Peter H. Rubin
Mount Sinai Hospital
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Featured researches published by Peter H. Rubin.
Gastroenterology | 1999
Peter H. Rubin; Sonya Friedman; Noam Harpaz; Eric S. Goldstein; Jeffrey Weiser; Jeremy Schiller; Jerome D. Waye; Daniel H. Present
BACKGROUND & AIMS Adenomatous polyps are by definition dysplastic and pathologically indistinguishable from the dysplasia-associated lesion or mass (DALM) described in 1981. Yet, adenomatous polyps in noncolitic colons are usually removed definitively endoscopically, whereas DALMs are regarded as harbingers of colon cancer, mandating colectomy. METHODS Since 1988, all of our patients with chronic ulcerative or Crohns colitis and dysplastic polyps and no coexistent dysplasia in flat mucosa underwent colonoscopic polypectomy. Biopsy specimens were obtained also adjacent to polypectomy sites, from strictures, and throughout the colon at 10-cm intervals. Follow-up colonoscopies and biopsies were performed within 6 months after polypectomy and yearly thereafter. RESULTS Colonoscopy in 48 patients with chronic colitis (mean duration, 25.4 years) resected 70 polyps (60 in colitic and 10 in noncolitic mucosa). Polyps were detected on screening colonoscopies (29%) and on surveillance (71%). Pathology was tubular adenoma in all polyps from noncolitic mucosa and low-grade dysplasia (57), high-grade dysplasia (2), or carcinoma (1) in polyps from colitic mucosa. Subsequent colonoscopies (mean follow-up, 4.1 years) revealed additional polyps in 48% but no carcinomas. Surgical resection (6 patients) for recurrent polyps confirmed colonoscopic findings. No dysplasia or cancers in flat mucosa were found at surgery or on follow-up colonoscopies. CONCLUSIONS In patients with chronic colitis who have no dysplasia in flat mucosa, colonoscopic resection of dysplastic polyps can be performed effectively, just as in noncolitic colons.
The American Journal of Gastroenterology | 2004
David Norman Moskovitz; Carol Bodian; Mark L. Chapman; James F. Marion; Peter H. Rubin; Ellen Scherl; Daniel H. Present
OBJECTIVES:We reviewed data to investigate the effect of 5-ASA drugs, metronidazole, ciprofloxacin, prednisone, 6-mercaptopurine, azathioprine, and cyclosporine on pregnancy outcomes in patients with inflammatory bowel disease (IBD).METHODS:One hundred and thirteen female patients with a total of 207 documented conceptions were studied. Treatment information included: smoking history (patient and spouse), dates of conception and termination, and outcome of pregnancy (spontaneous abortion, therapeutic abortion, maternal or fetal illness resulting in abortion, premature birth, healthy full-term birth, multiple births, ectopic pregnancy, congenital defects), weight of baby, type of delivery (cesarian section, vaginal), medication history during each trimester (mean dose, maximum dose, frequency). We analyzed the effect on pregnancy outcome of medication use during the first trimester or at any time during the pregnancy.RESULTS:Thirty-nine patients (34.5%) had ulcerative colitis (UC), 73 (64.5%) had crohns disease (CD), and 1 patient (1%) had indeterminate colitis. For 100 of the 207 conceptions, the patients were on 5-ASA drugs at some time during the pregnancy, 49 on prednisone, 101 on an immunomodulator (6-MP/azathioprine), 27 on metronidazole, 18 on ciprofloxacin, and 2 on cyclosporine. In 85 (31%) of the conceptions, patients were on none of these medications. No significant differences were found among the groups in each pregnancy with respect to outcome (p values 0.091 to 0.9). In multivariate analyses controlling for age of mother, there was no evidence that 5-ASA type drugs or any type of drug influenced pregnancy outcome.CONCLUSIONS:In 113 female patients with 207 conceptions none of the drugs used to treat IBD is associated with poor pregnancy outcomes.
Inflammatory Bowel Diseases | 2001
Sonia Friedman; James F. Marion; Ellen Scherl; Peter H. Rubin; Daniel H. Present
BackgroundPyoderma gangrenosum complicates inflammatory bowel disease in 2–3% of patients and often fails to respond to antibiotics, steroids, surgical debridement or even colectomy. MethodsWe performed a retrospective chart analysis of 11 consecutive steroid-refractory pyoderma patients (5 ulcerative colitis, 6 Crohns disease) referred to our practice and then treated with intravenous cyclosporine. Pyoderma gangrenosum was present on the extremities in 10 patients, the face in 2, and stomas in 2. At initiation of intravenous cyclosporine, bowel activity was moderate in 3 patients, mild in 4, and inactive in 4. All patients received intravenous cyclosporine at a dose of 4 mg/kg/d for 7–22 days. They were discharged on oral cyclosporine at a dose of 4–7 mg/kg/d. ResultsAll 11 patients had closure of their pyoderma with a mean time to response of 4.5 days and a mean time to closure of 1.4 months. All seven patients with bowel activity went into remission. Nine patients were able to discontinue steroids, and nine were maintained on 6-mercaptopurine or azathioprine. One patient who could not tolerate 6-mercaptopurine had a recurrence of pyoderma. No patient experienced significant toxicity. ConclusionIntravenous cyclosporine is the treatment of choice for pyoderma gangrenosum refractory to steroids and 6-mercaptopurine should be used as maintenance therapy.
