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Brunner’s gland hamartoma simulating a pancreatic mass with obstruction
AJG – September, Suppl., 2001
reducible incisional hernia. Two months ago: AST 79, ALT 103, ALP 114, T. Bili 0.6. CBC, Lytes normal. Ultrasound of abdomen revealed focal area of decreased echogenicity in right lobe of liver, neoplasm vs possible focal fatty sparing. Prominent CBD. CT SCAN: Intra and extrahepatic ductal dilation. Soft mass in the region of head of pancreas vs CBD. Possible thrombosis of posterior segment of right portal vein. Indeterminate 5mm hypervascular lesion in left lobe of liver. 2 weeks later presented with dark urine, jaundice but no fever or chills. Labs now: AST 207, ALT 293, ALP 224, T. Bili 4.1(c.bili 2.1), amylae 296, lipase 887. Normal CBC and lytes. ERCP demonstrated multiple filling defects in markedly dilated CBD, limited exam of intrahepatics. After papillotomy and an attempt at balloon extraction of stones, a soft friable, polypoid mass prolapsed through the ampulla. Endoscopic biopsy revealed tubulovilllous adenomatous fragments with low grade dysplasia. Repeat CT of abdomen revealed again ductal dilatation, thickening of distal 4 cm of CBD but no intrahepatic lesions or portal vein thrombosis. No lymph nodes. Exploratory laparotomy and intraoperative choledochoscopy and ultrasonograpghy demonstrated duplication of bileduct proximally, the anterior duct supplying the right anterior and left lateral segments and was free of tumor. The posterior duct was supplying the right posterior and left medial segments, both filled with tumor. Distally tumor extended to just above the ampulla. No masses in the liver outside the ducts. Underwent right trisegmentectomy, pylorus preserving whipple’s. Surgical margins were free of tumor. Surgical path shows papillary adenocarcinoma stage T1NOMx. Discussion: Papillary cholangiocarcinoma of extrahepatic bile duct is rare. It is possible that these lesions start off as adenomas and evolve into adenocarcinomas, with tendency to grow more towards lumen causing early obstructive symptoms. Minimally invasive or non-invasive papillary carcinomas of bile ducts have excellent prognosis. One differential here is “Biliary Papillomatosis” a rare disorder with multifocal papillary adenomas, which could be recurrent and has about 25% risk of malignancy. In our patient given the extent of disease is this a tumor with multicenteric origin? Could this be biliary papillomatosis with malignant transformation?
717 Diabetic gastroparesis a possible new indication for botulinum toxin injection Pavani Muddasani1 and Farhad Ismail-Beigi1*. 1Dept. of Gastroenterology, UPMC Shadyside, Pittsburgh, PA, United States. Purpose: Gastroparesis affects about 50% of diabetics. The exact pathophysiology is not clear but there is evidence for antral motor dysfunction which includes antral hypomotility, “pylorospasm” or isolated pyloric pressure waves and also failure of proximal gastric contraction. With very few pharmacological agents being available for treatment of this condition there is an increasing demand for identification of newer agents and newer treatment modalities. Case History: 47 y female with 32 year history of diabetis complicated by nephropathy, neuropathy and retinopathy, hypertension, CAD, GERD, cholecystectomy, chronic intermittent diarrhea due to bacterial overgrowth was admitted with 4 –5 day history of severe nausea, several episodes of vomiting and upper abdominal discomfort. She was on insulin, calcium, tricor and also reglan (for last 2 years). Had about 4 admissions in the last one and half years, upper endoscopy showing severe ulcerative distal esophagitis. Improved increasing doses of PPI and intravenous reglan. Lab at admission: WBC 13.9, H/H 13.7/41.5, platatelets 323 no left shift. BUN/Cr 63/14.1, CI 90, Hco3 28, Normal Na, K, Lfts and amylase, lipase. She was started on intravenous reglan, the dose was increased upto 15mg QID but 7– 8 days after admissions was still vomiting. Upper endoscopy again ulcerative esophagitis, no barrett’s on biopsies. On gastric emptying scan the T 1-1/2 curve for solid emptying was 160 minutes which was abnormal. A repeat endoscopy was performed and botulinum toxin was injected into pyloric muscle, in 4 quadrants, 50units each (total 200 units). She continued to take reglan. Repeat emptying scan 4 weeks later shows T
