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Dive into the research topics where Jeremiah J. Levine is active.

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Featured researches published by Jeremiah J. Levine.


Journal of Pediatric Gastroenterology and Nutrition | 2007

Wireless capsule endoscopy in the pediatric age group : Experience and complications

Libia Moy; Jeremiah J. Levine

Background: The development of wireless capsule endoscopy (CE) provides a unique opportunity to visualize the entire small bowel in a minimally invasive manner. Studies in adult patients have demonstrated that the disposable capsule is well tolerated and highly effective, but few studies have been done in children. The aims of our study were to compare the diagnostic yield of CE and small bowel series in children being evaluated for possible small intestine disease and to determine the risk of developing an adverse event following capsule endoscopy. Patients and Methods: We retrospectively reviewed the records of all children who underwent CE at 1 institution between August 2002 and July 2005. Results of CE were compared with those of small bowel radiographic studies when available. Results: There were 46 CE studies from 45 patients, 28 male and 17 female, with a mean age of 14.9 ± 3.6 years and mean weight of 49.7 ± 17.5 kg. The indications for CE included unresponsive Crohn disease (n = 16), possible intestinal polyps (n = 11), unexplained iron deficiency anemia (n = 7), growth failure (n = 5), unresponsive ulcerative colitis (n = 3), persistent abdominal pain (n = 1), protein-losing enteropathy (n = 1), and allergic enteropathy with occult gastrointestinal bleeding (n = 1). Of the 46 CE studies, 41 were completed and 5 were incomplete studies. Based on the CE, 9 patients were newly diagnosed with Crohn disease, 9 patients with Crohn disease were newly diagnosed with small bowel involvement, 8 patients had upper intestinal polyps, 1 patient had findings consistent with Ménétrièr disease, and 1 had a duodenal ulcer. Thirty-three patients had small bowel series before CE: 24 studies were normal, 6 had abnormal thickening of the small bowel, 2 had polyps, and 1 patient had antral narrowing. All 9 patients with abnormal small bowel series had abnormal CE studies. Of the 24 patients with normal small bowel series, 20 had completed CE studies, and in 10 children, the study was abnormal. Nine of the 45 subjects had adverse events. Five patients had delayed passage from the stomach, with 2 needing endoscopic retrieval of the CE, and 4 had delayed passage from the small intestine (>5 days), with 2 requiring surgical removal, 1 responding to steroids, and the final patient requiring an ileocolic resection 2 months after the CE for an undiagnosed ileal stricture. The only significant association noted was that older patients were more likely to have intestinal retention. Conclusions: CE provides a valuable tool in the evaluation of pediatric patients for possible small bowel disease. However, the risk of developing complications appears to be greater in the pediatric population, with 20% of our patients having an adverse event.


Journal of Pediatric Gastroenterology and Nutrition | 2007

Failure to respond to hepatitis B vaccine in children with celiac disease

Seung-Dae Park; James Markowitz; Michael J. Pettei; Toba Weinstein; Cristina P Sison; Steven R Swiss; Jeremiah J. Levine

Objectives: To determine whether children with celiac disease (CD) fail to show a response to hepatitis B virus (HBV) vaccine more frequently than children without CD. Patients and Methods: This was a prospective study that compared the response to HBV, tetanus, rubella, and Haemophilus influenzae type b (Hib) vaccines between children with CD and age- and sex-matched control subjects. Results: The study population included 26 patients with CD and 18 age- and sex-matched controls. All had received the full complement of childhood vaccinations. A significantly higher proportion of subjects in the CD group (14 of 26) failed to respond to HBV vaccine compared with controls (2 of 18; 53.9% vs 11.1%; P < 0.05). Patients with CD were 8.33 times more likely to test negative for hepatitis B surface antigen than control subjects (95% CI, 1.5–46.5). By contrast, all of the subjects in both groups tested positive for rubella antibodies; only 1 subject in the CD group tested negative for tetanus antibody versus none in the control group (3.9% vs 0%; P = 1.0). The percentage of subjects who tested negative for Hib antibodies was similar in the 2 groups (CD, 33.3%; control, 44.4%; P = 0.53). Conclusions: More than 50% of children with CD do not show a response to standard vaccination regimens for HBV. Given the large number of children with CD throughout the world, this observation suggests that there is a large HBV-susceptible population despite widespread vaccination. Current immunization strategies may need to be reassessed to protect this population and achieve the goal of universal protection.


