VIEWS: 12 PAGES: 15 POSTED ON: 8/5/2011
Clinical Vignette Poster Session II Friday, November 13, 2009 12:15pm – 2:15pm Esophagus/Stomach cv 25 IS THERE A ROLE FOR UPPER ENDOSCOPY IN THE EVALUATION OF FAILURE TO THRIVE? Stuart Berezin, Michael S. Halata, Howard E. Bostwick. Pediatrics, NY Medical College, Valhalla, NY Fifteen patients with poor weight gain, 5 months to 2 years of age, were evaluated for failure to thrive due to inadequate caloric intake based on dietary history. All patients had weight for length less than 5% and experienced a significant decrease in weight percentile on the growth curve. None had gastrointestinal symptoms of vomiting, diarrhea, constipation or dysphagia. Evaluation included CBC, total protein, albumin, ALT, AST, BUN, creatinine, T4, TSH and electrolytes. Patients over 10 months had lab testing for celiac disease. Abdominal ultrasound was performed in eight patients and upper gastrointestinal series in four patients. Evaluations were normal for all patients, except for two with positive celiac disease serology. All patients had an upper endoscopy with biopsies of the duodenum, stomach and esophagus. Seven of fifteen patients were under one year of age. Two had biopsy‐confirmed eosinophilic esophagitis (> 100 eosinophils/high power field (HPF)). Two patients had normal appearing endoscopies, but had histological evidence of reflux esophagitis (5‐7 eosinophils/HPF). One patient had a duodenal bulbar ulcer. Two patients had normal endoscopies. Eight of fifteen were over 1 year of age and also had upper endoscopies. One had eosinophilic esophagitis (> 30 eosinophils/HPF). This patient had previously been treated with omeprazole for 2 months. Two patients had biopsy‐proven celiac disease that confirmed their abnormal celiac serology. Five patients had normal endoscopies. In this young population of failure to thrive patients, upper endoscopic examinations with biopsies were useful in obtaining a diagnosis in more than 50% of those examined. Upper endoscopy is therefore a useful evaluation in children under 2 years of age with failure to thrive due to inadequate caloric intake and who do not exhibit overt gastrointestinal symptoms. In children under 1 year of age eosinophilic and reflux esophagitis were the most common diagnosis; in children over one year of age, celiac disease was the most common diagnosis in this patient population. cv 26 ENDOSCOPIC REMOVAL OF A LARGE GASTRIC TRICHOBEZOAR IN A PEDIATRIC PATIENT Ahmet Aybar, Anca M. Safta. Pediatrics, University of Maryland, Baltimore, MD A trichobezoar is an accumulation of swallowed hair in the stomach that fails to pass through the intestines. The incidence is greater among the mentally retarded or emotionally disturbed children. Endoscopic removal is usually not successful and can cause severe complications. Surgical or laparoscopic removal is the preferred method. Many endoscopic techniques have been described for breaking up the trichobezoar. We report a young patient with a large trichobezoar which was removed using hot biopsy forceps and electrocautery snare. A 5 ½ year‐old girl presented to the Pediatric ED with symptoms of small bowel obstruction. Exploratory laparotomy revealed a trichobezoar in the ileum and was removed with resection of the distal ileum. She had persistent nausea and vomiting with poor appetite for 6 weeks. A follow up CT of the abdomen and UGI study confirmed a large residual trichobezoar in the stomach extending through duodenal bulb. Endoscopic removal was attempted to avoid a second operation. Initially, the retrieval of the intact bezoar through the lower esophageal sphincter failed. Subsequently the bezoar was broken into 13 smaller pieces using hot biopsy forceps and snare via ERBE™ and completely removed. After the procedure, mucosal abrasions and small superficial mucosal burns noted in the greater curvature and treated with a course of lansoprazole and sucralfate. She was symptom‐free at follow up. Trichobezoar is a rare condition in which swallowed hair accumulates in the stomach. It is indigestible and slippery in character, can not be propulsed distally and may cause small bowel obstruction. Surgery is recommended for the removal of large bezoars. Endoscopic removal is very seldom successful due to a distal tail extending into small bowel or imbedding of hair in the gastric mucosa. We describe a safe and successful endoscopic removal of a large gastric trichobezoar without immediate complications. To our knowledge this is the first published report in the English literature removing a large trichobezoar endoscopically by cutting into small pieces using electrocautery. cv 27 RELATIONSHIP BETWEEN BMI AND REFLUX ESOPHAGITIS(GERD) IN CHILDREN Radha Nathan, Nidhi Rawal. Pediatrics, Brookdale University Hospital and Medical Center, Brooklyn, NY BACKGROUND: Obesity is a rising public health concern, because of various co‐morbidities. Studies in adults have shown a positive correlation between obesity and GERD. However, data in children have shown conflicting results. AIM: To evaluate the relationship between BMI and GERD in children. METHODS: In a retrospective case control study, we identified patients between ages 3‐18 years, from Jan’06 to Feb’08, with histological evidence of GERD. Charts were reviewed for age, sex, weight, height and symptoms. BMI was calculated and BMI percentiles were obtained using CDC growth charts. We defined overweight as BMI between the 85th and 95th percentiles and obese as >or equal to the 95th percentile. Exclusion criteria included patients with neurological conditions, IBD, prematurity and age<3years. Pediatric patients seen in the Well Child Clinic with no history of reflux symptoms, served as controls. Cases and controls were age and gender matched. Information was obtained for 47 matched pairs. Demographic data were collected. Analysis was performed with STATA software using logistic regression and t test. RESULTS: About 48.9% of cases (GERD +) were overweight/obese compared to 25.7% of controls (GERD ‐). The percentage of overweight and obese children in the control group corresponded closely to the population norm as per the CDC data. When regressed, GERD correlated well with BMI percentiles (OR=1.97, P=0.008) and female gender (OR=2.3, P value=0.026). No statistically significant relationship was found between GERD and age/simple BMI value. CONCLUSION: We report that children with BMI>85%ile have twice the risk of having GERD, as compared to the normal weight population. Prevalence is significantly higher in females. Variables Cases(47)GERD+ Controls(47)GERD‐ Weight(kg) 15.3‐127.8 10.3‐110 2 BMI(kg/m ) 12.6‐48 Mean=24.1±8.06 14‐37.9 Mean=22.04±6.3 BMIpercentiles <85th%ile 85‐95th%ile ‐ 24(51.06%) 8(17.02%)P=0.008 ‐ 35(74.4%) 6(12.7%) >95th%ile 15(31.9%) 6(12.7%) cv 28 ARGON PLASMA COAGULATION FOR TREATMENT OF RADIATION‐INDUCED HEMORRHAGIC GASTRITIS KATTAYOUN KORDY, MD, BRADLEY BARTH, MD, MPH UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER AT DALLAS, CHILDREN’S MEDICAL CENTER Kattayoun Kordy, Bradley Barth. University of Texas