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Gastrointestinal histoplasmosis involving the stomach and colon defining a patient with aids
S130
Abstracts
394 INLET PATCH–ASSOCIATED UPPER ESOPHAGEAL RING AND PSEUDODIVERTICULUM COMPLICATED BY FOOD BOLUS IMPACTION Christopher P. Shaver, M.D. and Martin E. Avalos, M.D., FACG*. Division of Digestive Diseases and Nutrition, University of South Florida, Tampa, FL and James A. Haley VA Medical Center, Tampa, FL. Purpose: An inlet patch is described as isolated ectopic gastric mucosa located in the upper esophagus at the level of the upper esophageal sphincter. This is a congenital abnormality and is identified in approximately four percent of patients undergoing diagnostic endoscopy. The inlet patch appears as a round or oval patch of red epithelium in the upper third of the esophagus that is flat and sharply demarcated. These lesions are incidental findings and rarely cause symptoms. Sample biopsies are consistent with gastric–type epithelium and may contain acid–secreting parietal cells. Several notable associations and complications have been linked to the inlet patch. The presence of pancreatic acinar metaplasia has been reported. There have been reports of associations with Barrett’s esophagus and adenocarcinoma arising from inlet patches. Upper esophageal strictures, rings, webs, mucosal ulcerations, and perforation have been reported. Complications are thought to be secondary to acid secretion from the inlet patch. We present a case of a patient with an acute, upper esophageal food bolus impaction requiring emergent EGD. Follow– up endoscopy revealed the presence of an inlet patch with an adjacent esophageal ring and pseudodiverticulum. Case Report: A 70 YO male presented to the ER complaining of food being “stuck in his throat.” He was in distress and hypersalivating. History was negative for prior GERD, dysphagia, or peptic strictures. Emergent EGD was performed which revealed the presence of a food bolus impaction at 20cm which was removed. EGD was performed two weeks later secondary to mild, persistent dysphagia. Careful examination of the proximal esophagus revealed the presence of an oval, 1cm by 1cm inlet patch at 21cm. A mucosal ring was observed at the level of the inlet patch. A 2cm pseudodiverticulum protruded proximal to the ring in close proximity to the inlet patch. Biopsies taken from the inlet patch, ring, and pseudodiverticulum were consistent with cardia–type gastric mucosa. Dilation was performed with complete relief of dysphagia. A BA swallow revealed an upper esophageal mucosal ring and a 2cm cervicothoracic pseudodiverticulum. Conclusion: Inlet patches are incidental findings but can be associated with significant symptoms and morbidity. Meticulous inspection of the proximal esophagus under adequate sedation is invaluable in picking up inlet patch and associated complications.
395 COPE’S SYNDROME REVISITED Terrence A. Smith, M.D.*. Div of Gastroenterology, Vanderbilt Univ Med Ctr, Nashville, TN. Background: In 1936, Cope noted that the side– effects of milk and alkali therapy for peptic ulcer disease occasionally produced a milk–alkali syndrome (MAS) of marked hypercalcemia, azotemia, and elevated plasma bicarbonate with decreased serum chloride. Biochemical abnormalities quickly normalized when the offending agents were discontinued but the impaired renal function often took weeks to resolve. This case exemplifies Cope’s form of MAS, which, with the advent of H2RA’s and PPI’s, has become exceedingly rare. Case Report: A 46 YO male complained of a 2–wk H/O severe, sharp epigastric pain. He described increasing episodes of nausea and vomiting, anorexia, constipation, weakness, and fatigue. New– onset polydipsia and polyuria were also reported. In an effort to control his pain, he steadily increased his use of an NSAID– based OTC analgesic. He coupled this with ever–increasing amounts of calcium– carbonate for his nausea and extraordinary amounts of milk (up to 2– gallons a day) to “settle his stomach”. PE revealed a pale thin WM in obvious discomfort. He had mild confusion and
