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PNEUMATOSIS CYSTOIDES INTESTINALIS A RARE CAUSEOF RECTAL BLEEDINGMartin E. Maldonado, M.D., F.A.C.P.* and Janice McCall, M.D.Department of Gastroenterology, Florida Medical Clinic, Tampa, FLand Department of Pathology, University Community Hospital, Tampa,FL.

Purpose: Pneumatosis cystoides intestinalis (PCI) is a rare disease. Itsincidence varies from 0.03% to 0.2%. PCI can be idiopathic or secondary(85%). Although symptoms associated with PCI are nonspecific; symptomsof abdominal distention, diarrhea, abdominal pain, constipation, mucousdischarge, hematemesis, rectal bleeding, volvulus and pneumoperitoneumhave been described. We present a case of a 37 year old male whopresented with hematochezia secondary to PCI.Methods: The patient complained of bloody stools four times per day forsix days. Colonoscopic examination revealed a cluster of multiple cysticand polypoid lesions in the ascending colon ranging in size from 5mm toseveral centimeters in diameter. Two of the larger lesions had fresh bloodover them. The smaller lesions demonstrated a cushion sign. This wasabsent in the two larger lesions. One of the larger polypoid lesions wassnared.Results: The differential diagnosis includes colon polyps, enterogenouscysts, lipomas, lymphosarcoma and colitis cystica profunda. Histologicexam confirmed the diagnosis of PCI.Conclusions: Most of the time the diagnosis of PCI can be confirmedendoscopically by puncturing the cystic structure causing its collapse. Thismay not be possible in larger lesions in which the cushion sign may beabsent. In this case histology confirmed the diagnosis.

PCI should be considered as a possible cause of rectal bleeding inhealthy patients.

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GLUTARALDEHYDE INDUCED COLITIS MIMMICKING ASISCHEMIC COLITISShailender Singh, M.D., Manjushree Gautam, M.D., Manzoor Rather,M.D.* and Steven Lichtenstein, D.O. Department of Medicine, MercyCatholic Medical Center, Darby, PA.

Purpose: A 61–year–old Asian woman presented with chills, abdominalcramps, diarrhea and bleeding per rectum. These symptoms developedabout six hours after undergoing screening colonoscopy in her physician’soffice. The procedure was uncomplicated and colonoscopy was reported asnormal. Her past medical history was unremarkable and she was not takingany medications. On examination she was found to be febrile and tachy-cardic with a normal blood pressure. Her abdomen was soft, diffuselytender with hypoactive bowel sounds. Investigations revealed a white cellcount of 15,400/cc with a normal metabolic panel. The stool analysis wasnegative for clostridium difficile toxin and other enteric pathogens. Ab-dominal radiography showed colonic thumb printing suggestive of isch-emic colitis. CT scan of abdomen revealed diffuse thickening of caecum,ascending colon and transverse colon consistent with colitis. In view of thetemporal relationship between the development of symptoms and colonos-copy, the diagnosis of chemical colitis rather than ischemic colitis wasentertained. She was treated conservatively with complete resolution of hersymptoms in two days. This rapid recovery also makes ischemic colitisunlikely and favors chemical colitis.Discussion: Two percent glutaraldehyde solution used as disinfectant andretained in the endoscope channels has been known to cause direct injuryto the colonic mucosa resulting in chemical colitis. The main characteristicin these cases is the time relationship with colonoscopy, symptoms ofsystemic reaction along with the abdominal complaints. Spontaneous re-covery occurs in most cases as seen in our patient. Glutaraldehyde–inducedcolitis is similar to ischemic colitis in biopsy specimens and cannot bediagnosed by histological analysis alone. This complication should besuspected in patients who develop hemorrhagic colitis immediately after

undergoing colonoscopy and should lead to an investigation of proceduresused for cleaning and disinfecting endoscopic equipment.

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SCHISTOSOMIASIS: AN UNUSUAL CAUSE OF ISOLATEDPROCTITISShailender Singh, M.D., Naushad Shaik, M.D., Manjushree Gautam,M.D. and Rafael Amaral, M.D.*. Department of Medicine, MercyCatholic Medical Center, Darby, PA.

