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Sarcomatoid hepatocellular carcinoma, a rare neoplasm in united states
S174
Abstracts
abdomen showed hepatomegaly, ascites, small bowel edema, and thrombosis of the hepatic, portal, superior mesenteric, and splenic veins. The patient did not have any previous history of liver disease and was not taking oral contraceptives. Hepatic and splanchnic venography confirmed thrombosis of the hepatic, superior mesenteric, portal, and splenic veins compatible with BCS and MVT. Because of worsening liver failure, a DIPS was established between the inferior vena cava and the left portal vein. A direct puncture from the inferior vena cava into the left portal vein had to be done because there was no hepatic vein remnant identified. MT with an Expedior Angiojet device was then performed to debulk the clot and restore flow in the superior mesenteric, splenic, and main portal veins. Follow-up thrombectomy of the right portal vein had to be performed the next day to allow full decompression. Post-procedure anticoagulation was complicated by significant lower gastrointestinal bleeding. Colonoscopy revealed severe colitis and total colectomy was performed. Work-up was negative for genetic and acquired causes of hypercoagulable states. Discussion: BCS is defined as thrombosis of the hepatic veins and/or the intrahepatic or suprahepatic inferior vena cava. In untreated patients, the mortality rate at 2 years is over 50%. Common causes of this syndrome include genetic defects leading to hypercoagulable states, myeloproliferative diseases, PNH, pregnancy, malignancy, and oral contraceptives. Patients with UC also appear to be at increased risk for BCS. The treatment for BCS includes anticoagulation, thrombolytic therapy, TIPS, surgical shunts, and liver transplantation. Our patient underwent DIPS and MT resulting in decompression of the congested segments of liver. Conclusion: This is first case report using DIPS and MT to treat BCS with MVT in the United States. Our patient was placed on coumadin. At the six-month follow-up, she has no clinical evidence of liver disease and duplex ultrasound shows patent DIPS and spontaneous recanalization of the left portal vein. 515 INFLAMMATORY BOWEL DISEASE AND AEROMONAS INFECTION: A COMMENSAL OR AN INITIATING AGENT OR A CAUSATIVE AGENT? Jessica A. Haffajee, B.A., Faten Aberra, M.D., Joanne Linevsky, M.D., Thomas Judge, M.D., Julius Deren, M.D.*, Radhika Srinivasan, M.D. University of Pennsylvania School of Medicine, Philadelphia, PA. It has been postulated that the cause of idiopathic inflammatory bowel disease (IBD) may be infectious in origin. Shigella, Campylobacter, and enteropathogenic E. coli have been implicated as causative agents in precipitating IBD in predisposed individuals and in causing relapses in those with documented IBD. The role of Aeromonas species in causing human gastrointestinal disease is controversial, but there is evidence to suggest that this gram-negative rod causes gastroenteritis, ranging from mild self-limited diarrhea to chronic diarrhea. The organism elaborates toxins that aid in its infectivity and ability to cause symptoms. Aeromonas has been reported to potentially cause and precede a chronic colitis, indistinguishable from ulcerative colitis, and has been established as a pathogen that can provoke relapses in patients with known IBD. Therefore, it is important to distinguish Aeromonas-colitis (as acute self-limited colitis) from idiopathic IBD. Previous studies suggest that the two are reliably distinguished based on histopathological parameters, most notably the presence of distorted crypt architecture and chronic inflammatory cells in the lamina propria with IBD. These changes are seen in patients even at time of first diagnosis of IBD. Although prior series have reliably noted these chronic changes 7 days after onset of symptoms, index colonoscopy in case 1 did not have these findings. These histopathologic features were, however, subsequently observed raising the possibility that Aeromonas initiated IBD in this patient. In this series, we describe 4 patients who had stool cultures positive for Aeromonas; in 2 known IBD patients it resulted in a relapse while in the other 2 IBD was subsequently diagnosed several weeks later. Although it is likely that the Aeromonas infection was coincidental, it is possible that the infection may have provoked these attacks of IBD or that the organism contains a factor that initiates the process responsible for chronic IBD.
