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Menetrier’s disease: assessment of treatment options
2620
Abstracts
Metformin is known to cause lactic acidosis, however, development of cholestatic hepatitis due to metformin has not been reported. A 63 yr-old female with a history of insulin requiring diabetes mellitus and hypothyroidism, who had been receiving insulin and synthroid for a number of years, was started on metformin 1g daily for better control of her blood sugar. One month later she developed fatigue, jaundice, pruritus and non-bloody diarrhea. She denied fever, rash or abdominal pain. She also denied the use of alcohol or non-prescription medications, history of blood transfusion or foreign travel, exposure to toxins, or family history of liver disease. On physical exam her skin was icteric and excoriated. Abdominal exam was unremarkable, with no hepatosplenomegaly. Laboratory studies revealed a total bilirubin 16.5 mg/dL with direct bilirubin 7.4 mg/dL, alkaline phosphatase 572 U/L, GGT 216 U/L, AST 66 U/L, ALT 87 U/L, LDH 162 U/L, total protein 5.4 g/dL, albumin 2.7 g/dL, cholesterol 293 g/dL, INR 1.42 U and PTT 46 sec. CBC was normal. Hepatitis A, B and C serologies were negative. ANA, smooth muscle antibodies, AMA and antiendomysial antibodies were negative. Thyroid function tests were normal. Abdominal ultrasound showed a normal liver and biliary tree. Stool was negative for leukocytes, pathogens and fat. Colonoscopy was normal. Metformin was discontinued but the bilirubin continued to rise. Liver biopsy showed marked intracellular and intracanalicular bile stasis, bile duct proliferation, and a predominantly neutrophilic infiltration of the portal fields consistent with drug-induced hepatitis. She was started on ursodeoxycholic acid 300 mg tid. Her symptoms gradually improved with normalization of liver chemistries over a period of 4 months. Metformin-induced hepatotoxicity appears to be a rare, idiosyncratic reaction characterized by marked intrahepatic cholestasis and resolution of symptoms only several months following discontinuation of the drug.
719 Small cell carcinoma of the gallbladder Behara Shailaja M.D., Attar Bashar M. M.D., FACG, Pothamsetty Srikirin M.D., Demetria Melchor M.D., Appavu Samuel M.D., Fronda Gerardo M.D., Harper Terrence M.D., Abrahamian Frida M.D. Departments of Medicine, Surgery and Pathology, Cook County Hospital and Rush Medical College, Chicago, IL. Small cell carcinoma of the gall bladder is extremely rate and limited only to a few case reports. We report a case of small cell carcinoma of the gallbladder. A 67 yr-old female presented with a 2 month history of crampy right upper quadrant pain aggravated by meals, and associated with nausea, anorexia and weight loss of 10 lbs. On physical examination she was icteric, and there was fullness and mild tenderness in the right upper quadrant. Lab studies showed hematocrit 28%, WBC 13,500 mm. AST 68 U/L, ALT 152 U/L, LDH 236 U/L, alkaline phosphatase 224 U/L, GGT 269 U/L, total bilirubin 3.4 mg/dL, direct bilirubin 1.6 mg/dL, and albumin 3.7 g/dL. Ultrasound showed cholelithiasis with thickening of the gallbladder wall, and no biliary ductal dilatation. Exploratory laparotomy revealed a firm, contracted and inflamed gallbladder with adhesions to the surrounding structures and extensive lymphadenopathy in the porta hepatis. The cystic and common bile ducts were not visualized secondary to lymphadenopathy. The gallbladder was transected and histopathology revealed small cell carcinoma extending into the cystic duct. Hilar lymph nodes also showed small cell carcinoma. Small cell carcinoma of the gall bladder is a rare, highly lethal malignancy. It is predominantly a disease of elderly women with cholelithiasis. At the time of diagnosis, these tumors are typically large and bulky, showing early locoregional metastasis. There have been only rare associations with paraneoplastic syndromes. This aggressive tumor behaves more like gallbladder adenocarcinoma than small cell carcinoma of the lung. For gallbladder small cell carcinoma, surgery is the main-stay of treatment for local disease: response to chemotherapy and radiation therapy is poor.