Clinical Gastroenterology and Hepatology | 2008
Sonia Friedman; Peter H. Rubin; Carol Bodian; Noam Harpaz; Daniel H. Present
BACKGROUND & AIMS Since 1980, we have followed 259 patients with chronic Crohns colitis in a prospective colonoscopic surveillance program. Our initial results through August 1998 showed a 22% chance of developing definite dysplasia or cancer by the fourth surveillance examination. We now update the results of all examinations since September 1998 until April 2005. METHODS All patients had at least 7 years of Crohns colitis affecting at least one third of the colon. Patients were recalled every 1 to 2 years or sooner if dysplasia was found. Pathology was classified as normal, dysplasia (indefinite, low-grade [LGD], or high-grade [HGD]), or carcinoma. Lesions were classified as flat, polyp, or mass. RESULTS A total of 1424 examinations were performed on 259 patients. Ninety percent had extensive colitis. The median age at diagnosis was 22 years (range, 2-61 y), and the median disease duration was 18 years (range, 7-49 y). On screening examination, definite dysplasia or cancer was found in 18 patients (7%). Thirteen had LGD, 2 had HGD, and 3 had cancer. On surveillance examinations, a first finding of definite dysplasia or cancer was found in an additional 30 patients (14%). Twenty-two had LGD, 4 had HGD, and 4 had cancer. The cumulative risk of detecting an initial finding of any definite dysplasia or cancer after a negative screening colonoscopy was 25% by the 10th surveillance examination. The cumulative risk of detecting an initial finding of flat HGD or cancer after a negative screening colonoscopy was 7% by the ninth surveillance examination. CONCLUSIONS Periodic surveillance colonoscopy should be part of the routine management of chronic extensive Crohns colitis.
The American Journal of Gastroenterology | 2001
Kimberly Persley; Ellen Scherl; Peter H. Rubin
Avoidance of steroids by the early use of infliximab and 6-mercaptopurine in an adolescent with active Crohns colitis
Gastroenterology | 2008
Juan Luis Mendoza; Melissa Marotta; Ruth Ann Denchy; Asher Kornbluth; Thomas A. Ullman; Lloyd Mayer; Monica Erazo; Sari Feldman; Jane Im; Peter H. Rubin; Simon Lichtiger; Anthony Weiss; James Aisenberg; Kenneth M. Miller; Eric S. Goldstein; Joel J. Bauer; Barry W. Jaffin; Daniel H. Present; Maria T. Abreu; Adele A. Mitchell
ively). Furthermore, IL-17A -197A allele was significantly associated with chronic relapsing phenotype (OR, 2.36; 95%CI, 1.34-4.15; p=0.0028) and steroid-dependent cases (OR, 2.14; 95%CI, 1.03-4.45; p=0.040), whereas IL-17F 7488T allele was associated with chronic continuous phenotype (OR, 2.71; 95%CI, 1.13-6.49; p=0.025). [Conclusion] Our results provided the first evidence that IL-17A and -17F gene polymorphism was significantly associated with the development of UC. IL-17A -197A and -17F 7844T alleles may influence the susceptibility to and pathophysiological features of UC independently.
Gastroenterology | 2003
Andrew P. Francella; Alan Dyan; Carol Bodian; Peter H. Rubin; Mark Chapman; Daniel H. Present
The American Journal of Gastroenterology | 1996
James George; Daniel H. Present; R. Pou; Carol Bodian; Peter H. Rubin
Gastroenterology | 2001
Sonia Friedman; Peter H. Rubin; Carol Bodian; Eric S. Goldstein; Noam Harpaz; Daniel H. Present
Diseases of The Colon & Rectum | 2007
Naris Nilubol; Ellen J. Scherl; David S. Bub; Stephen R. Gorfine; James F. Marion; Michael T. Harris; Asher Kornbluth; Simon Lichtiger; Peter H. Rubin; James George; Mark Chapman; Noam Harpaz; Daniel H. Present; Joel J. Bauer