Abstracts
S225
1-1/2 for solids this time 91 minutes, significant improvement. Four and half months after treatment she is still asymptomatic. Discussion: Botulinum toxin is a neurotoxin which acts at presynaptic level of neuromuscular junction preventing calcium dependent release of acetycholine. It produces a temporary state of denervation until new nerve filbrils grow. It is being used safely for the last few years, for several indications but has not been used so far for gastroparesis. Recently preliminary results of couple small studies on small group of (5– 6) patients have shown it’s effectiveness in diabetic gastroparesis and also idiopathic gastroparesis in doses 80 to 200 units. However the data is still preliminary and we need studies involving larger group of patients and longer follow-up before implementing in clilnical practice. We have done this after explaining the experimental nature of it’s use to the patient. This report is just to share our experience and not to recommend its routine use.
718 Brunner’s gland hamartoma simulating a pancreatic mass with obstruction Rushda Mumtaz MD and Francisco C Ramirez MD FACG*. 1 Gastroenterology, Carl T Hayden VA Medical Center, Phoenix, Arizona, United States. Purpose: Brunner’s gland hamartomas are rare benign submucosal tumors of duodenum. Usually asymptomatic but can present with gastrointestinal bleeding or symptoms of intestinal obstruction, or an incidental finding at endoscopy. Exact pathogenesis of this tumor is unknown but association with hyperacidity, chronic pancreatitis and Billroth II reconstruction have been suggested. Endoscopic ultrasound is the best imaging modality for diagnosing these tumors. In symptomatic patients, surgical or endoscopic resection is performed with good long-term prognosis. Methods: A 50-year old man presented with recurrent episodes of postprandial epigastric pain, nausea and vomiting of 6 months duration associated with 40 lb weight loss. Abdominal pain was sharp with radiation to back and relieved by vomiting. There was no history of hematemesis, melena, anemia or hematochezia. Past medical history was significant for hypertension. Had heavy drinking and smoking history and was taking lisinopril only. Family history was negative for gastrointestinal disease. Physical examination was unremarkable except diffuse upper abdominal tenderness. Laboratory data showed Blood urea nitrogen of 45 mg/dl, creatinine 1.5 mg/dl, bicarbonate of 31 mmol/L, chloride of 84 mmol/L, amylase of 362 U/L and lipase of 2620 U/L. Complete blood count and liver function tests were normal. Results: Hospital Course: Working diagnosis was pancreatitis and patient was treated conservatively. His symptoms were relieved with nasogastric decompression and NG output was 4 – 6 liters/day. EGD showed a mass arising from posterior wall of the duodenal bulb completely obstructing the lumen, biopsies obtained showed normal duodenal mucosa. At this point he underwent CT scan of abdomen which showed a mass in the head of pancreas extending into the duodenum causing compression. Endoscopic ultrasound revealed mass in the head of pancreas with no vascular involvement. Ca 19-9 was 0 U/ml. At laparotomy,inflammatory mass contiguous with uncinate process and head of pancreas with 5 cm nodule on serosal surface of duodenum was found and Whipple procedure was performed. On pathological examination, fungating circumferential mass measuring 6.6 ⫻ 4.5 cm was found in the area of ampulla of Vater. No mass lesions were found in the pancreas but small areas of necrosis and fibrosis was present. Frozen section was negative for malignancy. Histologically, the mass was confined within the muscularis propria, characterized by normal-appearing Brunner’s glands and small duct structures within firomuscular structure. Conclusions: Brunner’s gland hamartomas can mimic cancer of the head of pancreas & can be correctly diagnosed only after pancreatico-duodenectomy as seen in our case.