AJG – Vol. 97, No. 9, Suppl., 2002
depressed affect. His vitals were all wnl and his HEENT exam was significant for b/l band keratopathy with corneal injection and dry mucus membranes. Lungs were clear and the cardiovascular exam was normal. Abdominal exam revealed normoactive bowel sounds, epigastric tenderness without rebound, guarding, or distention. DTR’s were depressed and there was generalized muscle hypotonia. Lab data: sCa– 16.3 mg/dL (decreasing to nl after 4 d of treatment), BUN– 18 mg/dL, Cr– 1.8 mg/dL (correcting to nl at 4 –wk f/u), CO2– 29 mmol/L, Cl– 94 mEq/L. Other labs including PO4, Mg, Alk Phos, PTH, and TSH were wnl. An EGD revealed a very large clean– based prepyloric ulcer. Discussion: Given the high cost of prescription antiacids, some with dyspepsia may seek relief in the form of OTC and home remedies. This case reviews several features of Cope’s syndrome, felt to have a more reversible renal course than the more severe form of MAS known as Burnett’s syndrome. In general, MAS involves the prolonged excessive intake of milk and absorbable alkali leading to hypercalecemia without a fall in serum phosphate and without hypercalciuria. Azotemia and a mild alkalosis typically ensue. Hyperparathyroidism must be ruled out and treatment focuses on calcium and alkali restrictions along with a full dyspepsia evaluation with standard ulcer treatment as indicated. While now quite rare, MAS should still be considered in those presenting with dyspepsia and hypercalcemia.
396 GASTROINTESTINAL HISTOPLASMOSIS INVOLVING THE STOMACH AND COLON DEFINING A PATIENT WITH AIDS Garth J. Garramone, D.O., Daniel Freese, D.O., Carylann Hadjiyane, M.D., Crescens Pellecchia, M.D. and Ali S. Karakurum, M.D.*. Department of Gastroenterology, Nassau University Medical Center, East Meadow, NY. Introduction: We discuss a patient who presented to our intstitution complaining of intermittant rectal bleeding and weight loss. After a full gastrointestinal work– up was obtained, stomach and colonic histoplasmosis was discovered. The new diagnosis of AIDS was given because of this disseminated disease. Case: A 24 year old female without significant medical problems came to our institution complaining of a two month hisotry of occasional nausea associated with bilious vomiting. She also had loose watery stools that were blood–streaked. She developed dull, right upper quadrant pain in the past month. The patient also noted a decrease in appetite and a 25 lb weight loss. The patient denied fever, chills, black stools, vomining blood, urinary or respiratory symptoms. There were no sick contacts or recent foreign travel. On examination; temp. 99, blood pressure 90/60, pulse 100, the patient was thin and in mild distress complaining of right upper quadrant pain. Right cervical adenopathy and hepatosplenomegaly were appreciated. Rectal exam revealed no blood or stool in the vault. Conclusions: A CT scan showed fatty liver, splenomegaly , thickened ascending and transverse colon. A colonoscopy revealed diffuse, friable, ulcerated, pseudotumors, which ranged form 1–5cm throughout. Also, small polypoid lesions were noted. An EGD revealed small 5mm–1cm polypoid lesions. Biopsies and brushing were obtained from both areas. Biopsies in the colon consisted of necrotizing granulomatous inflammation with numerous fungal elements. CMV was also present in the colon. The polypoid lesions in the stomach were consistant with histoplasmosis. A lymph node biopsy was done and showed granulomatous inflammation consistant with disseminated histoplasmosis. Gastrointestinal histoplasmosis is usually associated with peripheral adenopathy, hepatosplenomgegaly and disseminated disease. Fever and respiratory symptoms are usually uncommon. The most common site of involvement are the ileum and cecum and rarely affects the stomach, however any area can be involved. The colonic and stomach histoplasmosis was treated with amphotericin B with a total dose of 2 grams. CMV was treated with ganciclovir. On re– evaluation 4 months later, the colon and stomach lesions had resolved and she is maintained on itraconazole 200mg twice daily.