Journal of Pediatric Gastroenterology and Nutrition | 2011

Pediatric inflammatory bowel disease and imaging-related radiation: are we increasing the likelihood of malignancy?

Yonathan Fuchs; James Markowitz; Toba Weinstein; Nina Kohn; Jeanne Choi-Rosen; Jeremiah J. Levine

Background and Aims: Increasing use of diagnostic radiography has led to concern about the malignant potential of ionizing radiation. We aimed to quantify the cumulative effective dose (CED) from diagnostic medical imaging in children with inflammatory bowel disease (IBD) and to identify which children are at greatest risk for high amounts of image-related radiation exposure. Patients and Methods: A retrospective chart review of pediatric IBD patients seen between January 1 and May 30, 2008 was conducted. The effective dose of radiation received from all of the radiology tests performed during the course of each patients treatment was estimated using typical effective doses and our institutions computed tomography dose index. A CED ≥50 mSv was considered high. Results: Complete records were available for 257 of 372 screened subjects. One hundred seventy-one had Crohn disease (CD) and 86 had ulcerative colitis (UC). The mean CED was 17.56 ± 15.91 mSv and was greater for children with CD than for those with UC (20.5 ± 17.5 vs 11.7 ± 9.9 mSv, P < 0.0001). Fifteen children (5.8%) had a CED ≥50 mSv, including 14 of 171 (8.2%) with CD and 1 of 86 (1.2%) with UC (P = 0.02). In children with CD, factors associated with high CED per multivariate analysis were any IBD-related surgery (odds ratio 42, 95% confidence interval 8–223, P < 0.0001) and platelet count (odds ratio 16, 95% confidence interval 1.5–175, P = 0.02). Conclusions: Although all doses of ionizing radiation have some malignancy-inducing potential, a small but important percentage of children with IBD are exposed to particularly high doses of ionizing radiation from diagnostic tests and procedures. Physicians caring for such patients must seek to limit radiation exposure whenever possible to lessen the lifetime risk of malignancy.


Journal of Pediatric Gastroenterology and Nutrition | 1998

Nitric oxide and inflammatory bowel disease: evidence for local intestinal production in children with active colonic disease.

Jeremiah J. Levine; Michael J. Pettei; Elsa Valderrama; David M. Gold; Bradley H. Kessler; Howard Trachtman

BACKGROUND Active colitis in patients with inflammatory bowel disease is associated with mucosal vasodilation, increased intestinal permeability and abnormal colonic motility. Nitric oxide is a messenger molecule with many functions, including regulation of local blood flow, vasomotor tone, and inflammation. Increased nitric oxide production and inducible nitric oxide synthase activity have been demonstrated in experimental models of colitis. This study was designed to determine the relationship between nitric oxide production and colonic inflammation in children with active colitis and in control subjects and whether expression of inducible nitric oxide synthase protein is demonstrable in the intestinal epithelium of these patients. METHODS Nitrate + nitrite were measured in urine, stool, and plasma using the Griess assay. Expression of inducible nitric oxide synthase protein in intestinal tissue was determined by immunohistochemical localization. RESULTS Urinary nitrate + nitrite levels were not significantly different in patients and control subjects. In contrast, stool and plasma nitrate + nitrite concentrations were significantly higher in children with inflammatory bowel disease compared with levels in control children (stool: 162.4 +/- 31.0 mumol/l versus 77.2 +/- 22.1 mumol/l; plasma: 65.2 +/- 9.9 mumol/l versus 38.1 +/- 6.6 mumol/L; p < 0.05). Stool nitrate + nitrite levels significantly correlated with plasma values. Immunohistochemical staining of colonic tissue from children with inflammatory bowel disease demonstrated inducible nitric oxide synthase protein located exclusively in epithelial cells. CONCLUSION Increased nitric oxide production and enhanced intestinal epithelial cell expression of inducible nitric oxide synthase protein are associated with active colonic inflammation.


Pediatric Transplantation | 2006

Capsule endoscopy as a diagnostic tool in the evaluation of graft-vs.-host disease.