AJG – Vol. 98, No. 9, Suppl., 2003
Profile of Patients with Positive Aeromonas Stool Culture Age/Gender/ Prior diagnosis of IBD
Timing of colonoscopy after onset of new symptoms
24/F/No 23/F/No 43/F/Yes
4 wks 6 months 7 wks
68/M/Yes
3 wks
Histopathology crypt architecture preserved architectural distortion present Significant acute inflammation and architectural distortion no colonoscopy
Response to antibiotic treatment Partially Yes Yes Yes
All patients on steroids/immunomodulators currently
516 DUODENAL EMBEDMENT OF AN INGESTED BAY LEAF: AN UNUSUAL CAUSE OF ACUTE ABDOMINAL PAIN Basher M. Atiquzzaman, M.D., Jagdish Gupta, M.D., Irwin M. Grosman, M.D.* Long Island College Hospital, Brooklyn, NY. A 59 year-old man, with no significant past medical history, developed acute epigastric and retrosternal chest pain while on his way home from a local restaurant where he had curried beef for dinner. He presented to his local emergency room where he was evaluated. A EKG did not reveal any acute changes and the cardiac enzymes were normal; an acute myocardial infarction was ruled out. He was reassured and discharged home on famotidine. The severe epigastric and chest pain persisted. The next day he was referred to a gastroenterologist and an urgent EGD was done. EGD showed mild esophagitis and erosive gastritis. Upon entering the duodenum, a large fragment of a dried bay leaf was noted to be embedded in the mucosa of the duodenal bulb at the stem. Utilizing biopsy forceps and polypectomy snare the bay leaf was disimpacted from the duodenal mucosa and retrieved. Upon subsequent examination a small ulceration was noted in the duodenem where the stem of the bay leaf was embedded. This was surrounded by edema and nodularity. The remainder of the duodenum was normal. Immediately after the procedure the patient reported relief of his pain symptoms. He was given a course of esomeprazole 40mg daily and had no subsequent recurrence of symptoms. Accidental bay leaf ingestion has been described as a rare cause of duodenal obstruction, upper gastrointestinal tract hemorrhage and perforation of the small intestine. Cases of pharyngeal and esophageal impaction have been reported. To our knowledge this is the first report of acute abdominal pain resulting from the accidental ingestion of a dried bay leaf which embedded in the duodenal mucosa. 517 SARCOMATOID HEPATOCELLULAR CARCINOMA, A RARE NEOPLASM IN UNITED STATES Sailaja M. Cheruku, M.D., John O’Brien, M.D.*, Brian Webb, M.D. Southern Illinois University School Of Medicine, Springfield, IL and Memorial Medical Center, Springfield, IL. A 66 year-old caucasian male was admitted to hospital for evaluation of increasing right upper quadrant pain for three weeks. He denied nausea, vomitting, jaundice or other significant complaints. His past medical history included Diabetes and Hypertension. Family history was negative for malignancy. He denied tobacco and alcohol use. Physical examination was only significant for tenderess in right upper quadrant with gaurding but no rebound. Laboratory evaluation showed hemoglobin of 8.5 mg/dl, low serum iron but normal electrolytes, amylase, lipase and liver fuction tests. An ultrasound of abdomen showed a hypoehoic mass in right hepatic lobe, no gall stones or ductal dialatation. Further evaluation with a CT scan showed, an irregular lesion 7.5cm in diameter along the inferolateral right lobe of liver highly suspicious for neoplasm. Alpha feto protein level was normal. Biopsy of the lesion was performed and histology showed extensive infiltration of liver parenchyma by a markedly cellular pleomorphic malignant neoplasm arranged in solid sheets and apparent fascicles.The cells demonstrated in some areas a spindled or sarcomatoid appearance and immunohistochemical stains for vimentin, cytokeratin AE1 and 3 were strongly positive but stains for cytokeratin 7, 20, S100, CD34, actin, and
AJG – September, Suppl., 2003
desmin were negative. The morphologic and immunohistochemical features were consistent with a “sarcomatoid carcinoma”. Further evaluation with endoscopy, CT of chest and PET scan did not demonstrate any other tomor focus. The final diagnosis was “unusual primary hepatocellular carcinoma”. Oncology recommended local therapy : surgery, hepatic artery embolization or radiofrequency ablation. Despite discussions, Pt declined above therapies. His pain worsened despite pain medications. A repeat CT scan in 3 weeks showed increase in size of tumor, peritoneal metastases with extensive ascitis and new 1.5cm metastatic lesion in right lobe of liver. He went to hospice care and expired in two weeks. Hepato cellular carcinoma ( HCC) with sarcomatous features is a rare neoplasm which has been found in only 1.8% of surgically resected HCC and prognosis is poor due to early development of intrahepatic and distal metastases.The frequency of tumor was about 4% of all HCCs, according to the literature. Alpha feto protein level is usually normal. Immunohistochemical staining for vimentin and cytokeratin are helpful in diagnosis. Literature review did not show any case from united states.
