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Sarcoidosis of the esophagus presenting macroscopically as Barrett’s esophagitis
AJG – July, 2003
13. Moore JG, Tweedy C, Christian PE, Datz FL. Effect of age on gastric emptying of liquid–solid meals in man. Dig Dis Sci 1983;28:340 –4. 14. Horowitz M, Maddern GJ, Chatterton BE, et al. Changes in gastric emptying rates with age. Clin Sci 1984;67:213–8. 15. Greiff JMC, Rowbotham D. Pharmacokinetics drug interactions with gastrointestinal motility modifying agents. Clin Pharmacokinet 1994;27:447–61. 16. Kahraman H, Kaya N, Demircali A, et al. Gastric emptying time in patients with primary hypothyroidism. Eur J Gastroenterol Hepatol 1997;9:901–4. 17. Folstein MF, Folstein SE, Mc Hugh PR. “Mini Mental State:” A practical method for grading the cognitive state of patients for the clinician. J Psychiat Res 1975;12:189 –98. 18. Mahoney FI, Barthel DW. Functional evaluation: The Barthel Index. Maryland State Med J 1965;14:61–5. 19. Madsen JL. Effects of gender, age and body mass index on gastrointestinal transit times. Dig Dis Sci 1992;37:1548 –53. Reprint requests and correspondence: Philippe Chassagne, M.D., Service de Me´decine Interne Ge´riatrique—CHU Rouen, 76 031, Rouen Cedex, France. Received Dec. 17, 2002; accepted Dec. 18, 2002.
Sarcoidosis of the Esophagus Presenting Macroscopically as Barrett’s Esophagitis TO THE EDITOR: Sarcoidosis is a systemic granulomatous disease of unknown cause. Involvement of the GI tract is very infrequent, with an incidence between 0.1% and 0.9% (1, 2), and is symptomatically rare. It has been believed that as endoscopy proceeds, the operator should be able to recognize— or at least to suspect—sarcoidosis from the macroscopic appearance (3). We report a case of sarcoidosis appearing with the macroscopic appearance of Barrett’s esophagitis. We believe this to be the first reported case of sarcoidosis affecting the esophagus so as to present in this way. A 54-yr-old woman was referred for investigation of a 4-month history of anemia. She was diagnosed with sarcoidosis in 1973 and treated from 1983 to 1998 with immunosuppressants for neurological complications. Her sarcoidosis had been clinically and radiologically quiescent since 1998. There was no history of any blood loss, upper or lower GI symptoms, or weight loss. She did not smoke. Her diet was varied and good. Medication consisted of iron supplements and two laxative preparations. There was no record of any use of nonsteroidal anti-inflammatory drugs. Abdominal examination did not reveal any abnormalities. Hb at referral was 9.7 with normal platelet and white cell count at MCV 90.3 and MCHC 31.6. At esophagogastroduodenoscopy (EGD), a macroscopic appearance of Barrett’s esophagitis was seen, with dark pink mucosa up to 28 cm (Fig. 1). Histology showed active inflammation with an infiltrate of lymphocytes, plasma cells, and granuloma. There was no evidence of intestinal
Letters to the Editor
1661
Figure 1. Endoscopic appearance of the esophagus at 28 cm.