Ari Silbermintz; Indira Sahdev; Libia Moy; Adrianna Vlachos; Jeffrey M. Lipton; Jeremiah J. Levine

Abstract:  Capsule endoscopy is a relatively new technology that has allowed gastroenterologists to visualize the mucosa of the small intestine. This technology is playing an expanding role in both adult and pediatric gastroenterology. In this report, we present an 8‐yr‐old child following allogeneic hematopoietic cell transplantation who developed large volume bloody diarrhea requiring multiple packed red blood cell transfusions that was resistant to aggressive therapy for GVHD. The capsule endoscopy performed on this patient provided significant information not provided by upper endoscopy and colonoscopy that allowed for successful treatment changes. This case demonstrates that capsule endoscopy is a diagnostic tool that may play an important role in the assessment of patients, including children, with possible GVHD.


Journal of Pediatric Gastroenterology and Nutrition | 2009

Capsule endoscopy in the evaluation of patients with unexplained growth failure.

Libia Moy; Jeremiah J. Levine

Background: Poor weight gain and growth can be caused by many medical, nutritional, behavioral, and psychological factors. Crohn disease is one of the more common gastrointestinal etiologies associated with growth failure. The aim of this study is to determine the role of capsule endoscopy (CE) in the evaluation of older children and adolescents who were referred to a pediatric gastroenterology service for a chief complaint of unexplained growth failure. Patients and Methods: We retrospectively reviewed the records of children with growth failure undergoing CE between August 2002 and November 2005. Height and weight (expressed as z scores) were recorded at least 6 months before study, at the time of the study, and at least 6 months poststudy. All of the patients had celiac disease and Crohn disease excluded using standard biochemical, radiologic, endoscopic, and histologic assessment. Results: Seven children (4 males and 3 females) were included in the study—mean age 11.7 ± 3.6 years. Indications for CE were growth failure associated with abdominal pain (3 patients), diarrhea and apthous ulcers (2 patients), delayed puberty (1 patient), or a family history of Crohn disease (1 patient). The mean z score for weight at the time of the study was −2.10 ± 1.0 and for height was −1.50 ± 0.7 All 7 children had normal small bowel series performed before the CE. All had both endoscopically and histologically normal esophagogastroduodenoscopy and colonoscopy. In 4 of 7 patients, multiple small bowel apthous ulcerations consistent with Crohn disease were identified by CE. All 4 patients who had abnormal CE were treated and started gaining weight. The mean z score for weight after 6 months of treatment was −1.35 ± 1.2 and for height was −0.50 ± 1.7. The mean z score for weight after treatment was significantly improved compared with the mean z score at diagnosis (P < 0.05). Conclusions: In our study, 4 of the 7 older children and adolescents with unexplained growth failure and normal small bowel series were found to have Crohn disease involving the small intestine. In addition, we were able to show the improvement on the mean z score for weight after treatment of small bowel Crohn disease was instituted.


Journal of Pediatric Gastroenterology and Nutrition | 2008

Polymorphisms in the tumor necrosis factor/lipopolysaccharides pathway in Crohn disease in the Jewish Ashkenazi population.

Ari Silbermintz; Jeremiah J. Levine; Toba Weinstein; Jack Silver

Objective: Tumor necrosis factor (TNF)-α plays a role in the inflammatory process in Crohn disease, a disease with an apparent polygenic basis. We investigated whether polymorphisms in multiple genes involved in the lipopolysaccharide–TNF inflammatory pathway are independently associated with Crohn disease in the Jewish Ashkenazi population. Polymorphisms in CD14, Toll-like receptor 4 (TLR4), and TNF-α were studied. In addition, we investigated polymorphisms in the TNF-α converting enzyme (TACE) gene, which to date has not been studied for an association with Crohn disease. Patients and Methods: To examine whether TLR4 Asp299Gly, CD14-260C/T, TNF-1031T/C, TNF-863C/A, TNF-857C/T, TACE-172C/T, and TACE-154C/A polymorphisms are associated with Crohn disease in the Ashkenazi Jewish population, we analyzed families with at least 1 child with Crohn disease for association with these mutations using a family-based association test (transmission disequilibrium test) for analysis. Results: The allelic frequency in the patient population of TLR4 G allele was 8.0%, CD14 T allele was 51.3%, TNF-1031C was 18.8%, TNF-863A was 14.2%, TNF-857T was 25.2%, TACE172T was 20.7%, and TACE154A was 24.5%. The transmission disequilibrium test transmitted:untransmitted (T:U) result for TLR4G was T:U = 32:20, for CD14T was T:U = 103:88, for TNF-1031C was T:U = 48:56, for TNF-863A was T:U = 39:42, for TNF-857T was T:U = 63:62, for TACE-172C/T was T:U = 48:59, and for TACE-154C/A was T:U = 52:55. No statistically significant associations were observed. Conclusions: The transmission disequilibrium test did not demonstrate preferential transmission of these variants in Jewish Ashkenazi patients with Crohn disease. These results suggest that these polymorphisms in the TNF/lipopolysaccharide pathway play little or no role in susceptibility to Crohn disease in the Jewish Ashkenazi population.