AJG – Vol. 95, No. 9, 2000
720 Menetrier’s disease: assessment of treatment options Carrere Juan MD, Riback Harvey MD, Culpepper-Morgan Joan MD, FACG. Norwalk Hospital, Yale University. Menetrier’s Disease is an uncommon idiopathic gastropathy, characterized by giant gastric folds, protein losing gastropathy, causing hypoproteinemia, and histologic features of foveolar hyperplasia and gland atrophy. Treatment options are not well defined, ranging from medical treatment with anticholinergics, acid antisecretory drugs, corticosteroids, H Pylori eradication and ocreotide to gastrectomy. We present a case of a 69 year old white male with past medical history of Colon Cancer who presented with a three week history of diarrhea and vomiting associated with weight loss of 16 lb. He denied anorexia, fever, bleeding diathesis, and jaundice. On Admission, he appeared dehydrated and had marked lower extremity edema. He had severe hypoalbuminemia (1.5) and hypoproteinemia (3.2) with normal liver function test. Prealbumin was 22.8. Urinalysis showed no protein. Upper Endoscopy revealed giant folds with a nodular appearance in the fundus and body with erosions and a thick serous exudate. The antrum was spared. Jumbo biopsies demonstrated chronic and acute gastritis. Fasting Gastrin was 23. Laparoscopic full thickness biopsy revealed the diagnosis of Menetrier’s Disease: Exuberant hypertrophy of foveolar glands; negative for H Pylori, dysplasia, intestinal metaplasia or malignancy. The patient was treated sequentially with the following medical treatment: acid antisecretory drugs (ranitidine and lansoprazole), steroids and ocreotide without success. After approximately two months of medical treatment the patient underwent a total gastrectomy with complete clinical recovery. From our review of the literature and our case outcome we can conclude that: Those patients with Menetrier’s Disease who present with severe hypoalbuminemia should undergo surgical treatment as the initial therapeutic option. If H Pylori present, eradication should be performed since several reports point to reversal of the disease. For those with mild to moderate disease and H Pylori negative, ocreotide treatment may be successful.
721 A case of acute necrotizing pancreatitis complicating Salmonella enteritis Elfarra Hossam MD., Fares Joseph MD., Al-Khatatneh Salim MD., Baddoura Walid MD. Seton Hall University School of Graduate Medical Education, South Orange, NJ, Division of Gastroenterology, St. Joseph’s Hospital and Medical Center, Paterson, NJ. Background: Infectious causes of acute pancreatitis are rare. It is still unusual for certain bacterial pathogens like salmonella to present with acute pancreatits. Till now there is no general agreement about the possibility that pancreatitis could be caused by Salmonella infection. The most common intraabdominal localized infections due to Salmonella are cholecystitis and splenic abscess. We report a rare case of acute necrotizing pancreatitis caused by Salmonella paratyphi A. Case Report: 23 year old Hispanic male with no significant past medical history presented with two days history of severe abdominal pain, vomiting and bloody diarrhea 2 days after he ate in the park with his wife. The patient denied drinking alcohol or illicit drug use, denied previous similar attack and he was not on any medications. Examination was remarkable for dehydration and upper abdominal tenderness. Initial laboratory data showed WBC 22,000, amylase 3200 U/L and lipase 2800 U/L, BUN 48 mg/dl and creatine 1.2 mg/dl. Serum calcium liver enzymes, bilirubin and triglycerides were all normal. He was admitted and was given aggressive intravenous fluid hydration. Abdominal ultrasound was unremarkable. Abdominal CT with intravenous contrast was consistant with necrotizing pancreatitis. Stool and blood culture were both positive for Salmonella paratyphi A. He was started on intravenous Levofloxacin 500 mg daily on the second day of admission. On the seventh day of admission he became asymptomatic and all of his laboratory data normalized by the third week.