metaplasia or the appearance of goblet cells to suggest Barrett’s metaplasia. The diagnosis of sarcoidosis requires a compatible clinical picture, histology of noncaseating granulomas, and exclusion of other differentials. In light of this patient’s medical history we made a diagnosis of sarcoidosis involving the esophagus. In the literature, cases of sarcoidosis involving the esophagus have mainly presented with dysphagia. The esophagus can be affected via a number of different pathways, such as pressure exerted from outside the walls (4), involvement of the walls themselves (5, 6), or nervous control of contractility causing achalasia (9). Oral steroids are stated as the treatment of choice for GI sarcoidosis, starting with high doses (30 – 40 mg prednisolone daily) before tapering down once there is clinical and subjective improvement (7). Sarcoid ulceration has also been treated with antacids (8). Follow-up endoscopy is recommended, as it is likely that the granulomatous process will only be stalled and not completely healed (3). Esophageal motility disorders have been treated with surgery alone, steroids alone, and a combination of both (5, 9). Because of the extremely low frequency of sarcoidosis affecting the esophagus, there are no trials comparing the various treatment modalities for the various presentations. This case shows esophageal involvement of sarcoidosis in a patient without any upper intestinal complaints. Endoscopy should be considered in sarcoidosis even if the markers of systemic activity are negative. Steroid therapy should be considered if there is involvement of the GI tract. In this case, however, steroid therapy was withheld because the patient was asymptomatic, and she was commenced on long term proton pump inhibitor treatment. A. Murdock, MB Bch BAO, MRCP G. Jacob, M.D., F.R.C.P. Department of Medicine Downe Hospital Downpatrick, North Ireland, United Kingdom
1662
Letters to the Editor
AJG – Vol. 98, No. 7, 2003
REFERENCES 1. Mayock RL, Bertard P, et al. Manifestations of sarcoidosis, analysis of 145 patients and a review of nine series selected from the literature. Am J Med 1963;35:67–89. 2. Israel HL, Sones M. Sarcoidosis, clinical observations on 161 cases. Arch Intern Med 1958;102:766 –75. 3. Chlumsky J, Krtek V, Chlumska A. Sarcoidosis of the stomach: Endoscopic diagnosis and possibilities of conservative treatment. Hepato-Gastroenterology 1985;32:255–7. 4. Cook DM, Dines DE, Dycus DS. Sarcoidosis: Report of a case presenting as dysphagia. Chest 1970;57:84 –6. 5. Siegel CI, Honda M, Salik J, et al. Dysphagia due to granulomatous myositis of the cricopharyngeous muscle: Physiological and cineradiographic studies prior to and following successful surgical therapy. Trans Assoc Am Phys 1961;74:342–52. 6. Wiesner PJ, Kleiman MS, Condemi JJ, et al. Sarcoidosis of the oesophagus. Dig Dis 1971;16:943–51. 7. Sharma A, Kadakia J, Sharma OP. Gastrointestinal sarcoidosis. Semin Respir Med 1992;13:442–9. 8. Ona FV. Gastric sarcoid: Unusual cause of upper gastrointestinal haemorrhage. Am J Gastroenterol 1981;75:286 –8. 9. Dufresne CR, Jeyasingham K, Baker RR. Achalasia of the cardia associated with pulmonary sarcoidosis. Surgery 1983; 94:32–5. Figure 1. Endoscopic view of disopyrobezoars in the stomach. Reprint requests and correspondence: G. Jacob, M.D., F.R.C.P., Consultant Gastroenterologist, Downe Hospital, Pound Lane, Downpatrick, Northern Ireland BT30 6JA, Northern Ireland, UK. Received Oct. 18, 2003; accepted Feb. 13, 2003.