Southwestern Medical Center at Dallas, Children's Medical Center Dallas, Dallas, TX Argon plasma coagulation (APC) is a non‐contact, through the scope, monopolar, electrocoagulation technique that has potential benefit in children requiring endoscopic therapy for GI bleeding. It is especially well suited for patients who are at high risk for perforation or with diffuse lesions, including those undergoing chemotherapy. Case Report: We describe a 4 year old boy with history of biliary rhabdomyoscarcoma who recently completed a 5 week course of radiation therapy. He presented with transfusion dependent upper GI bleeding secondary to severe radiation‐induced hemorrhagic gastritis. Several multimodal endoscopic therapies failed to control his chronic GI bleeding, including epinephrine injections and endoscopic clip placement. Due to the diffuse nature of the lesion, APC was applied to 80%‐90% of circumferential bleeding in the antrum with successful achievement of hemostasis. One week follow‐up endoscopy revealed improved gastritis limited to the antrum with some areas of oozing that was again treated with APC. Subsequent follow‐up endoscopy revealed complete resolution of GI bleeding without evidence of ulceration, and a significant drop in transfusion requirement post‐APC treatment. Discussion: To our knowledge, this is the first reported case of APC in the management of GI bleeding secondary to radiation induced hemorrhagic gastritis in a pediatric patient. Data is limited on APC in children with yet unknown long term effects. However, the non‐contact nature of this therapy, along with minimal depth of penetration make it ideally suited for this indication. REFERENCES 1. Kahn K, Scharzenberg S, Sharp H, Weisdorf‐Schindele S. Argon plasma coagulation: Clinical experience in pediatric patients. Gastrointestinal Endoscopy 2003; 57 (1): 110‐112. 2. Watson J, Bennett M, Griffin S, Matthewson K. The tissue effect of argon plasma coagulation on esophageal and gastric mucosa. Gastrointestinal Endoscopy 2000; 52(3):342‐5. cv 29 GASTRIC ADENOCARCINOMA IN A 14 YEAR‐OLD WITH HISTORY OF GIARDIA AND CMV INFECTIONS. Jeffrey H. Ho, Marvin E. Ament. Division of Pediatric GI, Hepatology and Nutrition, UCLA, Los Angeles, CA We describe a case of a 14 year old male with history of chronic abdominal pain and intermittent vomiting since two years of age. Family history is remarkable for members with gastric adenocarcinoma. At age two, patient began vomiting and was reported to have hypoalbuminemia and protein losing enteropathy. Endoscopy was normal but stool studies showed presence of Giardia. At age four, he presented with persistent vomiting. Endoscopy grossly showed antral ulcers. Biopsies showed severe gastritis, intestinal metaplasia and CMV intranuclear inclusions. Immunodeficiency work‐up showed reversal of CD4 and CD8 lymphocytes. He was then treated with Ganciclovir with resolution of symptoms. At age 14, he was evaluated for chronic abdominal pain. Endoscopy showed a friable and necrotic appearing gastric mass arising from mid‐body of the greater curvature. Biopsies showed high grade dysplasia. Patient underwent endoscopic ultrasound and the tumor appeared to penetrate through certain areas of muscularis propria. Patient then underwent subtotal gastrectomy with resection of gastric tumor, regional D2 lymphadenectomy and Roux‐en‐Y gastrojejunostomy. Frozen section analysis showed clear margins and benign reactive lymph nodes. Pathology revealed a 6.2 cm tubular/intestinal type gastric adenocarcinoma that was moderately differentiated. Tumor invaded into superficial submucosa and 76 resected lymph notes were negative for metastatic carcinoma. Tumor was classified as a Stage IA malignancy or T1N0M0. Interestingly, EBV EBER was positive in dysplasia but negative in adjacent normal mucosa. There have been limited studies on standardized treatment protocols for pediatric gastric adenocarcinoma, therefore approach was made to treat our patient as an adult. Patient received adjuvant chemotherapy with 11 courses of 5‐FU over six months. At one year post‐surgery, surveillance endoscopies with biopsies and imaging showed no recurrence of tumor or any evidence of metastatic lesions. cv 30 GASTROCOLIC FISTULA AFTER PERCUTANEOUS ENDOSCOPIC GASTROSTOMY (PEG) PLACEMENT K. Nguyen1, P. De Angelis2, N. Gupta3, A. S. Day3, J. Teitelbaum4, J. Dias5, A. Bautista6, C. Wilson7, R. Gill1, J. Xu1, S. Schwarz1, W. Treem1. 1SUNY Downstate Medical Center, Brooklyn, NY; 2Ospedale Pediatrico Bambino Gesù, Rome, Italy; 3Sydney Children's Hospital, Randwick, NSW, Australia; 4Children's Hospital at Monmouth Medical Center, Long Branch, NJ; 5Hospital de S. João, Porto, Portugal; 6University Hospital Santiago de Compostela, Galicia, Spain; 7Lucille Packard Children's Hospital, Palo Alto, CA Introduction:Gastrocolic fistulas (GCF) are a known complication of PEG placement in children but have only been described in case reports.Aims:We determined signs/symptoms, predisposing factors, natural history, and management strategies for GCF after PEG in a series of children.Methods:A questionnaire was designed and distributed to physicians who cared for pts with GCF after PEG.Each physician performed a retrospective chart review. No specific pt identifiers were provided.Consent waiver was obtained from SUNY Downstate IRB.Results:12 pts were included.7 had cerebral palsy, 3 of whom had scoliosis.7 had previous abdominal surgery.The number of PEGs/year by each physician ranged from < 5 and up to 40.Finger indentation/stomach insufflation alone was used in 11 cases.In 1 case, fluoroscopy was also used.The time from PEG to diagnosis of GCF ranged from <1 wk to >6 mo.The most common symptoms of GCF were feculent vomiting, diarrhea, and weight loss.Diagnosis was made by contrast study in 10, by EGD in 1, and at surgery in 1. GCF spontaneously closed in 4, was surgically closed in 6,and was endoscopically clipped in 1 pt.3 pts had repeat PEG and 7 had G‐tube replacement by surgery.Modifications to PEG after GCF included adoption of safe track technique,fluoroscopy w/transverse colon opacification,reduced stomach insufflation,or increased referrals to interventional radiology.Conclusions:GCF can present in the immediate post‐procedure period and as long as 10 months after PEG.Previous abdominal surgery is a key risk factor for GCF.Surgical closure or spontaneous closure was used in the majority of cases.The varied number of PEGs/year suggests that increased experience with PEG does not necessarily mitigate the risk for the development of GCF. cv 31 COIN RETRIEVAL AND EOSINOPHILIC ESOPHAGITIS Nicole Jordan1, Aeri Moon2. 