Abstracts
S175
ileostomy. A dermatologist evaluated his peristomal skin lesion and diagnosed pyoderma gangrenosum with biopsies of the lesion showing peristomal granulation tissue with collections of neutrophils. On physical examination a 3 cm ulcerated violaceous lesion was seen beneath the ileostomy. A complete blood count, sedimentation rate, and C-reactive protein were normal. A small bowel series was normal. The patient refused treatment with corticosteroids and/or 6-mercaptopurine. Infliximab in a dose of 5 mg/kg iv was given. The ulcerated skin lesion healed in 2 weeks. Follow-up infliximab infusions were given at 3 weeks and at 4 months after the initial treatment. The peristomal pyoderma gangrenosum had not recurred 6 months after initial infliximab therapy.
518 CONTROL OF HEMORRHAGE FROM A GASTRIC DIEULAFOY’S LESION USING ARGON PLASMA COAGULATION Poneh Rahimi, M.D., Irwin Grosman, M.D., Adnan Khdair, M.D.* Long Island College Hospital, Brooklyn, NY. A 52 year-old male with a history of hypertension presented to the emergency room with multiple episodes of hematemesis. He denied any history of prior GI bleeding episodes, PUD, NSAID use, or heavy alcohol use. There was no abdominal pain or melena associated with the presenting symptoms. The physical exam was remarkable for tachycardia and borderline hypotention. The initial blood results revealed normal chemistries, liver function tests, coagulation factors and a hematocrit of 40.5 %. Nasogastric lavage revealed fresh blood, which did not clear after lavaging with 2 liters of saline. Urgent EGD was performed and revealed a single spurting vessel with normal surrounding mucosa and no evidence of ulceration (diagnosed as Dieulafoy’s lesion) in the greater curvature within 3cm from GE junction. After applying epinephrine injection (12 CC of 1: 10,000) and thermocoagulation (BICAP setting 20 W in the continuous mode), the lesion still continued to bleed. Using the argon plasma coagulator (setting of 60 W and 1L/min), bleeding was stopped successfully after three applications. The repeat hemoglobin dropped to 8.5 but patient refused blood transfusion. Over the course of the hospital stay hemoglobin stabilized and there was no recurrent bleeding. He was discharged on hospital day 5.The Dieulafoy’s lesion is a rare cause of severe gastrointestinal hemorrhage. Several endoscopic modalities have been used to treat this condition including: thermal, schlerotherapy (using epinephrine, alcohol and ethanolamine) and mechanical means (hemoclips, sewing, band ligation and endoloop). Combination therapy with two or more modalities is purported to be superior to single modality therapy. Use of the APC in treating Dieulafoy’s lesion has not previously been reported in the literature. The successful result with APC in this case may introduce a new means of therapy for Dieulafoy’s lesion.
