI:10.1097/01.MIB.0000438566.10388.bc · 4.46 Impact Factor
  • Gut 07/2013; 62(11). DOI:10.1136/gutjnl-2013-305300 · 14.66 Impact Factor
  • Fernando S Velayos · Thomas A Ullman
    Gastroenterology 05/2013; 145(1). DOI:10.1053/j.gastro.2013.05.023 · 16.72 Impact Factor
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    ABSTRACT: T helper type (Th17) cytokines such as interleukin (IL)-17A and IL-22 are important in maintaining mucosal barrier function and may be important in the pathogenesis of inflammatory bowel diseases (IBDs). Here, we analyzed cells from the colon of IBD patients and show that Crohn's disease (CD) patients had significantly elevated numbers of IL-17+, CD4+ cells compared with healthy controls and ulcerative colitis (UC) patients, but these numbers did not vary based on the inflammatory status of the mucosa. By contrast, UC patients had significantly reduced numbers of IL-22+ cells in actively inflamed tissues compared with both normal tissue and healthy controls. There was a selective increase in mono-IL-17-producing cells from the mucosa of UC patients with active inflammation together with increased expression of transforming growth factor (TGF)-β and c-Maf. Increasing concentrations of TGF-β in lamina propria mononuclear cell cultures significantly depleted Th22 cells, whereas anti-TGF-β antibodies increased IL-22 production. When mucosal microbiota was examined, depletion of Th22 cells in actively inflamed tissue was associated with reduced populations of Clostridiales and increased populations of Proteobacteria. These results suggest that increased TGF-β during active inflammation in UC may lead to the loss of Th22 cells in the human intestinal mucosa.Mucosal Immunology advance online publication 22 May 2013; doi:10.1038/mi.2013.31.
    Mucosal Immunology 05/2013; 7(1). DOI:10.1038/mi.2013.31 · 7.37 Impact Factor
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    ABSTRACT: Background: Inflammatory bowel disease (IBD) patients are at increased risk for venous thromboembolism (VTE) compared to the general population. Practice guidelines recommend pharmacologic prophylaxis for IBD inpatients. Aim: Our aim was to determine the rates of pharmacologic VTE prophylaxis in ulcerative colitis (UC) inpatients at a tertiary referral center. We also assessed potential predictors of pharmacologic prophylaxis. Methods: We conducted a retrospective cohort study of 377 UC patients between January 1st, 2007 and December 31st, 2011. The medical record of each patient was examined to determine whether pharmacologic VTE prophylaxis was ordered and administered. We conducted multiple logistic regression to determine predictors of pharmacologic prophylaxis. Results: The overall VTE pharmacologic prophylaxis rate was 67.6%. The rate of patients admitted to the medical service was 57.4% compared to 93.5% for those admitted to surgery. In medical patients who received pharmacologic VTE prophylaxis, 34.0% of ordered doses were not given compared to 17.4% of doses in surgical patients (P < 0.001). In the multiple logistic regression analysis, having an additional VTE risk factor (OR 2.46, 95% CI 1.41–4.30), extensive colitis (OR 2.26, 95% CI 1.32–3.87) or being admitted to a surgical service (OR 12.03, 95% CI 5.29–27.38) was associated with VTE pharmacologic prophylaxis. Conclusions: A substantial proportion of medical patients admitted with UC were not ordered for VTE pharmacologic prophylaxis despite current guidelines. Even in patients who were ordered for pharmacologic prophylaxis, one third of doses were not given. Inappropriate prophylaxis may lead to unnecessary morbidity and mortality.