1Pediatric Gastroenterology, NYPH Weill Cornell Medical Center, NY, NY; 2 Pediatric Gastroenterology, NYPH Weill Medical College of Cornell University, NY, NY Coins are the most commonly ingested foreign body in children, and spontaneous passage occurs in up to a third. Of those lodged in the esophagus, approximately 10‐20% lodge in the mid‐esophagus. Retained esophageal coins occur most often in those who are small or with underlying esophageal pathology. Eosinophilic esophagitis (EE) is a chronic inflammatory condition of the esophagus. Although esophageal food impaction is a fairly common presentation of EE in adolescents, there are no published case reports on non‐food‐related foreign body impactions in children as an initial clinical manifestation of EE. This is the first case report of EE diagnosed in a child who underwent an esophagogastroduodenoscopy (EGD) for retrieval of a coin. Case: A four year‐old healthy male presented to the emergency department after having swallowed a coin the night prior. He was asymptomatic and a chest x‐ray showed a radiopaque foreign body within the esophagus. He underwent an EGD in which a coin was found in the mid‐esophagus. Gross endoscopic inspection noted linear exudates of the esophagus. Three‐level esophageal biopsies were taken and histologically reported as active esophagitis with eosinophilic infiltrates. The patient was placed on Prevacid. A repeat EGD was performed 3 months later which confirmed the diagnosis of EE whereby a swallowed topical steroid was added. Conclusion: In young children, EE is reported to present most often as dysphagia, pain and emesis, and in adolescents, as food impaction requiring endoscopic removal. This is not the first case in our institution where an EGD was performed on a child for coin retrieval in which the child was subsequently diagnosed with EE. This case illustrates two points: 1) presentation of a non‐food‐related foreign body impaction may be the first manifestation of EE in an otherwise normal child without symptoms of dysphagia or food impaction; therefore 2) it should be considered that all children undergoing an EGD for foreign body retrieval have biopsies taken when the foreign body is impacted in the esophagus. cv 32 RAPUNZEL SYNDROME: NOT JUST A FAIRY TALE Ryan K. Brislin1, Samantha Cook1, Bonnie Beaver2, Yoram Elitsur1. 1Pediatrics, Marshall, Huntington, WV; 2 Surgery, Marshall, Huntington, WV Rampion (campanula rapunculus) is a pot‐erb plan, characterized by its long stems and white hair. The plan was the main subject of the Grimms' brothers famous fairy tale, Rapunzel. Rapunzel syndrome was later described as a gastric trichobezoar that extended into the small intestine. Rapunzel syndrome is rarely described in the USA. Case report: A 12 year old female presented with intermittent and sharp abdominal pain with emesis, decreased appetite, early satiety, and weight loss. The patient reported history of trichotillomania, but denies hair swallowing. Physical examination : A diffuse abdominal pain with hyperactive bowel sounds. A mobile firm mass (approx. 15cm x 8cm) in the epigastric region was palpated. Abdominal CT scan showed a gastric bezoar that extended as far as the proximal jejunum and intestinal edema. Initial laboratory investigation showed normal CBC and electrolytes. A prliminary diagnosis of trichobezoar and partial bowel obstruction was made. An upper endoscopy documented the presence of a gastric trichobezoar occupying the entire gastric cavity. The hair was visualized exiting the pylorus and extending beyond the duodenal bulb, suggesting the diagnosis of Rapunzel syndrome. Surgical laparotomy revealed a firm trichobezoar occupying the entire gastric cavity. After removing the gastric portion, the distal portion of the bezoar was located 70 cm beyond the ligament of Treitz, well into the jejunum. A longitudinal incision was made and the removal of the remaining portion of the trichobezoar was performed. As a result of hair entrapment, a partial intestinal obstruction was present and was relieved. The patient tolerated the procedure uneventfully and was discharged at day 6. Surgical follow up was uneventful. The patient was referred for psychiatric evaluation. After few therapeutic sessions the patient was discharged in excellent condition. At 1.5 year post surgery, the patient is asymptomatic and his trichotillomania is under control. Conclusion : Rapunzel syndrome is a rare complication of trichotillomania that requires surgical therapy. cv 33 GASTRIC POLYPS IN MENKES DISEASE ASSOCIATED WITH GASTROINTESTINAL BLEEDING AND OUTLET OBSTRUCTION Melissa Kennedy, Rose Graham. Gastroenterology, Hepatology, and Nutrition, Childrens Hospital of Philadelphia, Philadelphia, PA A 19 month old male with Menkes Disease was admitted to the intensive care unit with metapneumovirus bronchiolitis and pnueomococcal bacteremia. Admission history and laboratory studies revealed severe anemia and a recent history of melena and intermittent hematemesis. The patient was treated with intravenous pantoprazole, antibiotic therapy, and supportive respiratory care. Endoscopy was postponed pending improvement in respiratory status as bleeding was manageable with supportive therapy. One week after admission, the patient developed acute hematemesis. Upper endoscopy revealed a large polypoid mass with numerous large fronds obstructing the pyloric outlet. As this could not be managed endoscopically, the procedure was converted to a surgical case, when the lesion was noted to be emanating from the gastric antrum. Antrectomy with a Bilroth Type 1 reconstruction was performed to surgically remove the mass. Microscopic pathology revealed hyperplastic gastric foveolar epithelium with edema, inflammation and areas of ulceration. Menkes Disease is an X‐linked recessive disorder of impaired copper membrane transport secondary to mutations in the ATP7A gene. Depleted serum copper levels lead to copper dependent enzyme deficiencies causing most of the clinical features of Menkes Disease. Deficiency in lysyl oxidase, a copper dependent enzyme required in the first step of collagen cross linkage, results in connective tissue fragility and predisposition towards mucosal redundancy including polypoid masses in the gastrointestinal tract. Hypertrophic polyp formation is more common at the pyloric outlet which is exposed to persistent localized pressure during peristalsis. These lesions are more prone to bleeding secondary to the underlying vascular abnormalities associated with Menkes Disease. Gastric polyps in Menkes Disease have been reported infrequently in the literature but are likely an underappreciated clinical feature of Menkes and may lead to gastrointestinal bleeding or obstruction. cv 34 17‐YEAR‐OLD IMMUNOCOMPETENT MALE WITH HERPES SIMPLEX VIRUS ESOPHAGITIS; COULD THIS BE PRECIPITATED BY ESOPHAGEAL EOSINOPHILIA? M. Samer Ammar. Pediatric, SIU School of Medicine, Springfield, IL Introduction: Herpes simplex virus (HSV) may cause esophagitis in immunocompromised patients and seldom in immunocompetent ones. In immunocompetent patients, risk factors are yet to be identified. In this patient, follow up histological examination of esophageal biopsies supported the diagnosis of Eosinophilic Esophagitis. Case report: 17‐year‐old male with history of intermittent dysphagia for years, developed odynophagia 2‐3 days before he was evaluated by pediatric gastroenterologist. Mucosal irregularity was seen on the contrast esophogram. Patient underwent an Esophagogastroduodenoscopy (EGD) with biopsies. Grossly, esophageal mucosa appeared thickened with blunted vasculature and whitish, nonwashable adherent materials. Fungal culture of esophageal brushing was negative. Distal esophageal biopsies had extensive ulceration with focal squamous mucosa demonstrating viropathic changes. Proximal esophageal biopsies demonstrated focal findings similar to those in the distal. The immuno stain for HSV was positive in distal and proximal esophageal biopsies confirming the diagnosis of HSV related esophagitis. GMS stain for fungal organisms was negative. Patient was then determined to be immunocompetent. He was treated with proton pump inhibitor and acyclovir, intravenously initially, followed by oral administration with improvement in symptoms. Patient underwent EGD with biopsies about 3.5 weeks and 6 months from the first endoscopic evaluation. The diagnosis of eosinophilic esophagitis was confirmed. Conclusion: HSV may cause esophagitis in immunocompetent patients. Esophageal eosinophilia was the only identifiable risk factor in this patient. Esophageal eosinophilia may be a risk factor for HSV esophagitis. cv 35 CHRONIC COUGH CAN IT BE HELICOBACTER PYLORI Vaibhav Goyal, Rima Jibaly. Pediatrics, Hurley Medical Center, Flint,, MI Chronic cough is defined as cough present for more than 4 weeks.Asthma,allergic rhinitis,foreign body ingestion and sinusitis are few of the common causes of chronic cough.Only one study looked at H.pylori as a possible etiology of chronic cough in adult patients.No similar publication was identified in the literature in the pediatrics age group.We are presenting a child with persistent cough who was found to have H.Pylori gastritis. His symptoms resolved after he was treated for H. Pylori. Case:13 year old child with a history of asthma came to the clinic complaining of cough since past three month.It was affecting his sleep and daily activities.He had been in and out of the asthma clinic where his medications were adjusted with no relief.PPI were added for possible reflux with no improvement.He was referred to the ENT specialist where a direct laryngoscopy showed erythema of larynx. GERD was suspected and he was referred to the GI clinic because of failure of reflux treatment.His chief complaint included cough with no abdominal pain, dyspepsia or vomiting.His exam revealed epigastric tenderness.GI endoscopy was done which showed: decreased vascularity of the oesophagus but no lesions were present.Stomach was erythematous with red streaks especially in the antrum. The esophageal biopsy was normal,but the Gastric antral biopsy revealed gastritis and Helicobacter pyori organisms were identified.Patient was treated with amocixillin and clarithromycin for 2 wks and prevacid for 4 weeks. Cough subsided within next couple of days after starting the treatment. Patient came for follow up one month after treatment and was asymptomatic.His last coughing was before initiating the treatment. Conclusion:Our case supports the possible association between H pylori and persistent cough.It was suggested by Petar Rouev et al that it may be a result of the pro inflammatory nature of the bacteria.The possibility of reflux as contributing to the cough can not be completely ruled out in this patient. We suggest keeping H. pylori in the differential of patients with persistent cough after the common causes have been ruled out. cv 36 ANTRAL POLYPS IN A CHILD WITH HYPOPROTEINEMIA, ANEMIA AND ABDOMINAL PAIN Yilda Alvarado, Iona Monteiro. Pediatrics, UMDNJ‐NJMS, Newark, NJ 12 year old male was initially seen in ‘02 with generalized swelling, abdominal pain and blood‐streaked vomiting. On exam he had macrocephaly and generalized edema. Lab studies showed anemia and hypoproteinemia. Esophagogastroduodenoscopy (EGD) showed few pedunculated antral polyps. Pathology: inflammatory/hamartomatous polyp. Colonoscopy: no polyps. Small bowel series: questionable filling defects. MRI of head was normal. He was lost to follow‐up till ‘09, when he came in with abdominal pain, hypoproteinemia and anemia. EGD revealed marked increase in polyps. Pathology revealed hyperplastic polyps. His pain decreased post polypectomy. Hyperplastic polyps are the commonest polyps in the stomach occuring in either gender and common in the 7th decade of life1. They are small solitary antral lesions, usually asymptomatic but can present with dyspepsia, abdominal pain or gastrointestinal (GI) bleeding and anemia1. Pathogenesis is unknown, but may occur with chronic gastritis ‐ autoimmune or H. pylori2. They can cause GI blood loss in older patients3. Removal of the polyps using endoscopic or surgical methods is required for resolution of the blood loss together with iron therapy3. In children there are very few case reports of hyperplastic polyps causing hypoproteinemia, anemia4 or gastric outlet obstruction5. We feel that this child's pain was likely secondary to obstruction at the pylorus as it improved post polypectomy. 1. Gastric hyperplastic polyps. A Review. R Jain, P Chetty. Dig Dis Sci, Nov 27, 2008 (E pub) 2. Hyperplastic polyps of the stomach: Associations with histologic patterns of gastritis and gastric atrophy. Abraham SC et al. Am J Surg Pathol, April 2001:25 (4) 500‐7 3. Hyperplastic polyps of the gastric antrum in patients with GI blood loss. M. Al‐Haddad et al. Dig Dis Sci. Jan 2007:52 (1):105‐9 4. Juvenile polyposis of the stomach: clinicopathological features and its malignant potential. Hizawa K. et al. J Clin Pathol Sep1997;50(9):771‐4 5. Prolapsed hyperplastic gastric polyp causing gastric outlet obstruction, hypergastrinemia, and hematemesis in an infant. Brooks GS et al. J Pediatr Surg Dec 1992:27(12):1537‐8 cv 37 DELAYED SPONDYLODISCITIS AFTER BUTTON‐BATTERY INGESTION Rupinder K. Gill, J. Amodio*, K. Nguyen, J. Xu, S. Schwarz, W. R. Treem. Pediatric Gastroenterology and Radiology*, Children's Hospital at SUNY Downstate Medical Center, Brooklyn, NY Ingestion of a button‐battery requires immediate endoscopic removal to avoid tissue necrosis, perforation, TE fistula, or death. We report a case complicated by spondylodiscitis, an unusual complication of button‐battery ingestion. Case report: A 14‐mo. old female presented with 4 wk history of persistent cough and a normal physical exam. A CXR revealed a round battery in the mid‐esophagus. The battery was removed by rigid endoscopy with only mild irritation of the esophagus reported. A barium swallow (BS) performed two days later showed a focal area of dilatation in the thoracic esophagus and a scalloped appearance of the posterior wall of the esophagus. There was no evidence of perforation or fistualization. The patient began oral feeds and was discharged home. Six weeks later the patient returned with torticollis but no fever or dysphagia. The CBC was normal with an elevated ESR (76) and CRP (12). MRI of the neck showed spondylodiscitis with erosion of the inferior endplate of T1 and the superior endplate of T2 vertebral bodies; with abnormal contrast enhancement of the T1 and T2 intervertebral disc and prevertebral tissue; and with extension into the posterior wall of the esophagus at the level of the previous button battery. Repeat BS showed a filling defect in the proximal esophagus without evidence of contrast leak. An upper endoscopy revealed a smooth, movable, polypoid lesion. The endoscope was easily passed beyond the lesion into the distal esophagus. Biopsy of the polyp showed granulation tissue. The patient was treated with IV antibiotics for 6 weeks and the torticollis resolved. Blood cultures obtained prior to IV antibiotics were negative and ESR and CRP returned to normal with treatment. Conclusion: We present a case of button‐battery ingestion complicated by spondylodiscitis 6 weeks later in the absence of esophageal necrosis, perforation, or fistualization at the time of battery removal. The onset of torticollis weeks after removal of a button battery should prompt imaging for this complication. cv 38 RECURRENCE OF RAPUNZEL SYNDROME Sheela Raikar1, Prateek Wali2, Seema Khan2,1. 