Abstracts
Metformin is known to cause lactic acidosis, however, development of cholestatic hepatitis due to metformin has not been reported. A 63 yr-old female with a history of insulin requiring diabetes mellitus and hypothyroidism, who had been receiving insulin and synthroid for a number of years, was started on metformin 1g daily for better control of her blood sugar. One month later she developed fatigue, jaundice, pruritus and non-bloody diarrhea. She denied fever, rash or abdominal pain. She also denied the use of alcohol or non-prescription medications, history of blood transfusion or foreign travel, exposure to toxins, or family history of liver disease. On physical exam her skin was icteric and excoriated. Abdominal exam was unremarkable, with no hepatosplenomegaly. Laboratory studies revealed a total bilirubin 16.5 mg/dL with direct bilirubin 7.4 mg/dL, alkaline phosphatase 572 U/L, GGT 216 U/L, AST 66 U/L, ALT 87 U/L, LDH 162 U/L, total protein 5.4 g/dL, albumin 2.7 g/dL, cholesterol 293 g/dL, INR 1.42 U and PTT 46 sec. CBC was normal. Hepatitis A, B and C serologies were negative. ANA, smooth muscle antibodies, AMA and antiendomysial antibodies were negative. Thyroid function tests were normal. Abdominal ultrasound showed a normal liver and biliary tree. Stool was negative for leukocytes, pathogens and fat. Colonoscopy was normal. Metformin was discontinued but the bilirubin continued to rise. Liver biopsy showed marked intracellular and intracanalicular bile stasis, bile duct proliferation, and a predominantly neutrophilic infiltration of the portal fields consistent with drug-induced hepatitis. She was started on ursodeoxycholic acid 300 mg tid. Her symptoms gradually improved with normalization of liver chemistries over a period of 4 months. Metformin-induced hepatotoxicity appears to be a rare, idiosyncratic reaction characterized by marked intrahepatic cholestasis and resolution of symptoms only several months following discontinuation of the drug.
719 Small cell carcinoma of the gallbladder Behara Shailaja M.D., Attar Bashar M. M.D., FACG, Pothamsetty Srikirin M.D., Demetria Melchor M.D., Appavu Samuel M.D., Fronda Gerardo M.D., Harper Terrence M.D., Abrahamian Frida M.D. Departments of Medicine, Surgery and Pathology, Cook County Hospital and Rush Medical College, Chicago, IL. Small cell carcinoma of the gall bladder is extremely rate and limited only to a few case reports. We report a case of small cell carcinoma of the gallbladder. A 67 yr-old female presented with a 2 month history of crampy right upper quadrant pain aggravated by meals, and associated with nausea, anorexia and weight loss of 10 lbs. On physical examination she was icteric, and there was fullness and mild tenderness in the right upper quadrant. Lab studies showed hematocrit 28%, WBC 13,500 mm. AST 68 U/L, ALT 152 U/L, LDH 236 U/L, alkaline phosphatase 224 U/L, GGT 269 U/L, total bilirubin 3.4 mg/dL, direct bilirubin 1.6 mg/dL, and albumin 3.7 g/dL. Ultrasound showed cholelithiasis with thickening of the gallbladder wall, and no biliary ductal dilatation. Exploratory laparotomy revealed a firm, contracted and inflamed gallbladder with adhesions to the surrounding structures and extensive lymphadenopathy in the porta hepatis. The cystic and common bile ducts were not visualized secondary to lymphadenopathy. The gallbladder was transected and histopathology revealed small cell carcinoma extending into the cystic duct. Hilar lymph nodes also showed small cell carcinoma. Small cell carcinoma of the gall bladder is a rare, highly lethal malignancy. It is predominantly a disease of elderly women with cholelithiasis. At the time of diagnosis, these tumors are typically large and bulky, showing early locoregional metastasis. There have been only rare associations with paraneoplastic syndromes. This aggressive tumor behaves more like gallbladder adenocarcinoma than small cell carcinoma of the lung. For gallbladder small cell carcinoma, surgery is the main-stay of treatment for local disease: response to chemotherapy and radiation therapy is poor.