    Journal of Crohn s and Colitis 05/2013; 7(12). DOI:10.1016/j.crohns.2013.05.002 · 6.23 Impact Factor
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    ABSTRACT: Background: In ulcerative colitis, total proctocolectomy is the treatment of choice for patients with colonic dysplasia or cancer because of the high risk for metachronous neoplasia. It is unknown whether patients with Crohn's disease and colon cancer or dysplasia have a similar risk. Methods: We retrospectively reviewed the charts of 75 patients treated at our center from 2001 to 2011 with Crohn's disease and colon cancer who underwent segmental resection or subtotal colectomy (STC). We then identified the presence or absence of subsequent colon cancer or dysplasia in these patients during the follow-up (0-19 years). Results: Of the 64 patients with colon cancer, 25 had at least 1 metachronous cancer (39%). The mean time to a new cancer was 6.8 years. Eighty-five percent of patients (21/25) were undergoing annual screening colonoscopy. Of the 11 patients with dysplasia, 5 (46%) had a new dysplasia. Mean time to a new dysplastic lesion was 5.0 years. Nineteen of the 47 patients (40%) who had a segmental resection for colon cancer developed metachronous cancer and 6/17 patients (35%) with a STC had metachronous cancer. Two of the 4 patients (50%) with STC for dysplasia (50%) had a new dysplasia and 3/7 patients (43%) with segmental resection had a new dysplasia. There was no significant difference (P = 0.61) between recurrence rates in patients with segmental resection versus STC. Conclusions: The high rate of metachronous colon cancer after surgical resection suggests that total proctocolectomy should be considered. Larger studies are required to determine if the same is true for dysplasia.
    Inflammatory Bowel Diseases 05/2013; 19(9). DOI:10.1097/MIB.0b013e318289c166 · 4.46 Impact Factor
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    ABSTRACT: Introduction: Variation in adherence to management guidelines for inflammatory bowel disease (IBD) suggests variable quality of care. Quality indicators (QIs) can be developed to measure the structure, processes, and outcomes of health care delivery. The RAND/UCLA appropriateness method was used to develop a set of process and outcome QIs to define quality of care for IBD. Methods: Guidelines and position papers for IBD published from 2006 to 2011 were reviewed for potential QIs, which were rated by a multidisciplinary panel. Potential process and outcome QIs were discussed at 3 moderated in-person meetings, with pre-meeting and post-meeting confidential electronic voting. Panelists rated the validity and feasibility of QIs on a 1 through 9 scale; disagreement was assessed using a validated index. QIs rated above 8 were selected for the final set. Results: More than 500 potential process QIs were extracted from guidelines. Following ratings and discussion by the first panel, 35 process QIs were selected for literature review. After the second panel, 10 process QIs were included in the final set. Candidate outcome QIs were then derived from physician, nurse, and patient input and ratings, in addition to outcomes associated with candidate process QIs. None of the top QIs exhibited disagreement. Conclusions: A set of QIs for IBD was developed with expert interpretation of the literature and multidisciplinary input. Outcome QIs focused largely on remission and quality of life, whereas process QIs were aimed at therapeutic optimization and patient safety. Evaluation of these QIs in clinical practice is needed to assess the correlation of performance on process QIs with performance on outcome QIs.
    Inflammatory Bowel Diseases 02/2013; 142(5). DOI:10.1097/mib.0b013e31828278a2 · 4.46 Impact Factor
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    ABSTRACT: Background: The expression and distribution of farnesoid X receptor (FXR) in colitis and colitis-associated neoplasia (CAN) is unknown. We investigated FXR expression in neoplastic and nonneoplastic tissue from ulcerative colitis (UC) patients, with or without primary sclerosing cholangitis (PSC), as well as the role of DNA methylation in FXR expression in colorectal cancer (CRC) cell lines. Methods: Samples from the right (RC) and left (LC) colon of patients with UC, with and without PSC, and with or without CAN, were stained by immunohistochemistry and scored semiquantitatively for nuclear FXR expression. FXR expression was analyzed by western blot and polymerase chain reaction (PCR) in nine different CRC cell lines before and after demethylation with 5-azacytidine. Results: In nondysplastic samples, FXR expression demonstrated a diminishing expression from proximal to distal colon (strong FXR expression: 39% RC samples vs. 14% LC samples; P = 0.007). With moderate-to-severe inflammation, FXR expression was almost always absent or weak in both UC and PSC-UC, regardless of location. With quiescent/mild inflammation, 56% of UC samples in the RC retained strong FXR expression versus 24% of PSC-UC samples (P= 0.017). FXR was absent in 72% of the neoplastic samples, with an inverse association with the grade of dysplasia. FXR expression was absent in all CRC cell lines, in some cases due to DNA methylation. Conclusions: FXR expression is inversely correlated with neoplastic progression and severity of inflammation in UC. Patients with PSC-UC have diminished FXR expression in the proximal colon compared to UC patients. This finding could contribute to the higher risk of proximal neoplasia in PSC patients.