Abstracts
394 INLET PATCH–ASSOCIATED UPPER ESOPHAGEAL RING AND PSEUDODIVERTICULUM COMPLICATED BY FOOD BOLUS IMPACTION Christopher P. Shaver, M.D. and Martin E. Avalos, M.D., FACG*. Division of Digestive Diseases and Nutrition, University of South Florida, Tampa, FL and James A. Haley VA Medical Center, Tampa, FL. Purpose: An inlet patch is described as isolated ectopic gastric mucosa located in the upper esophagus at the level of the upper esophageal sphincter. This is a congenital abnormality and is identified in approximately four percent of patients undergoing diagnostic endoscopy. The inlet patch appears as a round or oval patch of red epithelium in the upper third of the esophagus that is flat and sharply demarcated. These lesions are incidental findings and rarely cause symptoms. Sample biopsies are consistent with gastric–type epithelium and may contain acid–secreting parietal cells. Several notable associations and complications have been linked to the inlet patch. The presence of pancreatic acinar metaplasia has been reported. There have been reports of associations with Barrett’s esophagus and adenocarcinoma arising from inlet patches. Upper esophageal strictures, rings, webs, mucosal ulcerations, and perforation have been reported. Complications are thought to be secondary to acid secretion from the inlet patch. We present a case of a patient with an acute, upper esophageal food bolus impaction requiring emergent EGD. Follow– up endoscopy revealed the presence of an inlet patch with an adjacent esophageal ring and pseudodiverticulum. Case Report: A 70 YO male presented to the ER complaining of food being “stuck in his throat.” He was in distress and hypersalivating. History was negative for prior GERD, dysphagia, or peptic strictures. Emergent EGD was performed which revealed the presence of a food bolus impaction at 20cm which was removed. EGD was performed two weeks later secondary to mild, persistent dysphagia. Careful examination of the proximal esophagus revealed the presence of an oval, 1cm by 1cm inlet patch at 21cm. A mucosal ring was observed at the level of the inlet patch. A 2cm pseudodiverticulum protruded proximal to the ring in close proximity to the inlet patch. Biopsies taken from the inlet patch, ring, and pseudodiverticulum were consistent with cardia–type gastric mucosa. Dilation was performed with complete relief of dysphagia. A BA swallow revealed an upper esophageal mucosal ring and a 2cm cervicothoracic pseudodiverticulum. Conclusion: Inlet patches are incidental findings but can be associated with significant symptoms and morbidity. Meticulous inspection of the proximal esophagus under adequate sedation is invaluable in picking up inlet patch and associated complications.
395 COPE’S SYNDROME REVISITED Terrence A. Smith, M.D.*. Div of Gastroenterology, Vanderbilt Univ Med Ctr, Nashville, TN. Background: In 1936, Cope noted that the side– effects of milk and alkali therapy for peptic ulcer disease occasionally produced a milk–alkali syndrome (MAS) of marked hypercalcemia, azotemia, and elevated plasma bicarbonate with decreased serum chloride. Biochemical abnormalities quickly normalized when the offending agents were discontinued but the impaired renal function often took weeks to resolve. This case exemplifies Cope’s form of MAS, which, with the advent of H2RA’s and PPI’s, has become exceedingly rare. Case Report: A 46 YO male complained of a 2–wk H/O severe, sharp epigastric pain. He described increasing episodes of nausea and vomiting, anorexia, constipation, weakness, and fatigue. New– onset polydipsia and polyuria were also reported. In an effort to control his pain, he steadily increased his use of an NSAID– based OTC analgesic. He coupled this with ever–increasing amounts of calcium– carbonate for his nausea and extraordinary amounts of milk (up to 2– gallons a day) to “settle his stomach”. PE revealed a pale thin WM in obvious discomfort. He had mild confusion and
AJG – Vol. 97, No. 9, Suppl., 2002