Pancreas | 2012

Combination of CFTR gene mutation and autoimmune pancreatitis presenting as necrotizing pancreatitis.

Henna Patel; Jeremiah J. Levine; Toba Weinstein

To the Editor: Pancreatitis associated with decreased cystic fibrosis transmembrane conductance regulator (CFTR) function and autoimmune pancreatitis (AIP) are two separate and rare conditions that cause acute and chronic pancreatitis in the pediatric population.1,2 Autoimmune pancreatitis is an uncommon cause of chronic pancreatitis in children, typically presenting with relatively mild symptoms with an autoimmune association. There are multiple genetic etiologies associated with pancreatitis, including CFTR gene mutations. The CFTR gene mutations have never been confirmed to be related to the degree or intensity of the symptoms of pancreatitis, although some have been linked with the disease. Identifying gene mutations may help recognize those patients who are at risk of developing recurrent and severe pancreatitis. We report the first case of a child who presented with necrotizing pancreatitis found to have a CFTR gene mutation and features of AIP. A 13-year-old boy presented with acute epigastric pain, fever, and vomiting. On physical examination, the patient was febrile with a distended abdomen and marked epigastric tenderness. He had an elevated white blood cell count (neutrophil predominant). Serum amylase and lipase were 858 U/L (25Y123 U/L) and 2528 U/L (7Y60 U/L), respectively. The patient had a pleural effusion on chest radiography. The abdominal ultrasound showed moderate ascites with a well-distended gallbladder, no gallstones, and no gallbladder wall thickening. The pancreas appeared enlarged and heterogeneous, with septations and debris, suggestive of pancreatitis with an infectious component. There was no family history of pancreatic disease or cystic fibrosis (CF). Computed tomographic (CT) scan and magnetic resonance imaging findings showed an abnormal pancreas with severe phlegmon and suggestion of necrotic tissue. The patient was diagnosed as having necrotizing pancreatitis, and by the eighth hospital day, the patient had clinically improved. Dietary restrictions were modified, and he was advanced to a low-fat diet and discharged home. Genetic testing revealed a heterozygous presence of R75Q variant CFTR gene. Despite compliance with a low-fat diet and use of pancreatic enzyme replacement, the patient had eight hospitalizations for pancreatitis during the next 3 years, which prompted further investigation. Endoscopic retrograde cholangiopancreatography showed a small and fibrotic major papilla, a stricture in the supra-ampullary portion of the pancreatic duct, but no pancreatic divisum. The patient had a positive antinuclear antibody and an IgG4 level of 332 mg/dL (normal range, 0.3Y 111.0 mg/dL). The diagnosis of AIP was made based on these findings. The patient and his family refused a pancreatic biopsy. Steroid therapywasdiscussed,however,not instituted because the patient was responsive to conservative medical management. The AIP is correlated with specific clinical, laboratory, radiographic, and histopathologic findings. Clinical findings consist of obstructive jaundice, weight loss, abdominal pain, nausea, and vomiting. Radiographic findings supporting the diagnosis of AIP include magnetic resonance imaging or CT scans showing a diffuse sausage-shaped enlargement of the pancreas.6 An irregular narrow pancreatic duct and/or multiple strictures without upstream ductal dilatation on pancreatic imaging are suggestive of AIP. In our patient, the initial CT scan revealed phlegmon and necrotic changes but did not visualize the pancreatic duct, leading to the diagnosis of necrotizing pancreatitis. The subsequent endoscopic retrograde cholangiopancreatography found the pancreatic duct to be difficult to cannulate with a stricture in the supra-ampullary portion without ductal dilation. Based on these findings, serological testing for AIP was obtained. Elevated levels of IgG4 are felt to be the best markers of AIP, with a sensitivity of 73.3% and a specificity of 95.1%. Despite lack of histology and the decision to hold on systemic steroid therapy, given the clinical, radiographic, and laboratory findings, our patient met the criteria for AIP based on the criteria stated by the Japanese Pancreas Society. In children, CF associated with CFTR gene mutations is the most common cause of chronic and recurrent pancreatitis. A recent study of pancreatic-sufficient CF patients determined that patients with genotypes associated with mild phenotypic effects (at least one CFTR mutation) had a greater risk of developing pancreatitis than patients with more severe phenotypes. The CFTR gene, R75Q, found in our patient was tested as a part of a multicenter study. Patients with a combined mutation in both SPINK-1 and CFTR R75Q were found to have a higher risk of pancreatitis. The conclusions drawn from this study were that the combination of a CFTR gene R75Q and SPINK-1 mutation increases the risk of chronic pancreatitis in a multiplicative manner.13 One could speculate from this study that the presence of the CFTR R75Q gene may carry a more significant and severe risk of pancreatitis in the setting of other risk factors or underlying etiologies, such as hereditary pancreatitis, pancreatic duct divisum, or AIP. In our patient with AIP, the presence of the CFTR gene mutation leads us to believe the severity of our patient’s attacks, specifically, the development of necrotizing pancreatitis, is a result of this combination.