    Inflammatory Bowel Diseases 01/2013; 19(2). DOI:10.1097/MIB.0b013e318286ff2e · 4.46 Impact Factor
  • Inflammatory Bowel Diseases 12/2012; 18:S52. DOI:10.1097/00054725-201212001-00125 · 4.46 Impact Factor
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    ABSTRACT: BACKGROUND & AIMS: Some women with inflammatory bowel disease (IBD) require therapy with tumor necrosis factor (TNF) antagonists during pregnancy. It is not clear whether these drugs are transferred to the fetus, via the placenta, and then cleared, or whether structurally different TNF antagonists have different rates of transfer. METHODS: We studied 31 pregnant women with IBD receiving infliximab (IFX, n=11), adalimumab (ADA, n=10), or certolizumab (CZP, n=10). Serum concentrations of the drugs were measured at birth in the mother, infant, and in cord blood, and then monthly in the infant until the drugs were undetectable. Drug concentrations in the cord and the infant at birth were compared with those of the mother. RESULTS: Concentrations of IFX and ADA, but not CZP, were higher in infants at birth and their cords than in their mothers. The levels of CZP in infants and their cords were <2 μg/ml. The median level of IFX in the cord was 160% that of the mother, the median level of ADA in the cord was 153% that of the mother, and the median level of CZP in the cord was 3.9% that of the mother. IFX and ADA could be detected in the infants for as long as 6 months. No congenital anomalies or serious complications were reported. CONCLUSIONS: The TNF antagonists IFX and ADA are transferred across the placenta and can be detected in infants at birth; the drugs were detected in infants up to 6 months after birth. CZP has the lowest level of placental transfer, based on levels measured in cords and infants at birth, of the drugs tested.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 11/2012; 11(3). DOI:10.1016/j.cgh.2012.11.011 · 7.90 Impact Factor
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    ABSTRACT: : The role of intravenous (IV) cyclosporine in severe Crohn's colitis (CC) is poorly studied. : Our primary aim was to determine the in-hospital colonic resection rate in patients with severe CC who received IV cyclosporine, and the potential predictors of resection among these patients. : An inpatient pharmacy query of all patients who received IV cyclosporine at Mount Sinai Medical Center for 12.5 years after January 1, 1996 was reviewed. Patients with CC or indeterminate colitis favoring Crohn's were included and their medical records were reviewed. Subsequent need for colonic surgery was assessed. A Kaplan-Meier plot with log-rank testing was performed to determine the rate of colonic surgery avoidance. Forward stepwise logistic regression was performed to determine independent predictors of surgery. : Forty-eight patients met our inclusion criteria. Prior thiopurine and anti-tumor necrosis factor (anti-TNF) use was 85% and 69%, respectively. The median follow-up time was 12 months (range, 1 to 60 mo). 12.5% of patients required colonic resection during their admission for IV cyclosporine. Anti-TNF use in the 4 weeks preceding IV cyclosporine was the only predictor of surgery in this setting (P=0.05). The cumulative colonic surgery avoidance rate was 72±13% at 6 months and 59±15% at 12 months. : The use of IV cyclosporine resulted in a low rate of in-hospitalization colonic surgery among CC patients with severe disease, the majority of whom previously failed anti-TNFs and thiopurines.
    Journal of clinical gastroenterology 06/2012; 46(9):764-7. DOI:10.1097/MCG.0b013e31824e14a8 · 3.50 Impact Factor
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    The American Journal of Gastroenterology 06/2012; 107(6):951-2; author reply 952. DOI:10.1038/ajg.2012.73 · 10.76 Impact Factor

Publication Stats

2k Citations
877.71 Total Impact Points


  • 2002–2014
    • Icahn School of Medicine at Mount Sinai
      • • Department of Medicine
      • • Division of Gastroenterology
      • • Department of Surgery
      Borough of Manhattan, New York, United States
  • 2010–2013
    • Mount Sinai Medical Center
      New York City, New York, United States
  • 2009
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
  • 2005
    • Mount Sinai Hospital
      New York, New York, United States