Purpose: An 18–year–old African male presented with a 2 month historyof left lower quadrant abdominal pain and bright red blood in stoolsassociated with tenesmus. There was no history of nausea, vomiting,hematemesis, melena or mucus in stools. He had migrated to the UnitedStates two years ago. His past medical history was unremarkable and hewas not taking any medications. He had stable vital signs and abdominalexamination was unremarkable. Laboratory data: CBC and basic metabolicpanel were within normal limits. CT scan of abdomen revealed thickenedrectal wall suggestive of proctitis. On sigmoidoscopy the rectal ampullashowed mild to moderate erythema. There were no polyps. Microscopi-cally, rectal mucosa showed several granulomas containing eggs consistentwith schistosoma mansonii infection. He was treated with praziquantel withcomplete resolution of his symptoms and repeat sigmoidoscopy revealed anormal rectal mucosa.Discussion: Schistosomiasis is a snail–transmitted trematodiasis acquiredby immersion in water, which contains the cercariae. Gastrointestinalhemorrhages due to rupture of esophageal varices in case of hepaticinvolvement or moderate gastrointestinal hemorrhage due to colonic in-volvement may be observed. The diagnosis of schistosomiasis can be madeby identification of schistosoma in stool and urine, or by colonic or hepaticbiopsies. Patients massively eliminating eggs experience abdominal painand diarrhea with stools containing blood and mucus. We report a case ofrectal schistosoma mansoni infection presenting exclusively with recurrentepisodes of lower gastrointestinal bleeding. Finding the characteristic lat-eral–spined eggs in the biopsy specimens from the rectum made thediagnosis. If schistosomiasis is suspected, it can be diagnosed by lookingfor eggs in the stool specimen thus avoiding invasive investigations. Al-though rare in United States, parasitic causes of lower gastrointestinalbleeding should be considered, if there is history of travel to an endemicarea or the patient is originally from one of the endemic regions as in ourcase.

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CELIAC DISEASE AND PRIMARY HYPERPARATHYROIDISM:A RARE CLINICAL ASSOCIATIONShailender Singh, M.D., Manjushree Gautam, M.D., Naushad Shaik,M.D. and Edward Ruby, M.D.*. Department of Medicine, MercyCatholic Medical Center, Darby, PA and Department of Endocrinology,Thomas Jefferson University Hospital, Philadelphia, PA.

Purpose: A 32–year–old white female with history of celiac disease (CD)presented with gradually progressive fatigue of three months duration.Review of systems was unremarkable. She had been compliant with glu-ten–free diet with a favorable response. On examination she was 57 inchestall, had stable vitals and weighed 79 Ibs. Remainder of the physicalexamination was essentially unremarkable. Lab data: CBC revealed hemo-globin of 11.8 gm/dl. Coagulation profile, basic chemistry and thyroidfunctions were within normal limits. Liver function tests revealed AST 36,ALT 51, alkaline phosphatase 179, total serum proteins 7.1gm%, serumalbumin 3.8 gm% and total serum bilirubin of 0.5 mg%. Serum calciumdone on two occasions prior to this visit was 11.8 and 11.3 mg/dl (normal8.9–10.5 mg/dl) with a corresponding PTH (IRMA) level of 354 and 453(normal 10–65 PG/ML) respectively. 25–OH vitamin D and 1,25–OH

S145AJG – September, Suppl., 2002 Abstracts

vitamin D levels were normal. Urinary calcium excretion was 199 mg/24hours. Dexa scan showed generalized osteoporosis, parathyroid scan re-vealed a right inferior pole adenoma and she underwent resection for theadenoma. Few months after surgery she had worsening dietary intolerance,abdominal bloating, diarrhea and 15 pound weight loss. Investigations donerevealed serum calcium of 7.8mg/dl, serum phosphorous of 5.0 (2.7–4.4mg/dl) and PTH of 190 (10–65 PG/ML) consistent with secondary hyper-parathyroidism.Discussion: Hypocalcemia in CD leading to secondary hyperparathyroid-ism or masking the hypercalcemia of primary (or tertiary) hyperparathy-roidism is known to occur. Presence of hypercalcemia is uncommon andcan be due to progression of secondary to tertiary hyperparathyroidism orconcurrent primary hyperparathyroidism as seen in our case. Primaryhyperparathyroidism is seldom associated with other autoimmune disor-ders. In our case presence of hypercalcemia with raised PTH level, osteo-porosis and parathyroid adenoma in the background of clinically quiescentceliac disease suggest primary hyperparathyroidism as the initial abnor-mality. Later the development of hypocalcemia and raised PTH level(secondary hyperparathyroidism) few months after resection of parathyroidadenoma was coincidental with clinical recrudescence of CD. Calciumlevels can demonstrate a wide variation in CD depending on the durationand disease activity. Although rare, the possibility of primary hyperpara-thyroidism should be considered in celiac disease patients presenting withnormal or high calcium levels.