reducible incisional hernia. Two months ago: AST 79, ALT 103, ALP 114, T. Bili 0.6. CBC, Lytes normal. Ultrasound of abdomen revealed focal area of decreased echogenicity in right lobe of liver, neoplasm vs possible focal fatty sparing. Prominent CBD. CT SCAN: Intra and extrahepatic ductal dilation. Soft mass in the region of head of pancreas vs CBD. Possible thrombosis of posterior segment of right portal vein. Indeterminate 5mm hypervascular lesion in left lobe of liver. 2 weeks later presented with dark urine, jaundice but no fever or chills. Labs now: AST 207, ALT 293, ALP 224, T. Bili 4.1(c.bili 2.1), amylae 296, lipase 887. Normal CBC and lytes. ERCP demonstrated multiple filling defects in markedly dilated CBD, limited exam of intrahepatics. After papillotomy and an attempt at balloon extraction of stones, a soft friable, polypoid mass prolapsed through the ampulla. Endoscopic biopsy revealed tubulovilllous adenomatous fragments with low grade dysplasia. Repeat CT of abdomen revealed again ductal dilatation, thickening of distal 4 cm of CBD but no intrahepatic lesions or portal vein thrombosis. No lymph nodes. Exploratory laparotomy and intraoperative choledochoscopy and ultrasonograpghy demonstrated duplication of bileduct proximally, the anterior duct supplying the right anterior and left lateral segments and was free of tumor. The posterior duct was supplying the right posterior and left medial segments, both filled with tumor. Distally tumor extended to just above the ampulla. No masses in the liver outside the ducts. Underwent right trisegmentectomy, pylorus preserving whipple’s. Surgical margins were free of tumor. Surgical path shows papillary adenocarcinoma stage T1NOMx. Discussion: Papillary cholangiocarcinoma of extrahepatic bile duct is rare. It is possible that these lesions start off as adenomas and evolve into adenocarcinomas, with tendency to grow more towards lumen causing early obstructive symptoms. Minimally invasive or non-invasive papillary carcinomas of bile ducts have excellent prognosis. One differential here is “Biliary Papillomatosis” a rare disorder with multifocal papillary adenomas, which could be recurrent and has about 25% risk of malignancy. In our patient given the extent of disease is this a tumor with multicenteric origin? Could this be biliary papillomatosis with malignant transformation?
717 Diabetic gastroparesis a possible new indication for botulinum toxin injection Pavani Muddasani1 and Farhad Ismail-Beigi1*. 1Dept. of Gastroenterology, UPMC Shadyside, Pittsburgh, PA, United States. Purpose: Gastroparesis affects about 50% of diabetics. The exact pathophysiology is not clear but there is evidence for antral motor dysfunction which includes antral hypomotility, “pylorospasm” or isolated pyloric pressure waves and also failure of proximal gastric contraction. With very few pharmacological agents being available for treatment of this condition there is an increasing demand for identification of newer agents and newer treatment modalities. Case History: 47 y female with 32 year history of diabetis complicated by nephropathy, neuropathy and retinopathy, hypertension, CAD, GERD, cholecystectomy, chronic intermittent diarrhea due to bacterial overgrowth was admitted with 4 –5 day history of severe nausea, several episodes of vomiting and upper abdominal discomfort. She was on insulin, calcium, tricor and also reglan (for last 2 years). Had about 4 admissions in the last one and half years, upper endoscopy showing severe ulcerative distal esophagitis. Improved increasing doses of PPI and intravenous reglan. Lab at admission: WBC 13.9, H/H 13.7/41.5, platatelets 323 no left shift. BUN/Cr 63/14.1, CI 90, Hco3 28, Normal Na, K, Lfts and amylase, lipase. She was started on intravenous reglan, the dose was increased upto 15mg QID but 7– 8 days after admissions was still vomiting. Upper endoscopy again ulcerative esophagitis, no barrett’s on biopsies. On gastric emptying scan the T 1-1/2 curve for solid emptying was 160 minutes which was abnormal. A repeat endoscopy was performed and botulinum toxin was injected into pyloric muscle, in 4 quadrants, 50units each (total 200 units). She continued to take reglan. Repeat emptying scan 4 weeks later shows T
Abstracts
S225
1-1/2 for solids this time 91 minutes, significant improvement. Four and half months after treatment she is still asymptomatic. Discussion: Botulinum toxin is a neurotoxin which acts at presynaptic level of neuromuscular junction preventing calcium dependent release of acetycholine. It produces a temporary state of denervation until new nerve filbrils grow. It is being used safely for the last few years, for several indications but has not been used so far for gastroparesis. Recently preliminary results of couple small studies on small group of (5– 6) patients have shown it’s effectiveness in diabetic gastroparesis and also idiopathic gastroparesis in doses 80 to 200 units. However the data is still preliminary and we need studies involving larger group of patients and longer follow-up before implementing in clilnical practice. We have done this after explaining the experimental nature of it’s use to the patient. This report is just to share our experience and not to recommend its routine use.