depressed affect. His vitals were all wnl and his HEENT exam was significant for b/l band keratopathy with corneal injection and dry mucus membranes. Lungs were clear and the cardiovascular exam was normal. Abdominal exam revealed normoactive bowel sounds, epigastric tenderness without rebound, guarding, or distention. DTR’s were depressed and there was generalized muscle hypotonia. Lab data: sCa– 16.3 mg/dL (decreasing to nl after 4 d of treatment), BUN– 18 mg/dL, Cr– 1.8 mg/dL (correcting to nl at 4 –wk f/u), CO2– 29 mmol/L, Cl– 94 mEq/L. Other labs including PO4, Mg, Alk Phos, PTH, and TSH were wnl. An EGD revealed a very large clean– based prepyloric ulcer. Discussion: Given the high cost of prescription antiacids, some with dyspepsia may seek relief in the form of OTC and home remedies. This case reviews several features of Cope’s syndrome, felt to have a more reversible renal course than the more severe form of MAS known as Burnett’s syndrome. In general, MAS involves the prolonged excessive intake of milk and absorbable alkali leading to hypercalecemia without a fall in serum phosphate and without hypercalciuria. Azotemia and a mild alkalosis typically ensue. Hyperparathyroidism must be ruled out and treatment focuses on calcium and alkali restrictions along with a full dyspepsia evaluation with standard ulcer treatment as indicated. While now quite rare, MAS should still be considered in those presenting with dyspepsia and hypercalcemia.
396 GASTROINTESTINAL HISTOPLASMOSIS INVOLVING THE STOMACH AND COLON DEFINING A PATIENT WITH AIDS Garth J. Garramone, D.O., Daniel Freese, D.O., Carylann Hadjiyane, M.D., Crescens Pellecchia, M.D. and Ali S. Karakurum, M.D.*. Department of Gastroenterology, Nassau University Medical Center, East Meadow, NY. Introduction: We discuss a patient who presented to our intstitution complaining of intermittant rectal bleeding and weight loss. After a full gastrointestinal work– up was obtained, stomach and colonic histoplasmosis was discovered. The new diagnosis of AIDS was given because of this disseminated disease. Case: A 24 year old female without significant medical problems came to our institution complaining of a two month hisotry of occasional nausea associated with bilious vomiting. She also had loose watery stools that were blood–streaked. She developed dull, right upper quadrant pain in the past month. The patient also noted a decrease in appetite and a 25 lb weight loss. The patient denied fever, chills, black stools, vomining blood, urinary or respiratory symptoms. There were no sick contacts or recent foreign travel. On examination; temp. 99, blood pressure 90/60, pulse 100, the patient was thin and in mild distress complaining of right upper quadrant pain. Right cervical adenopathy and hepatosplenomegaly were appreciated. Rectal exam revealed no blood or stool in the vault. Conclusions: A CT scan showed fatty liver, splenomegaly , thickened ascending and transverse colon. A colonoscopy revealed diffuse, friable, ulcerated, pseudotumors, which ranged form 1–5cm throughout. Also, small polypoid lesions were noted. An EGD revealed small 5mm–1cm polypoid lesions. Biopsies and brushing were obtained from both areas. Biopsies in the colon consisted of necrotizing granulomatous inflammation with numerous fungal elements. CMV was also present in the colon. The polypoid lesions in the stomach were consistant with histoplasmosis. A lymph node biopsy was done and showed granulomatous inflammation consistant with disseminated histoplasmosis. Gastrointestinal histoplasmosis is usually associated with peripheral adenopathy, hepatosplenomgegaly and disseminated disease. Fever and respiratory symptoms are usually uncommon. The most common site of involvement are the ileum and cecum and rarely affects the stomach, however any area can be involved. The colonic and stomach histoplasmosis was treated with amphotericin B with a total dose of 2 grams. CMV was treated with ganciclovir. On re– evaluation 4 months later, the colon and stomach lesions had resolved and she is maintained on itraconazole 200mg twice daily.