1Pediatrics, Thomas Jefferson University, Philadelphia, PA; 2 Pediatric Gastroenterology, Alfred I. duPont Hospital for Children, Wilmington, DE We report a case of a 12‐year‐old girl presenting with a three day history of severe, intermittent abdominal pain and vomiting. The pain was localized to the epigastric area. It was worse with meals and ambulation. She had one episode of diarrhea. Her history was negative for fever, back pain, dysuria or dymenorrhea. She reported similar symptoms three months earlier that resolved spontaneously. She had a history of depression. She had a history of prior trichobezoar and laparotomy at age four. On physical exam, she appeared in discomfort, had short cropped hair and was wearing a wig. Her abdominal exam was positive for generalized tenderness and guarding, otherwise unremarkable. CT of the abdomen revealed a mass in the stomach extending through the pylorus, into the proximal small bowel. An upper endoscopy revealed a large trichobezoar extending from the LES to the third part of the duodenum. Multiple attempts at endoscopic removal failed. She underwent laparotomy with removal of an extensive trichobezoar. She had an uncomplicated post‐operative course and was discharged home with psychiatric follow‐up. Trichobezoars result secondary to ingestion of hair with associated trichotillomania. Rapunzel syndrome is a rare complication of trichobezoar formation resulting in a mass extending through the pylorus into the small bowel. This mainly affects girls and has been linked to psychiatric conditions. The human body is unable to digest hair, leading to a ball formation in the stomach. Complications include FTT, chronic anemia, ulcer formation, perforation, pancreatitis, intussusception, and intestinal obstruction. Extent of the bezoar may be determined by CT or MRI. Endoscopic removal is generally unsuccessful due to large dimensions and firmness of the bezoar. Endoscopic fragmentation can lead to distal small bowel obstruction. If a large bezoar is present (greater than 20cm), surgical removal is required. Open laparotomy or laparoscopy remains the standard of treatment. After removal, psychiatric evaluation is essential to prevent recurrence of trichobezoar. cv38a DIEULAFOY LESION IN A CHILD A.N. Nasir, C.M. Wilhelm, J.N. Udall, Pediatrics, WVUHSC‐Charleston, Charleston, WV;J.A. Levien, Medicine, WVUHSC‐Charleston, Charleston, WV;W.P. Tomlison, Medicine/Pediatrics, WVUHSC‐ Charleston, Charleston, WV. Dieulafoy lesions are caused by a large tortuous artery that erodes as it approximates the mucosa of the GI tract leading to massive bleeding.The patient is a 7 year old boy who had a chronic fever and cough. He was treated with no improvement. A chest x‐ray showed a right lung pneumonia and large pleural effusion. The boy was hospitalized. The hemoglobin in gm% and hematocrit in % (H/H) were 11.3/32.3. A right‐sided chest tube was placed. On hospital day 2 he vomited 45 ml of blood. His H/H dropped to 7.4/21.7.He was transfused 2 units of PRBCs. I.V. pantoprazole and p.o. sucralfate were started. He was stable until day 8, when he had a 40 ml hematemesis. His H/H dropped from 10.3/29.5 to 8.5/25.3. Three units of PRBCs were given. At upper endoscopy there were clots of blood in the stomach but no active bleeding. Two ulcers approximately 3 cm apart in the duodenal bulb were noted. One had a white escar base (healing) and the other was covered with clot (recent bleed). There was no active bleeding. Following endoscopy octreotide and pantoprazole drips were started. A day later blood was aspirated from his NG tube, and his hemoglobin dropped from 9.0 to 6.8. He was returned to the OR for upper endoscopy. At endoscopy, a small clean based ulcer crater was found (healing) in the duodenal bulb. In the duodenal sweep there was a moderate sized blood clot. The clot was removed and a large blood vessel which had recently bled was noted. The area was injected with 2.5 ml of 1:10,000 epinephrine and cauterized.The boy remained stable with no signs of active bleeding during the rest of his hospital stay. However, he did require 4 more units of PRBCs. He had a third upper endoscopy just prior to discharge on hospital day 21. There was no active bleeding and healing of both duodenal ulcers was evident. Biopsies from the gastric antrum were negative for H. pylori, and a fasting serum gastrin level was normal. The H/H at discharge was 12.6/36.8. In outpatient clinic 2 months later the H/H was 14.2/42.0. This case illustrates the success of endoscopy in the diagnosis and treatment of a duodenal Dieulafoy lesion in a 7 year old boy. Intestine/Colon/IBD cv 39 AN UNUSUAL CASE OF GASTROINTESTINAL BLEEDING Kristin N. Fiorino1, Brian Lestini2, Asim Maqbool1. 1Gastroenterology, The Children's Hospital of Philadelphia, Philadelphia, PA; 2Oncology, The Children's Hospital of Philadelphia, Philadelphia, PA A previously healthy 10‐year‐old African American boy presented with a 3 day history of fever, headaches, and periumbilical abdominal pain, with the development of nonbloody, nonbilious emesis and melena 24 hours prior to presentation. No history of ingestion, trauma, travel, use of NSAIDs, or sick contacts; family history was negative for inflammatory bowel disease, peptic ulcer disease, and polyposis syndromes. Upon initial examination, HR 126, BP 116/56; he was afebrile and dehydrated. No oral lesions, rashes, joint swelling/effusions, or perirectal lesions. Abdomen was soft, with epigastric tenderness, no hepatosplenomegaly/masses. Stool was hemoccult positive. Laboratory studies included hemoglobin 4 g/dL, MCV 80.1 fL, sedimentation rate 42 mm/hr, lipase 202 U/L, BUN 12 mg/dL, creatinine 0.8 mg/dL. Infectious stool studies and abdominal x‐ray were negative. Within 8 hours, a palpable fullness was felt in the epigastric and suprapubic regions which rapidly progressed to a discrete, dense 10 cm firm mass. CT revealed a well‐defined, vascular 8 cm retroperitoneal mass near the pancreas, compressing the duodenum with near complete effacement of the inferior vena cava, with arterial branches from the gastroduodenal and superior mesenteric