Conclusion: Infliximab was an effective therapy for a patient with peristomal pyoderma gangrenosum associated with Crohn’s disease. 520
519 TREATMENT OF PERISTOMAL PYODERMA GANGRENOSUM ASSOCIATED WITH CROHN’S DISEASE WITH INFLIXIMAB Warren Finkelstein, M.D., FACG* The Gastroenterology Group of New Jersey, Glen Ridge, NJ.
GASTRIC ASCARIASIS PRESENTING AS RECURRENT MASSIVE UPPER GASTROINTESTINAL BLEEDING Thomas A. Scileppi, M.D., Joel Albert, M.D., John Trillo, M.D., Scott Tenner, M.D., FACG* Maimonides Medical Center, Mount Sinai School of Medicine, Brooklyn, NY.
Peristomal pyoderma gangrenosum is a very unusual painful complication of Crohn’s disease that may occur after total proctocolectomy with ileostomy. It is often misdiagnosed as a skin infection and mismanaged with ineffective therapy. Local wound care measures are usually unsuccessful and most patients require systemic medical therapy. I document a case of peristomal pyoderma gangrenosum in a patient with Crohn’s disease treated with infliximab. Case Report: A 51 year-old physician with a history of Crohn’s disease since age 5 and total proctocolectomy with ileostomy performed at age 12 presented with a 3-week history of a very painful ulcerated lesion adjacent to his
Ascaris lumbricoides is a parasitic nematode that, in its adult phase, lives in the human gastrointestinal tract. Ascaris lumbriciodes infects approxiamately one-fourth of the world’s population. Most persons infected have minimal symptoms. Less commonly, weight loss, pneumonia and gastrointestinal/biliary obstruction can occur. We present a patient with recurrent massive gastrointestinal bleeding found to have Ascaris lunbricoides. A 63 year-old Bangladeshi female presented to the medical center with symptoms of weakness, fatigue, dark stools and coffee ground emesis. One year prior, she had been hospitalized elsewhere with an upper gastrointestinal bleed. The etiology was unclear. The patient reported that the physicians found a “small
Abstracts
abdomen showed hepatomegaly, ascites, small bowel edema, and thrombosis of the hepatic, portal, superior mesenteric, and splenic veins. The patient did not have any previous history of liver disease and was not taking oral contraceptives. Hepatic and splanchnic venography confirmed thrombosis of the hepatic, superior mesenteric, portal, and splenic veins compatible with BCS and MVT. Because of worsening liver failure, a DIPS was established between the inferior vena cava and the left portal vein. A direct puncture from the inferior vena cava into the left portal vein had to be done because there was no hepatic vein remnant identified. MT with an Expedior Angiojet device was then performed to debulk the clot and restore flow in the superior mesenteric, splenic, and main portal veins. Follow-up thrombectomy of the right portal vein had to be performed the next day to allow full decompression. Post-procedure anticoagulation was complicated by significant lower gastrointestinal bleeding. Colonoscopy revealed severe colitis and total colectomy was performed. Work-up was negative for genetic and acquired causes of hypercoagulable states. Discussion: BCS is defined as thrombosis of the hepatic veins and/or the intrahepatic or suprahepatic inferior vena cava. In untreated patients, the mortality rate at 2 years is over 50%. Common causes of this syndrome include genetic defects leading to hypercoagulable states, myeloproliferative diseases, PNH, pregnancy, malignancy, and oral contraceptives. Patients with UC also appear to be at increased risk for BCS. The treatment for BCS includes anticoagulation, thrombolytic therapy, TIPS, surgical shunts, and liver transplantation. Our patient underwent DIPS and MT resulting in decompression of the congested segments of liver. Conclusion: This is first case report using DIPS and MT to treat BCS with MVT in the United States. Our patient was placed on coumadin. At the six-month follow-up, she has no clinical evidence of liver disease and duplex ultrasound shows patent DIPS and spontaneous recanalization of the left portal vein. 515 INFLAMMATORY BOWEL DISEASE AND AEROMONAS INFECTION: A COMMENSAL OR AN INITIATING AGENT OR A CAUSATIVE AGENT? Jessica A. Haffajee, B.A., Faten Aberra, M.D., Joanne Linevsky, M.D., Thomas Judge, M.D., Julius Deren, M.D.