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Pseudomyxoma peritonei presenting as a rectal mass
S248
Abstracts
days for melena, which revealed diffuse ulcerative esophagitis and gastritis. Repeat endoscopy after another 7 days for recurrent bleeding revealed a large gastric clot and resolving gastric injury. He did well until approximately one month post-ingestion when he developed symptoms of gastric outlet obstruction. Endoscopic exam revealed gastric scarring with marked pyloric stenosis. Endoscopic balloon dilation was performed with temporary improvement. Recurrent symptoms of gastric outlet obstruction 4 months later led to a gastrojejunostomy for relief of symptoms. A gastrectomy was considered, but at the time of surgery the stomach was too scarred to make this a viable procedure. After his surgery he has been asymptomatic for 2 months of follow-up. Conclusions: Caustic acid ingestion can lead to severe sequelae including esophageal and pyloric stenosis in a relatively short time. Endoscopy allows assessment and DPEJ placement for nutritional support. Continued evolution of pyloric stricturing following concentrated acid ingestion may occur over several months following caustic ingestion.
792 Pseudomyxoma peritonei presenting as a rectal mass Jorge Sotelo, M.D.1, Mitchell Chorost, M.D.1, Gerald Fruchter, M.D.1 and Ayse Aytaman, M.D.1*. 1Gastroenterology, VA NY Harbor HCS Brooklyn Campus, Brooklyn, New York, United States. Purpose: Pseudomyxoma peritonei (PMP) is characterized by gelatinous intraperitoneal fluid collections and mucinous implants on the peritoneal surfaces and omentum which usually is derived from an underlying appendiceal or intestinal mucin secreting adenoma or adenocarcinoma. Typical presentations are increasing abdominal girth, ovarian mass, new onset inguinal hernia or rarely acute appendicitis. We describe a case of PMP presenting with a rectal mass simulating a rectal carcinoma. Case History: The patient is a 69 year old male, who was evaluated 4 years earlier for right lower quadrant pain and constipation. A computed tomography (CT) scan of the abdomen revealed at that time a right lower quadrant mass and multiple hepatic lesions suspicious for metastasis. Two CT guided biopsies of the liver lesions revealed cavernous hemangioma. Colonoscopy was unremarkable except for a small ulceration at the appendiceal orifice with biopsy showing nonspecific inflammation. He re-presented with a 3 month history of weight loss, constipation, increasing abdominal girth and was found to have massive ascites and a painful, hard and fixed rectal mass. Repeat colonoscopy revealed a submucosal, 5cm rectal mass encroaching upon 50% of the lumen, biopsy was non-diagnostic; in addition there was a 4mm nodule overlying the appendiceal orifice, biopsy revealing acute and chronic inflammation and villotubular changes. CT scan showed extensive ascites with multiple areas of enhancement, and an extrinsic rectal mass. Paracentesis revealed well differentiated, bland and tall columnar cells noted in the background of mucus lakes, consistent with PMP. Patient underwent surgery for debulking and to relieve obstructive symptoms. Findings revealed bulky gelatinous masses throughout the peritoneum with omental, pelvic, bilateral subdiaphragmatic caking and near total extrinsic compression of the recto-sigmoid. Patient underwent transverse loop colostomy and limited debulking. Pathology was consistent with well differentiated mucinous adenocarcinoma consistent also with PMP. Conclusions: The treatment of PMP is aggressive debulking via laparotomy and possible use of chemotherapy. Except in patients with high-grade malignant process where only palliative therapy may be indicated, the median survival can be increased significantly with early diagnosis and treatment before large volume of disease leads to bowel entrapment by tumor. Conclusion: In the differential diagnosis of rectal obstructing lesions this rare entity has to be considered. It is important to pay special attention to lesions found at the level of the appendix.
AJG – Vol. 96, No. 9, Suppl., 2001
793 Successful treatment of hepatitis B-associated vasculitis with lamivudine Veslav Stecevic1, Martin M. Pevzner2 and Stuart C. Gordon1*. 1 Gastroenterology/Hepatology, William Beaumont Hospital, Royal Oak, Michigan, United States; and 2Rheumatology, William Beaumont Hospital, Royal Oak, Michigan, United States. Purpose: Vasculitis is a potentially serious extrahepatic manifestation of hepatitis B virus (HBV) infection. The treatment of HBV-associated vasculitis with corticosteroids and immunosuppressive agents may worsen the hepatic disease. We report a case of HBV-associated leukocytoclastic vasculitis that responded to oral lamivudine as monotherapy. Case report: A 59-year-old Caucasian woman with chronic HBV developed biopsy-confirmed leukocytoclastic vasculitis in 1978. She had recurrent flares of vasculitis over 20 years, treated continuously with prednisone, up to 30 mg/d. On initial evaluation in 1998 she had purpuric skin lesions about her upper and lower extremities and was on prednisone, 30 mg/d. She had no hepatosplenomegaly or stigmata of chronic liver disease. Laboratory studies showed normal AST and ALT. HBsAg and anti-HBc were positive, anti-HBs negative, HBeAg negative, anti-HBe positive, HBV DNA level of 9.3 pg/mL, anti-HCV negative. She was started on lamivudine 150 mg/d. One month later, quantitative HBV DNA was undetectable, and her vasculitis flares were less intense. Over the next seven months, the prednisone was tapered and eventually stopped. Twenty-one months later, her vasculitic lesions had completely resolved. She remains on oral lamivudine. Her HBV DNA is undetectable. She is still HBsAg and anti-HBe positive and anti-HBs negative. She has not taken any immunosuppressive agents for over 3 years. Conclusions: This case illustrates successful treatment of HBV-associated vasculitis with lamivudine that allowed the patient to stop high dose prednisone therapy. Acecdotal case reports suggest that lamivudine may be used in the treatment of HBV-related polyarteritis nodosa in combination with immunosuppressive agents, but there are no previous reports of lamivudine as a single agent in the treatment of vasculitis.