The First Report of Successful Nasogastric Coca-Cola Lavage Treatment for Bitter Persimmon Phytobezoars in Japan TO THE EDITOR: Bezoars are concretions or hard masses of foreign matter found in the intestinal tract. A disopyrobezoar is a type of phytobezoar that is caused by persimmons, and that is considered to be harder than other types of phytobezoars. Disopyrobezoars are often resistant to drug treatment and hence are usually removed endoscopically or surgically (1, 2). Recently, the efficacy of nasogastric administration of Coca-Cola for the dissolution of phytobezoar was reported from Greece (3). Here we report the first case of disopyrobezoars that was successfully treated by nasogastric Coca-Cola lavage in Japan. A 52-yr-old woman was admitted to Toyokawa City Hospital with lower abdominal pain and vomiting. She had experienced abdominal discomfort after eating bitter persimmons 3 days before admission. Seven years before the current admission she had experienced depression and had received antidepressants orally. On physical examination the abdomen was slightly distended, and moderate tenderness was noted in the lower abdominal region. Abdominal radiography and a computed tomographic scan revealed dilation and niveau formation at the small intestine. The patient was diagnosed with a small intestine obstruction of
unknown etiology and was treated by intestinal tube for 7 days. This decreased the frequency and severity of abdominal pain, and the abdominal distension disappeared. Despite cure of the obstruction of the small intestine, epigastric discomfort persisted. Esophagogastroduodenoscopy (EGD) revealed two white-greenish, round bezoars with irregular surfaces in the stomach (Fig. 1). A piece of the bezoars obtained using forceps during EGD was analyzed by infrared spectroscopy, which revealed that 98% of them was composed of tannin. Therefore, the bezoars were considered to be disopyrobezoars derived from bitter persimmons. After obtaining informed consent from the patient, we performed nasogastric Coca-Cola lavage treatment according to the procedure reported by Ladas et al. (3). Briefly, 3 L of “Coca-Cola light” (Coca-Cola (Japan) Co., Ltd., Tokyo, Japan) was infused through a 16F nasogastric tube over 12 h. The next day, EGD demonstrated the complete disappearance of the disopyrobezoars from the stomach. No major complication occurred during the Coca-Cola lavage. After the dissolution of the disopyrobezoars, abdominal radiography revealed the absence of any intestinal obstruction by the dissolved disopyrobezoars. Disopyrobezoars are considered to be distinct from other phytobezoars because of their particular features such as stony constitution and resistance to enzymatic treatment. Disopyrobezoars are generated by ingestion of the soluble tannin and shibuol found in unripe or astringent persimmons. In the presence of the dilute hydrochloric acid in the stomach, this tannin undergoes polymerization to a coagulum that includes cellulose, hemicellulose, and protein, which is the basis of the bezoar (4). A number of endoscopic techniques for the management of disopyrobezoars have been described, including fragmen-
13. Moore JG, Tweedy C, Christian PE, Datz FL. Effect of age on gastric emptying of liquid–solid meals in man. Dig Dis Sci 1983;28:340 –4. 14. Horowitz M, Maddern GJ, Chatterton BE, et al. Changes in gastric emptying rates with age. Clin Sci 1984;67:213–8. 15. Greiff JMC, Rowbotham D. Pharmacokinetics drug interactions with gastrointestinal motility modifying agents. Clin Pharmacokinet 1994;27:447–61. 16. Kahraman H, Kaya N, Demircali A, et al. Gastric emptying time in patients with primary hypothyroidism. Eur J Gastroenterol Hepatol 1997;9:901–4. 17. Folstein MF, Folstein SE, Mc Hugh PR. “Mini Mental State:” A practical method for grading the cognitive state of patients for the clinician. J Psychiat Res 1975;12:189 –98. 18. Mahoney FI, Barthel DW. Functional evaluation: The Barthel Index. Maryland State Med J 1965;14:61–5. 19. Madsen JL. Effects of gender, age and body mass index on gastrointestinal transit times. Dig Dis Sci 1992;37:1548 –53. Reprint requests and correspondence: Philippe Chassagne, M.D., Service de Me´decine Interne Ge´riatrique—CHU Rouen, 76 031, Rouen Cedex, France. Received Dec. 17, 2002; accepted Dec. 18, 2002.