AJG – Vol. 95, No. 9, 2000
720 Menetrier’s disease: assessment of treatment options Carrere Juan MD, Riback Harvey MD, Culpepper-Morgan Joan MD, FACG. Norwalk Hospital, Yale University. Menetrier’s Disease is an uncommon idiopathic gastropathy, characterized by giant gastric folds, protein losing gastropathy, causing hypoproteinemia, and histologic features of foveolar hyperplasia and gland atrophy. Treatment options are not well defined, ranging from medical treatment with anticholinergics, acid antisecretory drugs, corticosteroids, H Pylori eradication and ocreotide to gastrectomy. We present a case of a 69 year old white male with past medical history of Colon Cancer who presented with a three week history of diarrhea and vomiting associated with weight loss of 16 lb. He denied anorexia, fever, bleeding diathesis, and jaundice. On Admission, he appeared dehydrated and had marked lower extremity edema. He had severe hypoalbuminemia (1.5) and hypoproteinemia (3.2) with normal liver function test. Prealbumin was 22.8. Urinalysis showed no protein. Upper Endoscopy revealed giant folds with a nodular appearance in the fundus and body with erosions and a thick serous exudate. The antrum was spared. Jumbo biopsies demonstrated chronic and acute gastritis. Fasting Gastrin was 23. Laparoscopic full thickness biopsy revealed the diagnosis of Menetrier’s Disease: Exuberant hypertrophy of foveolar glands; negative for H Pylori, dysplasia, intestinal metaplasia or malignancy. The patient was treated sequentially with the following medical treatment: acid antisecretory drugs (ranitidine and lansoprazole), steroids and ocreotide without success. After approximately two months of medical treatment the patient underwent a total gastrectomy with complete clinical recovery. From our review of the literature and our case outcome we can conclude that: Those patients with Menetrier’s Disease who present with severe hypoalbuminemia should undergo surgical treatment as the initial therapeutic option. If H Pylori present, eradication should be performed since several reports point to reversal of the disease. For those with mild to moderate disease and H Pylori negative, ocreotide treatment may be successful.
721 A case of acute necrotizing pancreatitis complicating Salmonella enteritis Elfarra Hossam MD., Fares Joseph MD., Al-Khatatneh Salim MD., Baddoura Walid MD. Seton Hall University School of Graduate Medical Education, South Orange, NJ, Division of Gastroenterology, St. Joseph’s Hospital and Medical Center, Paterson, NJ. Background: Infectious causes of acute pancreatitis are rare. It is still unusual for certain bacterial pathogens like salmonella to present with acute pancreatits. Till now there is no general agreement about the possibility that pancreatitis could be caused by Salmonella infection. The most common intraabdominal localized infections due to Salmonella are cholecystitis and splenic abscess. We report a rare case of acute necrotizing pancreatitis caused by Salmonella paratyphi A. Case Report: 23 year old Hispanic male with no significant past medical history presented with two days history of severe abdominal pain, vomiting and bloody diarrhea 2 days after he ate in the park with his wife. The patient denied drinking alcohol or illicit drug use, denied previous similar attack and he was not on any medications. Examination was remarkable for dehydration and upper abdominal tenderness. Initial laboratory data showed WBC 22,000, amylase 3200 U/L and lipase 2800 U/L, BUN 48 mg/dl and creatine 1.2 mg/dl. Serum calcium liver enzymes, bilirubin and triglycerides were all normal. He was admitted and was given aggressive intravenous fluid hydration. Abdominal ultrasound was unremarkable. Abdominal CT with intravenous contrast was consistant with necrotizing pancreatitis. Stool and blood culture were both positive for Salmonella paratyphi A. He was started on intravenous Levofloxacin 500 mg daily on the second day of admission. On the seventh day of admission he became asymptomatic and all of his laboratory data normalized by the third week.