794 Pancreatic stenting as a treatment for pancreatic pseudocyst Deborah A Streletz, Fernando Ramos, Eric M Osgard and Darren S Baroni*. 1Medicine, Tripler Army Medical Center, Honolulu, HI, United States. Purpose: Often pancreatic duct strictures can be a cause of recurrent pancreatitis and lead to pseudocyst formation. We present a case of a patient with a high-grade stricture in the pancreatic head and secondary pseudocyst, both of which responded to endoscopic dilation and stenting of the pancreatic duct. Methods: Our patient is a 40-year-old African American female who presented in November 2000 with her first documented episode of alcoholic pancreatitis. A CT scan done at the time revealed diffuse pancreatic inflammation, a dilated pancreatic duct and a 3 to 4 cm peripancreatic pseudocyst. Her pancreatitis improved with medical management and she was eventually discharged. As an outpatient, however, even with discontinuation of alcohol, the patient continued to require daily narcotics for pain control for several months. She presented with recurrent pancreatitis requiring admission in both December 2000 and January 2001. Repeat CT scans done during both hospital admissions showed persistent dilation of the pancreatic duct and continued presence of the pseudocyst. In December 2000 the patient was also diagnosed with a right-sided pancreatic pleural effusion. Eventually, in January 2001 an ERCP was performed and revealed a single marked stricture in the pancreatic head with upstream dilation in the uncinate, body and tail of the pancreas. Also noted, just proximal (upstream) to the pancreatic head stricture, was a side branch that directly communicated with peripancreatic pseudocyst. Dilation of the stricture was performed with catheter dilators and a 5 Fr 7cm pancreatic stent was placed which transversed the stricture.
Abstracts
days for melena, which revealed diffuse ulcerative esophagitis and gastritis. Repeat endoscopy after another 7 days for recurrent bleeding revealed a large gastric clot and resolving gastric injury. He did well until approximately one month post-ingestion when he developed symptoms of gastric outlet obstruction. Endoscopic exam revealed gastric scarring with marked pyloric stenosis. Endoscopic balloon dilation was performed with temporary improvement. Recurrent symptoms of gastric outlet obstruction 4 months later led to a gastrojejunostomy for relief of symptoms. A gastrectomy was considered, but at the time of surgery the stomach was too scarred to make this a viable procedure. After his surgery he has been asymptomatic for 2 months of follow-up. Conclusions: Caustic acid ingestion can lead to severe sequelae including esophageal and pyloric stenosis in a relatively short time. Endoscopy allows assessment and DPEJ placement for nutritional support. Continued evolution of pyloric stricturing following concentrated acid ingestion may occur over several months following caustic ingestion.
792 Pseudomyxoma peritonei presenting as a rectal mass Jorge Sotelo, M.D.1, Mitchell Chorost, M.D.1, Gerald Fruchter, M.D.1 and Ayse Aytaman, M.D.1*. 1Gastroenterology, VA NY Harbor HCS Brooklyn Campus, Brooklyn, New York, United States. Purpose: Pseudomyxoma peritonei (PMP) is characterized by gelatinous intraperitoneal fluid collections and mucinous implants on the peritoneal surfaces and omentum which usually is derived from an underlying appendiceal or intestinal mucin secreting adenoma or adenocarcinoma. Typical presentations are increasing abdominal girth, ovarian mass, new onset inguinal hernia or rarely acute appendicitis. We describe a case of PMP presenting with a rectal mass simulating a rectal carcinoma. Case History: The patient is a 69 year old male, who was evaluated 4 years earlier for right lower quadrant pain and constipation. A computed tomography (CT) scan of the abdomen revealed at that time a right lower quadrant mass and multiple hepatic lesions suspicious for metastasis. Two CT guided biopsies of the liver lesions revealed cavernous hemangioma. Colonoscopy was unremarkable except for a small ulceration at the appendiceal orifice with biopsy showing nonspecific inflammation. He re-presented with a 3 month history of weight loss, constipation, increasing abdominal girth and was found to have massive ascites and a painful, hard and fixed rectal mass. Repeat colonoscopy revealed a submucosal, 5cm rectal mass encroaching upon 50% of the lumen, biopsy was non-diagnostic; in addition there was a 4mm nodule overlying the appendiceal orifice, biopsy revealing acute and chronic inflammation and villotubular changes. CT scan showed extensive ascites with multiple areas of enhancement, and an extrinsic rectal mass. Paracentesis revealed well differentiated, bland and tall columnar cells noted in the background of mucus lakes, consistent with PMP. Patient underwent surgery for debulking and to relieve obstructive symptoms. Findings revealed bulky gelatinous masses throughout the peritoneum with omental, pelvic, bilateral subdiaphragmatic caking and near total extrinsic compression of the recto-sigmoid. Patient underwent transverse loop colostomy and limited debulking. Pathology was consistent with well differentiated mucinous adenocarcinoma consistent also with PMP. Conclusions: The treatment of PMP is aggressive debulking via laparotomy and possible use of chemotherapy. Except in patients with high-grade malignant process where only palliative therapy may be indicated, the median survival can be increased significantly with early diagnosis and treatment before large volume of disease leads to bowel entrapment by tumor. Conclusion: In the differential diagnosis of rectal obstructing lesions this rare entity has to be considered. It is important to pay special attention to lesions found at the level of the appendix.