arteries and the infrarenal aorta. Histopathologic evaluations of tissue suggested a neuroendocrine tumor, specifically paraganglioma. Neo‐adjuvant chemotherapy was followed by surgical exploration and eventual resection. A malignant ulcer eroded into the third part of the duodenum, the primary source of the bleeding. Follow‐up imaging revealed no residual mass or MIBG‐avid disease. The patient remains disease‐free two years post‐resection. Paragangliomas are rare tumors of neuroendocrine origin with the potential for malignant progression. They may initially grow insidiously and lack biochemical secretion, and therefore may present with nonspecific symptoms dependent upon the site of origin. Abdominal paragangliomas are not typically associated with GI bleeding, unless invading the intestinal tract. cv 40 FURTHER EVIDENCE FOR EPCAM AS THE GENE FOR CONGENITAL TUFTING ENTEROPATHY Tiffany D. Schaible1, Mamata Sivagnanam2, Robert H. Byrd3, Milton J. Finegold3, Reka Szigeti3, Nina Tatevian3, Sarangarajan Ranganathan4, Richard Kellermayer1 1 Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX; 2Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of California San Diego, Rady Children's Hospital, San Diego, CA; 3Department of Pathology, Baylor College of Medicine, Texas Children's Hospital, Houston, TX; 4 Children's Hospital of Pittsburgh, Pittsburgh, PA Congenital tufting enteropathy (CTE) is a rare, but severe disorder resulting in early postnatal diarrhea. This entity has been recently shown to associate with mutations in the gene encoding epithelial cell adhesion molecule (EpCAM). However, this association was conclusively made in only 4 individuals thus far. We present an ethnically distinct patient with CTE affected by the first nonsense mutation described in EpCAM. Fluorescent immunohistochemistry of duodenal tissue from the patient, demonstrated lack of EpCAM staining. Our results underscore EpCAM as the gene for congenital tufting enteropathy. cv 41 DAIRY ALLERGY AS POTENTIAL CAUSE OF RECURRENT INTUSSUSCEPTION Crystal M. Knight1, Laura Finn2, David Suskind1, Ghassan Wahbeh1. 1Gastroenterology, Seattle Children's Hospital, Seattle, WA; 2Pathology, Seattle Children's Hospital, Seattle, WA Case. A 4 year old female presented with abdominal cramps and subsequently demonstrated ileocolic intussusception. Within 48 hours after air enema reduction, intussusception recurred twice with successful nonoperative reduction. Contrast enema studies showed residual ileocecal valve edema (figures 1, 2). A nuclear scan for Meckel’s diverticulum was normal. Milk protein allergy had been diagnosed in infancy due to vomiting and diarrhea, and later peanut allergy presented with facial rash and swelling. At age 1 year she had ileocolonic intussusception which was reduced by air enema. She was asymptomatic since on a dairy and peanut free diet. Milk was reintroduced 3 days prior to the latest episode. Colonoscopy (done to assess for lead points) was normal except for prominent edema and erythema in the terminal ileum. Capsule endoscopy revealed lymphoid hyperplasia in the distal ileum (figure 3). Histologic exam showed focal neutrophilic inflammation, reactive epithelium and moderate mucosal eosinophilia, raising the possibility of allergic enteritis (figure 4). She received oral steroids and was kept dairy free. After 1 year of follow up, she remained without symptoms. Discussion. Intussusception is the second most common cause of bowel obstruction in children, most commonly in the ileocecal region. The majority occur in children under one year of age. In children age > 1 year, a pathologic lead point is not uncommon. There are no prior reports of allergic enterocolitis association with intussusception. Given this temporal association to the reintroduction of dairy and the biopsy findings, as well as the resolution after treatment with steroids and resumption of a dairy‐free diet, we propose dairy allergy to be a plausible cause of intussusception in our patient. Allergic enterocolitis should be considered as a trigger of recurrent intussusception in the future, particularly in children with prior known allergies. cv 42 HERMANSKY PUDLAK SYNDROME; A PEDIATRIC CASE WITH SEVERE COLITIS AND GOOD RESPONSE TO INFLIXIMAB Lina M. Felipez, Ranjana Gokhale, Barbara Kirschner, Stefano Guandalini. Pediatric Gastroenterology, University of Chicago Hospitals, Chicago, IL Hermansky Pudlak Syndrome (HPS) is a rare autosomal recessive disorder characterized by tyrosine positive oculocutaneous albinism, bleeding diathesis resulting from platelet dysfunction and ceroid deposition within the reticuloendothelial system. HPS results from 1 of at least 7 different gene mutations. It has been associated with fatal pulmonary fibrosis and severe colitis. The colitis has been associated mostly with HPS 1 and HPS 4 genotypes and is severe and poorly responsive to medical therapy. We report a case of a pediatric patient with HPS type 1 with clinical, endoscopic and histologic features of Crohn's disease, refractory to medical treatment with azathioprine, sulfasalazine, flagyl and steroids. The patient was started on infliximab infusions with good response and quiescent colitis but later developed perianal fistulas. IBD serology was positive for ASCA IgA, Anti‐OMPC IgA and PANCA. These observations suggest there are many similarities between granulomatous colitis in HPS and Crohn's disease. The pathogenesis of granulomatous colits has been attributed to the lysosomal accumulation of ceroid lipofusion but this relationship is speculative. The findings of severe colitis at presentation and perianal fistulization refractory to infliximab suggest that HPS is a severe form of inflammatory bowel disease that may need aggresive treatment comparable to severe Cronh's disease. cv 43 COLLAGENOUS GASTROENTEROCOLITIS CAUSING PREOTEIN LOOSING ENTEROPATHY IN A TODDLER Osama F. Almadhoun, Megan Gabel, Thomas Rossi. Pediatric GI, University of Rochester Medical Ctr, Rochester, NY Collagenous Colitis (CC) is a cause of watery diarrhea in the elderly, but it is rarely reported in children. Protein losing enteropathy (PLE) in association with this disease has never been reported in children. We report a 15 month old boy who presented with severe diarrhea, diffuse edema, and hypoalbuminemia. Further testing revealed PLE associated with collagenous colitis and enteritis. Our patient is a 15 month old who presented with progressive peripheral edema for two weeks. Parents reported that the child had 4‐5 explosive diarrheal bowel movements per day for approximately 4 weeks prior to presentation in addition to vomiting after almost every meal. His physical exam was significant for facial, upper limb, and lower limb edema. Albumin level was 2.4, and total protein 3.6.Stool for alpha one antitrypsin was >1.33,consistent with protein losing enteropathy.Celiac panel, EBV and CMV profile,stool for bacterial and viral culture, were all negative.Upper endoscopy showed edematous antral and duodenal mucosa.The rectal and sigmoid mucosa appeared normal on flexible sigmoidoscopy.Biopsies showed wide subepithelial band of collagen typical of collagenous gastroenterocolitis.The patient was started on oral budesonide 3 mg per day for 5 days but he continued with diarrhea and protein loss requiring parenteral replacement. Methylprednisolone was then added at 2 mg/kg/day. A marked improvement of his symptoms was noticed, and gradually he tolerated oral intake and was weaned off TPN. Collagenous Colitis is a rare entity in Pediatrics. While there are 12 reported pediatric cases of CC none of them were found to have small intestinal involvement. This is a novel description of severe protein losing enteropathy as the presenting feature of collegenous gastroenterocolitis in child. Our patient was treated according to modified guidelines established for adults and has had a favorable response. cv 44 ULCERATIVE DUODENITIS IN A CHILD WITH CELIAC DISEASE Richard L. Mones1, Geraldine O. Mercer2. 