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SUCCESSFUL ENDOSCOPIC THERAPY OF BOUVERET’SSYNDROME USING HOLMIUM LASER LITHOTRIPSY: ACASE REPORTAnubha Sinha, M.D., Michelle Nazareth, M.D., Ashok N. Shah, M.D.,Etal Eurtuk, M.D. and Uma Sundaram, M.D.*. Digestive DiseaseGroup, University of Rochester, Rochester, NY.

Introduction: Bouverets syndrome is a rare clinical condition character-ized by gastric outlet obstruction due to gallstones. Surgery is the main stayof treatment. In patients with medical co morbidities, endoscopic therapywith mechanical electrohydraulic or extracorporeal shock wave lithotripsyas well as one case of intracorporeal laser lithotripsy with rhodamine hasbeen reported. Holmium YAG laser has been used in urinary calculi andinfrequently in the biliary tract.Case Report: This is the first case of Bouverets syndrome successfullytreated with Holmium YAG laser alone. Patient was an 86 WM with 3 dayhistory of nausea, vomiting, and abdominal pain. Physical exam wasunremarkable. Labs revealed WBC �25,000, HCT �37, lipase �618 andnormal LFT. During EGD, 2L of greenish fluid was suctioned enabling usto visualize the entire stomach that was dilated. A large gallstone measuringapprox 5 cm was seen beyond pylorus extending into the duodenumcausing complete pyloric obstruction. CT scan demonstrated 5.3 cm ob-structing intraluminal mass in the 2nd portion of the duodenum withpneumobliia, consistent with fistula to the gallbladder. Gallbladder wascollapsed with non–dilated biliary tree. UGI with SBFT demonstrated largebarium into the biliary tree. Diagnosis of Bouverets Syndrome was madeon the basis of the above classic finding. In view of his multiple comor-bidities, surgery was not an option. He underwent EGD with HolmiumYAG laser lithotripsy under general anesthesia using double channel ther-apeutic endoscope. A duodenal stone was visualized and 600 micron laserprobe was passed through the therapeutic channel aiming directly at thestone. Total of 6,961 pulses were used to deliver 3,297 joules of energy at10 watts for 12 minutes. Saline flushes were used judiciously. About 70%of the stone fragments were removed sucessfully.Conclusion: This case illustrates classic presentation of Bouverets syn-drome and its unique and novel management by endoscopic HolmiumYAG laser lithotripsy alone.

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GATIFLOXACIN INDUCED HEPATOTOXICITY: A CASEREPORTOnki Cheung, M.D., Michael Nalesnik, M.D. and Kapil Chopra, M.D. .Gastroenterology, Hepatology & Nutrition, University of PittsburghSchool of Medicine, Pittsburgh, PA.

Purpose: Quinolones may induce transient abnormalities in serumtransaminase levels. Severe hepatotoxicity is rare. We describe a case ofcholestatic hepatitis and acute pancreatitis after the administration of gati-floxacin, one of the newest fluroquinolones.Case report: A 41 year–old woman was referred for evaluation of cho-lestatic jaundice and elevated liver enzyme. Two weeks prior to admission,she was given gatifloxacin 400 mg daily for an upper respiratory tractinfection. After two days of gatifloxacin, she developed a rash on hershoulder, arms and back. She subsequently noted dark urine and acholicstools. She presented with right upper quadrant abdominal pain. On ex-amination, she had scleral icterus, an urticarial rash over her arms, back andlegs without cutaneous stigmata of chronic liver disease, hepatosplenomeg-aly, or ascites.

Laboratory data on admission showed total serum bilirubin of 5.1 mg/dlwith conjugated of 3.6 mg/dl, aspartate aminotransferase 139 IU/ml, ala-nine aminotransferase 145 IU/ml, Albumin 3.0 mg/dl, Alkaline phospha-tase 482 IU/ml and GGTP 517 IU/ml. Serologic studies for hepatitis A , B,C, Epstein–Barr virus and cytomegalovirus antibodies were negative. An-tinuclear, Antimitochondrial, Antismooth muscle, anti–liver, kidney andmicrosomal antibodies were undetectable. Abdominal sonograph revealedfocal hypoechogenicity of the body and tail of the pancreas. Lipase waselevated. CT abdomen was unremarkable. Endoscopic retrograde cholan-giopancreatography showed a normal cholangiogram and pancreatogram.A liver biopsy performed three weeks after the onset of symptoms revealedportal and subsinusoidal fibrosis; incomplete bridging fibrosis, focal mac-

S146 Abstracts AJG – Vol. 97, No. 9, Suppl., 2002