successful endoscopic therapy of bouveret’s syndrome using holmium laser lithotripsy: a case...
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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