*, Radhika Srinivasan, M.D. University of Pennsylvania School of Medicine, Philadelphia, PA. It has been postulated that the cause of idiopathic inflammatory bowel disease (IBD) may be infectious in origin. Shigella, Campylobacter, and enteropathogenic E. coli have been implicated as causative agents in precipitating IBD in predisposed individuals and in causing relapses in those with documented IBD. The role of Aeromonas species in causing human gastrointestinal disease is controversial, but there is evidence to suggest that this gram-negative rod causes gastroenteritis, ranging from mild self-limited diarrhea to chronic diarrhea. The organism elaborates toxins that aid in its infectivity and ability to cause symptoms. Aeromonas has been reported to potentially cause and precede a chronic colitis, indistinguishable from ulcerative colitis, and has been established as a pathogen that can provoke relapses in patients with known IBD. Therefore, it is important to distinguish Aeromonas-colitis (as acute self-limited colitis) from idiopathic IBD. Previous studies suggest that the two are reliably distinguished based on histopathological parameters, most notably the presence of distorted crypt architecture and chronic inflammatory cells in the lamina propria with IBD. These changes are seen in patients even at time of first diagnosis of IBD. Although prior series have reliably noted these chronic changes 7 days after onset of symptoms, index colonoscopy in case 1 did not have these findings. These histopathologic features were, however, subsequently observed raising the possibility that Aeromonas initiated IBD in this patient. In this series, we describe 4 patients who had stool cultures positive for Aeromonas; in 2 known IBD patients it resulted in a relapse while in the other 2 IBD was subsequently diagnosed several weeks later. Although it is likely that the Aeromonas infection was coincidental, it is possible that the infection may have provoked these attacks of IBD or that the organism contains a factor that initiates the process responsible for chronic IBD.
AJG – Vol. 98, No. 9, Suppl., 2003
Profile of Patients with Positive Aeromonas Stool Culture Age/Gender/ Prior diagnosis of IBD
Timing of colonoscopy after onset of new symptoms
24/F/No 23/F/No 43/F/Yes
4 wks 6 months 7 wks
68/M/Yes
3 wks
Histopathology crypt architecture preserved architectural distortion present Significant acute inflammation and architectural distortion no colonoscopy
Response to antibiotic treatment Partially Yes Yes Yes
All patients on steroids/immunomodulators currently
516 DUODENAL EMBEDMENT OF AN INGESTED BAY LEAF: AN UNUSUAL CAUSE OF ACUTE ABDOMINAL PAIN Basher M. Atiquzzaman, M.D., Jagdish Gupta, M.D., Irwin M. Grosman, M.D.* Long Island College Hospital, Brooklyn, NY. A 59 year-old man, with no significant past medical history, developed acute epigastric and retrosternal chest pain while on his way home from a local restaurant where he had curried beef for dinner. He presented to his local emergency room where he was evaluated. A EKG did not reveal any acute changes and the cardiac enzymes were normal; an acute myocardial infarction was ruled out. He was reassured and discharged home on famotidine. The severe epigastric and chest pain persisted. The next day he was referred to a gastroenterologist and an urgent EGD was done. EGD showed mild esophagitis and erosive gastritis. Upon entering the duodenum, a large fragment of a dried bay leaf was noted to be embedded in the mucosa of the duodenal bulb at the stem. Utilizing biopsy forceps and polypectomy snare the bay leaf was disimpacted from the duodenal mucosa and retrieved. Upon subsequent examination a small ulceration was noted in the duodenem where the stem of the bay leaf was embedded. This was surrounded by edema and nodularity. The remainder of the duodenum was normal. Immediately after the procedure the patient reported relief of his pain symptoms. He was given a course of esomeprazole 40mg daily and had no subsequent recurrence of symptoms. Accidental bay leaf ingestion has been described as a rare cause of duodenal obstruction, upper gastrointestinal tract hemorrhage and perforation of the small intestine. Cases of pharyngeal and esophageal impaction have been reported. To our knowledge this is the first report of acute abdominal pain resulting from the accidental ingestion of a dried bay leaf which embedded in the duodenal mucosa. 