Sarcoidosis of the Esophagus Presenting Macroscopically as Barrett’s Esophagitis TO THE EDITOR: Sarcoidosis is a systemic granulomatous disease of unknown cause. Involvement of the GI tract is very infrequent, with an incidence between 0.1% and 0.9% (1, 2), and is symptomatically rare. It has been believed that as endoscopy proceeds, the operator should be able to recognize— or at least to suspect—sarcoidosis from the macroscopic appearance (3). We report a case of sarcoidosis appearing with the macroscopic appearance of Barrett’s esophagitis. We believe this to be the first reported case of sarcoidosis affecting the esophagus so as to present in this way. A 54-yr-old woman was referred for investigation of a 4-month history of anemia. She was diagnosed with sarcoidosis in 1973 and treated from 1983 to 1998 with immunosuppressants for neurological complications. Her sarcoidosis had been clinically and radiologically quiescent since 1998. There was no history of any blood loss, upper or lower GI symptoms, or weight loss. She did not smoke. Her diet was varied and good. Medication consisted of iron supplements and two laxative preparations. There was no record of any use of nonsteroidal anti-inflammatory drugs. Abdominal examination did not reveal any abnormalities. Hb at referral was 9.7 with normal platelet and white cell count at MCV 90.3 and MCHC 31.6. At esophagogastroduodenoscopy (EGD), a macroscopic appearance of Barrett’s esophagitis was seen, with dark pink mucosa up to 28 cm (Fig. 1). Histology showed active inflammation with an infiltrate of lymphocytes, plasma cells, and granuloma. There was no evidence of intestinal
Letters to the Editor
1661
Figure 1. Endoscopic appearance of the esophagus at 28 cm.
metaplasia or the appearance of goblet cells to suggest Barrett’s metaplasia. The diagnosis of sarcoidosis requires a compatible clinical picture, histology of noncaseating granulomas, and exclusion of other differentials. In light of this patient’s medical history we made a diagnosis of sarcoidosis involving the esophagus. In the literature, cases of sarcoidosis involving the esophagus have mainly presented with dysphagia. The esophagus can be affected via a number of different pathways, such as pressure exerted from outside the walls (4), involvement of the walls themselves (5, 6), or nervous control of contractility causing achalasia (9). Oral steroids are stated as the treatment of choice for GI sarcoidosis, starting with high doses (30 – 40 mg prednisolone daily) before tapering down once there is clinical and subjective improvement (7). Sarcoid ulceration has also been treated with antacids (8). Follow-up endoscopy is recommended, as it is likely that the granulomatous process will only be stalled and not completely healed (3). Esophageal motility disorders have been treated with surgery alone, steroids alone, and a combination of both (5, 9). Because of the extremely low frequency of sarcoidosis affecting the esophagus, there are no trials comparing the various treatment modalities for the various presentations. This case shows esophageal involvement of sarcoidosis in a patient without any upper intestinal complaints. Endoscopy should be considered in sarcoidosis even if the markers of systemic activity are negative. Steroid therapy should be considered if there is involvement of the GI tract. In this case, however, steroid therapy was withheld because the patient was asymptomatic, and she was commenced on long term proton pump inhibitor treatment. A. Murdock, MB Bch BAO, MRCP G. Jacob, M.D., F.R.C.P. Department of Medicine Downe Hospital Downpatrick, North Ireland, United Kingdom
1662
Letters to the Editor
AJG – Vol. 98, No. 7, 2003
REFERENCES 1. Mayock RL, Bertard P, et al. Manifestations of sarcoidosis, analysis of 145 patients and a review of nine series selected from the literature. Am J Med 1963;35:67–89. 2. Israel HL, Sones M. Sarcoidosis, clinical observations on 161 cases. Arch Intern Med 1958;102:766 –75. 3. Chlumsky J, Krtek V, Chlumska A. Sarcoidosis of the stomach: Endoscopic diagnosis and possibilities of conservative treatment. Hepato-Gastroenterology 1985;32:255–7. 4. Cook DM, Dines DE, Dycus DS. Sarcoidosis: Report of a case presenting as dysphagia. Chest 1970;57:84 –6. 5. Siegel CI, Honda M, Salik J, et al. Dysphagia due to granulomatous myositis of the cricopharyngeous muscle: Physiological and cineradiographic studies prior to and following successful surgical therapy. Trans Assoc Am Phys 1961;74:342–52. 6. Wiesner PJ, Kleiman MS, Condemi JJ, et al. Sarcoidosis of the oesophagus. Dig Dis 1971;16:943–51. 7. Sharma A, Kadakia J, Sharma OP. Gastrointestinal sarcoidosis. Semin Respir Med 1992;13:442–9. 8. Ona FV. Gastric sarcoid: Unusual cause of upper gastrointestinal haemorrhage. Am J Gastroenterol 1981;75:286 –8. 9. Dufresne CR, Jeyasingham K, Baker RR. Achalasia of the cardia associated with pulmonary sarcoidosis. Surgery 1983; 94:32–5. Figure 1. Endoscopic view of disopyrobezoars in the stomach. Reprint requests and correspondence: G. Jacob, M.D., F.R.C.P., Consultant Gastroenterologist, Downe Hospital, Pound Lane, Downpatrick, Northern Ireland BT30 6JA, Northern Ireland, UK. Received Oct. 18, 2003; accepted Feb. 13, 2003.