AJG – Vol. 96, No. 9, Suppl., 2001
793 Successful treatment of hepatitis B-associated vasculitis with lamivudine Veslav Stecevic1, Martin M. Pevzner2 and Stuart C. Gordon1*. 1 Gastroenterology/Hepatology, William Beaumont Hospital, Royal Oak, Michigan, United States; and 2Rheumatology, William Beaumont Hospital, Royal Oak, Michigan, United States. Purpose: Vasculitis is a potentially serious extrahepatic manifestation of hepatitis B virus (HBV) infection. The treatment of HBV-associated vasculitis with corticosteroids and immunosuppressive agents may worsen the hepatic disease. We report a case of HBV-associated leukocytoclastic vasculitis that responded to oral lamivudine as monotherapy. Case report: A 59-year-old Caucasian woman with chronic HBV developed biopsy-confirmed leukocytoclastic vasculitis in 1978. She had recurrent flares of vasculitis over 20 years, treated continuously with prednisone, up to 30 mg/d. On initial evaluation in 1998 she had purpuric skin lesions about her upper and lower extremities and was on prednisone, 30 mg/d. She had no hepatosplenomegaly or stigmata of chronic liver disease. Laboratory studies showed normal AST and ALT. HBsAg and anti-HBc were positive, anti-HBs negative, HBeAg negative, anti-HBe positive, HBV DNA level of 9.3 pg/mL, anti-HCV negative. She was started on lamivudine 150 mg/d. One month later, quantitative HBV DNA was undetectable, and her vasculitis flares were less intense. Over the next seven months, the prednisone was tapered and eventually stopped. Twenty-one months later, her vasculitic lesions had completely resolved. She remains on oral lamivudine. Her HBV DNA is undetectable. She is still HBsAg and anti-HBe positive and anti-HBs negative. She has not taken any immunosuppressive agents for over 3 years. Conclusions: This case illustrates successful treatment of HBV-associated vasculitis with lamivudine that allowed the patient to stop high dose prednisone therapy. Acecdotal case reports suggest that lamivudine may be used in the treatment of HBV-related polyarteritis nodosa in combination with immunosuppressive agents, but there are no previous reports of lamivudine as a single agent in the treatment of vasculitis.
794 Pancreatic stenting as a treatment for pancreatic pseudocyst Deborah A Streletz, Fernando Ramos, Eric M Osgard and Darren S Baroni*. 1Medicine, Tripler Army Medical Center, Honolulu, HI, United States. Purpose: Often pancreatic duct strictures can be a cause of recurrent pancreatitis and lead to pseudocyst formation. We present a case of a patient with a high-grade stricture in the pancreatic head and secondary pseudocyst, both of which responded to endoscopic dilation and stenting of the pancreatic duct. Methods: Our patient is a 40-year-old African American female who presented in November 2000 with her first documented episode of alcoholic pancreatitis. A CT scan done at the time revealed diffuse pancreatic inflammation, a dilated pancreatic duct and a 3 to 4 cm peripancreatic pseudocyst. Her pancreatitis improved with medical management and she was eventually discharged. As an outpatient, however, even with discontinuation of alcohol, the patient continued to require daily narcotics for pain control for several months. She presented with recurrent pancreatitis requiring admission in both December 2000 and January 2001. Repeat CT scans done during both hospital admissions showed persistent dilation of the pancreatic duct and continued presence of the pseudocyst. In December 2000 the patient was also diagnosed with a right-sided pancreatic pleural effusion. Eventually, in January 2001 an ERCP was performed and revealed a single marked stricture in the pancreatic head with upstream dilation in the uncinate, body and tail of the pancreas. Also noted, just proximal (upstream) to the pancreatic head stricture, was a side branch that directly communicated with peripancreatic pseudocyst. Dilation of the stricture was performed with catheter dilators and a 5 Fr 7cm pancreatic stent was placed which transversed the stricture.