Journal of Pediatric Gastroenterology and Nutrition | 1997

FOLLOW UP EXPERIENCE IN PEDIATRIC LIVER TRANSPLANTATION IN AN ACADEMIC, NON-TRANSPLANT BASED GASTROENTEROLOGY GROUP: 143

Bradley H. Kessler; Dave Gold; Toba Weinstein; Jeremiah J. Levine; Michael J. Pettei

As pediatric liver transplantation has become relatively common since the early 1980s, most long-term follow-up care has shifted from transplant centers to the pediatric gastroenterologists at referring institutions. We reviewed our experience with 16 patients who have undergone liver transplantation at eight institutions from 1987 to 1996. Our initial follow-up visit took place at an average 4.1 months after the transplant. The mean duration of follow-up was 41 months. During this period 11 hospitalizations at the transplant center occured, including five that were to rule out lymphoma or post-transplant lymphoproliferative disease. At the Schneider Childrens Hospital, NY, USA, 158 outpatient visits were recorded. Forty-two hospitalizations occurred. Twenty of the hospital admissions were accounted for by two patients. Forty-nine outpatient/inpatient surgical or diagnostic procedures were performed, including 15 percutaneous liver biopsies. In only one biopsy was there a disagreement in the histologic diagnosis between our pathologist and the pathologist at the transplant center. In conclusion, comprehensive follow-up care can be provided by an academic hospital-based gastroenterology group in conjunction with a transplant center.


Pediatric Pulmonology | 2018

Airway and esophageal eosinophils in children with severe uncontrolled asthma

Jessica Erkman; Allen Vaynblat; Kristen Thomas; Leopoldo N. Segal; Jeremiah J. Levine; Libia Moy; Melanie K. Greifer; Robert Giusti; Rasik Shah; Mikhail Kazachkov

Children with severe uncontrolled asthma (SUA) have a high burden of symptoms and increased frequency of asthma exacerbations. Reflux esophagitis and eosinophilic esophagitis are important co‐morbid factors for SUA. Both are associated with the presence of eosinophils in esophageal mucosa. We hypothesized that esophageal eosinophils are frequently present and correlate with the presence of airway eosinophils in children with SUA.

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Dive into the Jeremiah J. Levine's collaboration.

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Toba Weinstein

Albert Einstein College of Medicine

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Michael J. Pettei

Albert Einstein College of Medicine

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David M. Gold

Albert Einstein College of Medicine

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James Markowitz

North Shore-LIJ Health System

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Ninfa Candela

University of Massachusetts Medical School

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Norman T. Ilowite

Albert Einstein College of Medicine

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Howard Trachtman

Boston Children's Hospital

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