1Pediatric Gastoenterology/Nutrition, Goryeb Children's Hospital, Morristown, NJ; 2Dept. of Pathology, Morristown Memorial Hospital, Morristown, NJ A 15 month old boy was seen because of a 2 month history of weight loss, vomiting, irritability and abdominal distension. His family history was non‐contributory.He had been having one to two formed bowel movements per day. The review of systems was otherwise non‐contributory. An UGI series, abdominal ultrasound, CBC, metabolic panel, TSH and T4, CRP, food allergy panel and celiac screen were all normal. Stool for infectious agents were negative. On exam, he was a thin, irritable, sallow appearing toddler with a distended abdomen. An UGI endoscopy was performed. There were multiple ulcers of the duodenal bulb and the second part of the duodenum. Biopsies of the duodenum showed ulceration of the mucosa, total villous atrophy, marked glandular hyperplasia and increased numbers of IELs. On the day following the endoscopy, the repeat celiac screen was received and was as follows: Anti‐Human Tissue Transglutaminase IgA >100U/ML, Anti‐Endomysial IgA Ab. positive, Anti‐Giadin IgG Ab 49.3U/ml and the Anti‐Gliadin IgA Ab was 21.9U/ml. The patient was treated with a brief course of oral corticosteroids and a gluten free diet. He is happy, totally asymptomatic and thriving. Ulceration of the duodenum is a rare finding in children with celiac disease. The first description of ulcerative duodenitis in children with celiac disease was reported by Eltumi et.al.(1) This case also illustrates the great variability of results when screening for celiac disease. 1.Eltumi M, Brueton MJ, Francis N. Ulceration of the Small Intestine in Children with Celiac Disease. Gut. 1996 Oct;39(4)613‐4 TTG IgA Ab <3U/ml 9/08/2008 EGD/Biopsy 11/18/2008 TTG IgA>100U/ml EMA not done EMA + Gliadan IgA Abs. <3U/ml Gliadin IgA Abs. 21.9U/ml (<5 WNL) cv 45 HEMATURIA & BLADDER GRANULOMA WITHOUT ENTEROVESICULAR FISTULA AS PRESENTATION OF CROHN'S DISEASE Kara M. Sullivan1, Aseem R. Shukla2, Glenn R. Gourley1. 1Pediatric Gastroenterology, University of Minnesota, Minneapolis, MN; 2Pediatric Urology, University of Minnesota, Minneapolis, MN 13‐year old male referred to pediatric GI for evaluation of elevated liver enzymes. His AST and ALT had been in the 300‐450 range, with normal bilirubin and alkaline phosphatase levels for four months. His past medical history included an 18‐month history of hematuria and dysuria. Previous evaluations by pediatric urology and nephrology had revealed hematuria with >150 rbc/hpf, 50 wbc/hpf, normal calcium and protein to creatinine ratios, multiple sterile urine cultures, a normal renal ultrasound, normal CT scan of chest, abdomen and pelvis, normal CRP, CBC, ESR, ANA, and electrolytes. Hepatic panel six months prior to referral was normal. Bladder biopsy showed inflammatory changes with foreign body reaction and noncaseating granulomas. Evaluation for tuberculosis, chronic granulomatous disease, and sarcoidosis were negative. Urine culture and PCR for viruses, Chlamydia and gonorrhea were negative. Viral hepatitis testing was negative. His ANCA was positive at 1:80 (reference range <1:20). He reported occasional abdominal discomfort when eating dairy products and having 4‐5 loose stools daily. There was a family history of rheumatoid arthritis in his grandfather and a cousin with an undefined autoimmune disease. His medications included pyridium 100 mg three times daily for bladder pain, and daily Tylenol and ibuprofen. IBD serology was consistent with ulcerative colitis. His liver enzymes returned to normal with discontinuing his medications. Endoscopy revealed an ulcer in the duodenum, but was otherwise grossly normal. Biopsies revealed granulomatous inflammation in the stomach, duodenum, terminal ileum and colon consistent with Crohn’s disease. He was treated for Crohn’s disease with steroids, 5‐ASA and 6‐MP with resolution of his symptoms and hematuria, gross and microscopic. While extraintestinal manifestations are common in IBD, granuloma without fistula is very rare, especially in a patient without a previous diagnosis of Crohn’s disease. cv 46 BEDSIDE SUCTION RECTAL BIOPSY FOR GRAFT‐VS‐HOST DISEASE IN CHILDREN Robert P. Dillard, Ashok Raj, Alexandra C. Cheerva. Pediatrics, University of Louisville, Louisville, KY Background. Graft‐vs‐host disease (GVHD) is often a major complication of hematopoietic stem cell transplantation (BMT) in children. Clinical criteria can be inadequate for accurate diagnosis and tissue biopsy of the intestinal tract is required. These seriously ill patients are at increased risk for procedural complications and routinely are emotionally exhausted. Our aim was to evaluate our experience with bedside suction rectal biopsy (SRB) to determine if it could establish the diagnosis of GVHD using minimal or no sedation. Others found rectal biopsy useful. However, this is the first report of bedside suction rectal biopsy as the initial test. Methods. A retrospective chart review was done of children who underwent bedside SRB for suspected GVHD following allogenic BMT at the Kosair Children’s Hospital in Louisville, KY. from August 2006 to February 2009. Results. Seven children required tissue biopsy to differentiate GVHD from other diagnoses. Six had bedside SRB and the diagnosis of GVHD was established from histology in 4 cases. One had a negative biopsy and no further evidence of GVHD. One had a negative SRB but subsequent endoscopic biopsies were positive. One had mild GVHD, evidence of infectious proctitis with repeat stool culture positive for an enteric pathogen. No complications occurred. One had minimal midazolam for anxiety, one a small dose of fentanyl by patient controlled analgesia and one distraction therapy. The remainder agreed to no intervention following assurance about the ease and painlessness of the procedure. No colon preparation was required and tissue was obtained within hours of gastroenterology service consultation. All patients and family members were relieved and pleased with the rapidity of diagnosis and ease of the procedure. Conclusions. We conclude that, in children, bedside SRB should be the