517 SARCOMATOID HEPATOCELLULAR CARCINOMA, A RARE NEOPLASM IN UNITED STATES Sailaja M. Cheruku, M.D., John O’Brien, M.D.*, Brian Webb, M.D. Southern Illinois University School Of Medicine, Springfield, IL and Memorial Medical Center, Springfield, IL. A 66 year-old caucasian male was admitted to hospital for evaluation of increasing right upper quadrant pain for three weeks. He denied nausea, vomitting, jaundice or other significant complaints. His past medical history included Diabetes and Hypertension. Family history was negative for malignancy. He denied tobacco and alcohol use. Physical examination was only significant for tenderess in right upper quadrant with gaurding but no rebound. Laboratory evaluation showed hemoglobin of 8.5 mg/dl, low serum iron but normal electrolytes, amylase, lipase and liver fuction tests. An ultrasound of abdomen showed a hypoehoic mass in right hepatic lobe, no gall stones or ductal dialatation. Further evaluation with a CT scan showed, an irregular lesion 7.5cm in diameter along the inferolateral right lobe of liver highly suspicious for neoplasm. Alpha feto protein level was normal. Biopsy of the lesion was performed and histology showed extensive infiltration of liver parenchyma by a markedly cellular pleomorphic malignant neoplasm arranged in solid sheets and apparent fascicles.The cells demonstrated in some areas a spindled or sarcomatoid appearance and immunohistochemical stains for vimentin, cytokeratin AE1 and 3 were strongly positive but stains for cytokeratin 7, 20, S100, CD34, actin, and
AJG – September, Suppl., 2003
desmin were negative. The morphologic and immunohistochemical features were consistent with a “sarcomatoid carcinoma”. Further evaluation with endoscopy, CT of chest and PET scan did not demonstrate any other tomor focus. The final diagnosis was “unusual primary hepatocellular carcinoma”. Oncology recommended local therapy : surgery, hepatic artery embolization or radiofrequency ablation. Despite discussions, Pt declined above therapies. His pain worsened despite pain medications. A repeat CT scan in 3 weeks showed increase in size of tumor, peritoneal metastases with extensive ascitis and new 1.5cm metastatic lesion in right lobe of liver. He went to hospice care and expired in two weeks. Hepato cellular carcinoma ( HCC) with sarcomatous features is a rare neoplasm which has been found in only 1.8% of surgically resected HCC and prognosis is poor due to early development of intrahepatic and distal metastases.The frequency of tumor was about 4% of all HCCs, according to the literature. Alpha feto protein level is usually normal. Immunohistochemical staining for vimentin and cytokeratin are helpful in diagnosis. Literature review did not show any case from united states.
Abstracts
S175
ileostomy. A dermatologist evaluated his peristomal skin lesion and diagnosed pyoderma gangrenosum with biopsies of the lesion showing peristomal granulation tissue with collections of neutrophils. On physical examination a 3 cm ulcerated violaceous lesion was seen beneath the ileostomy. A complete blood count, sedimentation rate, and C-reactive protein were normal. A small bowel series was normal. The patient refused treatment with corticosteroids and/or 6-mercaptopurine. Infliximab in a dose of 5 mg/kg iv was given. The ulcerated skin lesion healed in 2 weeks. Follow-up infliximab infusions were given at 3 weeks and at 4 months after the initial treatment. The peristomal pyoderma gangrenosum had not recurred 6 months after initial infliximab therapy.