718 Brunner’s gland hamartoma simulating a pancreatic mass with obstruction Rushda Mumtaz MD and Francisco C Ramirez MD FACG*. 1 Gastroenterology, Carl T Hayden VA Medical Center, Phoenix, Arizona, United States. Purpose: Brunner’s gland hamartomas are rare benign submucosal tumors of duodenum. Usually asymptomatic but can present with gastrointestinal bleeding or symptoms of intestinal obstruction, or an incidental finding at endoscopy. Exact pathogenesis of this tumor is unknown but association with hyperacidity, chronic pancreatitis and Billroth II reconstruction have been suggested. Endoscopic ultrasound is the best imaging modality for diagnosing these tumors. In symptomatic patients, surgical or endoscopic resection is performed with good long-term prognosis. Methods: A 50-year old man presented with recurrent episodes of postprandial epigastric pain, nausea and vomiting of 6 months duration associated with 40 lb weight loss. Abdominal pain was sharp with radiation to back and relieved by vomiting. There was no history of hematemesis, melena, anemia or hematochezia. Past medical history was significant for hypertension. Had heavy drinking and smoking history and was taking lisinopril only. Family history was negative for gastrointestinal disease. Physical examination was unremarkable except diffuse upper abdominal tenderness. Laboratory data showed Blood urea nitrogen of 45 mg/dl, creatinine 1.5 mg/dl, bicarbonate of 31 mmol/L, chloride of 84 mmol/L, amylase of 362 U/L and lipase of 2620 U/L. Complete blood count and liver function tests were normal. Results: Hospital Course: Working diagnosis was pancreatitis and patient was treated conservatively. His symptoms were relieved with nasogastric decompression and NG output was 4 – 6 liters/day. EGD showed a mass arising from posterior wall of the duodenal bulb completely obstructing the lumen, biopsies obtained showed normal duodenal mucosa. At this point he underwent CT scan of abdomen which showed a mass in the head of pancreas extending into the duodenum causing compression. Endoscopic ultrasound revealed mass in the head of pancreas with no vascular involvement. Ca 19-9 was 0 U/ml. At laparotomy,inflammatory mass contiguous with uncinate process and head of pancreas with 5 cm nodule on serosal surface of duodenum was found and Whipple procedure was performed. On pathological examination, fungating circumferential mass measuring 6.6 ⫻ 4.5 cm was found in the area of ampulla of Vater. No mass lesions were found in the pancreas but small areas of necrosis and fibrosis was present. Frozen section was negative for malignancy. Histologically, the mass was confined within the muscularis propria, characterized by normal-appearing Brunner’s glands and small duct structures within firomuscular structure. Conclusions: Brunner’s gland hamartomas can mimic cancer of the head of pancreas & can be correctly diagnosed only after pancreatico-duodenectomy as seen in our case.