initial test for suspected GVHD. It provides a readily available, safe and rapid method to obtain tissue. Potential complications from anesthesia and more invasive procedures are avoided as well as emotional trauma to already anxious children and their families. cv 47 CELIAC DISEASE DIAGNOSED IN A PEDIATRIC PATIENT WITH HIRSCHSPRUNG DISEASE Alexandra N. Menchise, Adria A. Condino, Michael J. Wilsey. University of South Florida College of Medicine, Tampa, FL Hirschsprung disease is a disorder of neural crest migration characterized by intestinal aganglionosis along a variable segment of the gastrointestinal tract. It is a complex disorder associated with several syndromes. Celiac disease is an autoimmune enteropathy characterized by a dietary intolerance to gluten proteins. Celiac disease can mimic Hirschsprung disease when it presents with constipation and megacolon. We present the case of celiac disease diagnosed in a pediatric patient with Hirschsprung disease. CASE REPORT: A five year old Caucasian male with history of delayed meconium passage (>48 hours) was diagnosed with Hirschprung disease during infancy by contrast barium enema and full‐ thickness rectal biopsy. Patient underwent a primary pull‐through procedure with resection of the rectum, sigmoid colon, and part of the descending colon and primary coloanal anastomosis without colostomy at seven months of age. Gross pathology and histology confirmed proximal megacolon, recto‐ sigmoid transition zone and aganglionosis of the rectum. The patient did well postoperatively until 18 months of age when he developed progressive constipation, abdominal distention and recurrent fecal retention, which was only partially responsive to laxative therapy and rectal irrigation. Celiac testing at age three revealed elevated TTG IgG (>100 U/mL) and IgA ( >100 U/ml) levels and he was homozygous for HLA‐DQB1*0201 allele. Duodenal biopsies showed severe villous atrophy and crypt hyperplasia consistent with celiac disease. The patient symptomatically improved with a gluten‐free diet, but later required surgical revision of his pull through at age four. Currently, the patient is maintained on laxative therapy and rectal irrigation as needed. CONCLUSIONS: To the authors’ knowledge, this is the first case of celiac disease diagnosed in a pediatric patient with concurrent Hirschsprung disease. Further research is warranted to establish whether an association exists between celiac disease and Hirschsprung disease or if celiac disease can complicate and delay the diagnosis of Hirschsprung disease. cv 48 OCCULT COLONIC DUPLICATION: A CASE REPORT Andrea C. Hernandez Troya1, Souheil Gebara1, David A. Bloom2, Winston K. Chan3. 1Department of Pediatrics, Beaumont Children’s Hospital, Royal Oak, MI; 2Department of Pediatric Radiology, Beaumont Children’s Hospital, Royal Oak, MI; 3Department of Pediatric Surgery, Beaumont Children’s Hospital, Royal Oak, MI Gastrointestinal (GI) duplication is uncommon and has a variety of clinical presentations. Colonic duplication (CD) is even less common, occurring in 4‐18% of all cases of GI duplication. We report the case of a 33 week GA female, born with neonatal bowel obstruction. The initial contrast enema (CE) demonstrated a microcolon and possible ileal atresia (IA). No other anatomic issues were identified. An IA was found at surgery, with resection and primary reanastamosis. At 6 weeks of age, the patient developed recurrent episodes of diarrhea and abdominal distention, suggestive of bacterial overgrowth, perhaps in relation to ileal stricture, dysmotility and prestenotic small bowel ectasia. An upper GI was performed at 5 months of age, demonstrating a dilated loop of bowel on the scout radiograph that eventually filled with barium. It extended into the pelvis, paralleling the rectosigmoid. Its exact etiology was unclear, so the patient underwent a CE one week later. The scout image showed retained contrast in the same dilated loop as seen by prior upper GI. During the CE this loop filled further with contrast, extended deep into the pelvis, appeared to be colonic in origin, and was blind ending at its distal extent. At laparotomy, a CD was found with a communication between native colon and the duplication at the level of the splenic flexure. The CD was resected without complication. Since then, the patient has been well, with resolution of all GI symptoms. To our knowledge, no case of a communicating CD that presented in a similar, delayed fashion, with an initial negative CE and surgery has been reported. We hypothesize that the communication between the CD and native colon was missed at CE due to meconium and other thick secretions obstructing the fistula, or that the size of the microcolon and adjacent dilated small bowel led to occlusion of the connection. Duplication must always be considered in patients with symptoms of bacterial overgrowth. cv 49 HEPATIC PELIOSIS AND GANULOMATOUS HEPATITIS IN A CHILD WITH CROHN'S DISEASE Chuan‐Hao Lin. Children Hospital LA, Los Angeles, CA Background: Increases in childhood Crohn's disease have paralleled overall population trends. Sulfasalazine and ‐ASA have been used as active and preventive treatment for Crohn's disease. Azathioprine (AZ)/6 MP, given as the immunomodulatory drugs, have become a mainstay of the management of pediatric Crohn's disease. However, there are potential adverse effects of both medications. OBJECTIVE: We report a pediatric Crohn's disease patient treated with Sulfasalazine and 6 MP. The patient developed adverse effects of both medications with hepatic peliosis and granulomatous hepatitis. DESIGN/METHODS: A 9 years old female presented with bloody diarrhea was diagnosed with Crohn's disease by endoscopic findings. She was initially treated with Prednisone, Sulfasalazine and 6 MP with improvement. The prednisone was tapered after 6 months treatment. She was found to have mild hepatomegaly and minimally elevated liver enzymes (ALT:68) after 14 months of treatment with both medications. A CT scan showed hepatic peliosis. 6 MP was discontinued after CT scan finding. RESULTS: Two months after discontinuation of 6 MP, a repeat CT scan showed resolution of hepatic peliosis. A liver biopsy was performed one month after discontinuation of 6 MP. The liver biopsy showed extensive granulomatous hepatitis and no micro‐organisms were found. Sulfasalazine was discontinued. Asacol was introducted as the only medication for treatment of her Crohn's disease. Prednisone was added again 4 months later due to active terminal iletis. CONCLUSIONS: 1)Potential adverse effects of 6 MP in the treatment of pediatric Crohn's disease include hepatic peliosis. 2) Granulomatous hepatitis can occur in pediatric Crohn's disease treated with Sulfasalazine. 3) Hepatobiliary involvement of pediatric Crohn's disease includes granulomatous hepatitis and fibrosis. 4) Early detection of hepatobiliary lesions using CT scan and/or liver biopsy is indicated with pediatric Crohn's disease with hepatomegaly and/or mildly elevated liver enzymes.
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