518 CONTROL OF HEMORRHAGE FROM A GASTRIC DIEULAFOY’S LESION USING ARGON PLASMA COAGULATION Poneh Rahimi, M.D., Irwin Grosman, M.D., Adnan Khdair, M.D.* Long Island College Hospital, Brooklyn, NY. A 52 year-old male with a history of hypertension presented to the emergency room with multiple episodes of hematemesis. He denied any history of prior GI bleeding episodes, PUD, NSAID use, or heavy alcohol use. There was no abdominal pain or melena associated with the presenting symptoms. The physical exam was remarkable for tachycardia and borderline hypotention. The initial blood results revealed normal chemistries, liver function tests, coagulation factors and a hematocrit of 40.5 %. Nasogastric lavage revealed fresh blood, which did not clear after lavaging with 2 liters of saline. Urgent EGD was performed and revealed a single spurting vessel with normal surrounding mucosa and no evidence of ulceration (diagnosed as Dieulafoy’s lesion) in the greater curvature within 3cm from GE junction. After applying epinephrine injection (12 CC of 1: 10,000) and thermocoagulation (BICAP setting 20 W in the continuous mode), the lesion still continued to bleed. Using the argon plasma coagulator (setting of 60 W and 1L/min), bleeding was stopped successfully after three applications. The repeat hemoglobin dropped to 8.5 but patient refused blood transfusion. Over the course of the hospital stay hemoglobin stabilized and there was no recurrent bleeding. He was discharged on hospital day 5.The Dieulafoy’s lesion is a rare cause of severe gastrointestinal hemorrhage. Several endoscopic modalities have been used to treat this condition including: thermal, schlerotherapy (using epinephrine, alcohol and ethanolamine) and mechanical means (hemoclips, sewing, band ligation and endoloop). Combination therapy with two or more modalities is purported to be superior to single modality therapy. Use of the APC in treating Dieulafoy’s lesion has not previously been reported in the literature. The successful result with APC in this case may introduce a new means of therapy for Dieulafoy’s lesion.
Conclusion: Infliximab was an effective therapy for a patient with peristomal pyoderma gangrenosum associated with Crohn’s disease. 520
519 TREATMENT OF PERISTOMAL PYODERMA GANGRENOSUM ASSOCIATED WITH CROHN’S DISEASE WITH INFLIXIMAB Warren Finkelstein, M.D., FACG* The Gastroenterology Group of New Jersey, Glen Ridge, NJ.
GASTRIC ASCARIASIS PRESENTING AS RECURRENT MASSIVE UPPER GASTROINTESTINAL BLEEDING Thomas A. Scileppi, M.D., Joel Albert, M.D., John Trillo, M.D., Scott Tenner, M.D., FACG* Maimonides Medical Center, Mount Sinai School of Medicine, Brooklyn, NY.
Peristomal pyoderma gangrenosum is a very unusual painful complication of Crohn’s disease that may occur after total proctocolectomy with ileostomy. It is often misdiagnosed as a skin infection and mismanaged with ineffective therapy. Local wound care measures are usually unsuccessful and most patients require systemic medical therapy. I document a case of peristomal pyoderma gangrenosum in a patient with Crohn’s disease treated with infliximab. Case Report: A 51 year-old physician with a history of Crohn’s disease since age 5 and total proctocolectomy with ileostomy performed at age 12 presented with a 3-week history of a very painful ulcerated lesion adjacent to his
Ascaris lumbricoides is a parasitic nematode that, in its adult phase, lives in the human gastrointestinal tract. Ascaris lumbriciodes infects approxiamately one-fourth of the world’s population. Most persons infected have minimal symptoms. Less commonly, weight loss, pneumonia and gastrointestinal/biliary obstruction can occur. We present a patient with recurrent massive gastrointestinal bleeding found to have Ascaris lunbricoides. A 63 year-old Bangladeshi female presented to the medical center with symptoms of weakness, fatigue, dark stools and coffee ground emesis. One year prior, she had been hospitalized elsewhere with an upper gastrointestinal bleed. The etiology was unclear. The patient reported that the physicians found a “small