The First Report of Successful Nasogastric Coca-Cola Lavage Treatment for Bitter Persimmon Phytobezoars in Japan TO THE EDITOR: Bezoars are concretions or hard masses of foreign matter found in the intestinal tract. A disopyrobezoar is a type of phytobezoar that is caused by persimmons, and that is considered to be harder than other types of phytobezoars. Disopyrobezoars are often resistant to drug treatment and hence are usually removed endoscopically or surgically (1, 2). Recently, the efficacy of nasogastric administration of Coca-Cola for the dissolution of phytobezoar was reported from Greece (3). Here we report the first case of disopyrobezoars that was successfully treated by nasogastric Coca-Cola lavage in Japan. A 52-yr-old woman was admitted to Toyokawa City Hospital with lower abdominal pain and vomiting. She had experienced abdominal discomfort after eating bitter persimmons 3 days before admission. Seven years before the current admission she had experienced depression and had received antidepressants orally. On physical examination the abdomen was slightly distended, and moderate tenderness was noted in the lower abdominal region. Abdominal radiography and a computed tomographic scan revealed dilation and niveau formation at the small intestine. The patient was diagnosed with a small intestine obstruction of
unknown etiology and was treated by intestinal tube for 7 days. This decreased the frequency and severity of abdominal pain, and the abdominal distension disappeared. Despite cure of the obstruction of the small intestine, epigastric discomfort persisted. Esophagogastroduodenoscopy (EGD) revealed two white-greenish, round bezoars with irregular surfaces in the stomach (Fig. 1). A piece of the bezoars obtained using forceps during EGD was analyzed by infrared spectroscopy, which revealed that 98% of them was composed of tannin. Therefore, the bezoars were considered to be disopyrobezoars derived from bitter persimmons. After obtaining informed consent from the patient, we performed nasogastric Coca-Cola lavage treatment according to the procedure reported by Ladas et al. (3). Briefly, 3 L of “Coca-Cola light” (Coca-Cola (Japan) Co., Ltd., Tokyo, Japan) was infused through a 16F nasogastric tube over 12 h. The next day, EGD demonstrated the complete disappearance of the disopyrobezoars from the stomach. No major complication occurred during the Coca-Cola lavage. After the dissolution of the disopyrobezoars, abdominal radiography revealed the absence of any intestinal obstruction by the dissolved disopyrobezoars. Disopyrobezoars are considered to be distinct from other phytobezoars because of their particular features such as stony constitution and resistance to enzymatic treatment. Disopyrobezoars are generated by ingestion of the soluble tannin and shibuol found in unripe or astringent persimmons. In the presence of the dilute hydrochloric acid in the stomach, this tannin undergoes polymerization to a coagulum that includes cellulose, hemicellulose, and protein, which is the basis of the bezoar (4). A number of endoscopic techniques for the management of disopyrobezoars have been described, including fragmen-