- Email: [email protected]
Alendronate-induced colon ulcers: case report of a new clinical entity
M Sawhney, D Nelson
Brief Reports
strongly considered in the evaluation of patients with portal hypertension and obstructive jaundice when other imaging modalities are unrevealing. REFERENCES
13.
14.
secondary to portal cavernoma. Ital J Gastroenterol Hepatol 1998;30:202-4. Colle I, VanVlierberghe H, Pattyn P, Troisi R, Vogelaers D, deHemptinne B, et al. Cholestasis as presenting symptom of portal cavernoma. Hepatol Res 2003;25:32-7. Mathieu D, Vasile N, Grenier P. Portal thrombosis: dynamic CT features and course. Radiology 1985;154:737-41. West MS, Garra BS, Horii SC, Hayes WS, Cooper C, Silverman PM, et al. Gallbladder varices: imaging findings in patients with portal hypertension. Radiology 1991;179: 179-82. Grimbert S, Vullierme MP, Dahan P, Hammel P, Bernades P. Value of color-Doppler ultrasound in the diagnosis of a diffuse intrahepatic portal cavernoma [French]. Gastroenterol Clin Biol 1993;17:295-7. Chawla A, Dewan R, Sarin SK. The frequency and influence of gallbladder varices on gallbladder functions in patients with portal hypertension. Am J Gastroenterol 1995;90: 2011-4. Condat B, Vilgrain V, Asselah T, O’ Toole D, Rufat P, Zappa M, et al. Portal cavernoma-associated cholangiopathy: a clinical and MR cholangiography coupled with MR portography imaging study. Hepatology 2003;37:1302-8. Petren T. Die extrahepatischen Gallenwegsvenen und ihre pathologischanatomische Bedeutung (The veins of the extrahepatic biliary system and their pathologic anatomic significance) [German]. Verh Anat Ges 1932;41: 139-43. Saint JA. The epicholedochal venous plexus and its importance as a means of identifying the common duct during operations on the extrahepatic biliary tract. Br J Surg 1961; 46:489-98. Gorgul A, Kayhan B, Dogan I, Unal S. Disappearance of the pseudocholangiocarcinoma sign after TIPSS. Am J Gastroenterol 1996;91:150-3. Chaudhary A, Dhar P, Sarin SK, Sachdev A, Agarwal AK, Vij JC, et al. Bile duct obstruction due to portal biliopathy in extrahepatic portal hypertension: surgical management. Br J Surg 1998;85:326-9. Palazzo L, Hochain P, Helmer C, Cuillerier E, Landi B, Roseau G, et al. Biliary varices on endoscopic ultrasonography: clinical presentation and outcome. Endoscopy 2000;32: 520-4.
1. Sarin SK, Bhatia V, Makwane U. Portal biliopathy in extra hepatic portal vein obstruction [abstract]. Indian J Gastroenterol 1992;2:A82. 2. Khuroo MS, Yattoo GN, Zargar SA, Javid G, Dar MY, Khan BA, et al. Biliary abnormalities associated with extrahepatic portal venous obstruction. Hepatology 1993;17: 807-13. 3. Chandra R, Kapoor D, Tharakan A, Chaudhary A, Sarin SK. Portal biliopathy: review. J Gastroenterol Hepatol 2001;16: 1086-92. 4. Chandra R, Tharakan A, Kapoor D, Sarin SK. Comparative study of portal biliopathy in patients with portal hypertension due to different etiologies [abstract]. Indian J Gastroenterol 1997;15(Suppl 2):A59. 5. Malkan GH, Bhatia SJ, Bashir K, Khemani R, Abraham P, Gandhi MS, et al. Cholangiopathy associated with portal hypertension: diagnostic evaluation and clinical implications. Gastrointest Endosc 1999;49:344-8. 6. Dhiman RK, Puri P, Chawla Y, Minz M, Bapuraj JR, Gupta S, et al. Biliary changes in extrahepatic portal venous obstruction: compression by collaterals or ischemic? Gastrointest Endosc 1999;50:646-52. 7. Dilawari JB, Chawla YK. Pseudosclerosing cholangitis in extrahepatic portal venous obstruction. Gut 1992;33:272-6. 8. Gibson JP, Johnston GW, Fulton TT. Extrahepatic portal vein obstruction. Br J Surg 1965;52:129-39. 9. Kim S, Chew FS. Choledochal varices. AJR Am J Roentgenol 1988;150:578-80. 10. Thervet L, Faulques B, Pissas A, Bremondy A, Monges B, Salducci J, et al. Endoscopic management of obstructive jaundice due to portal cavernoma. Endoscopy 1993;25:423-5. 11. Perlemuter G, Bejanin H, Fritsch J, Prat F, Gaudric M, Chaussade S, et al. Biliary obstruction caused by portal cavernoma: a study of 8 cases. J Hepatol 1996;25:58-63. 12. Solmi L, Rossi A, Conigliaro R, Sassatelli R, Gandolfi L. Endoscopic treatment of a case of obstructive jaundice
15.
BRIEF REPORTS
Thus, there is increasing use of bisphosphonates to prevent and to treat osteoporosis. These agents decrease bone resorption and increase bone mass, resulting in a decreased incidence of fractures.2 Esophageal injury caused by alendronate is well characterized, but there are no reports of injury to the colon. Two patients with colonic ulceration related to the use of alendronate are presented. Case report 1. A 62-year-old man presented to the emergency department with hematochezia. The medical history included severe osteoporosis, diabetes, chronic obstructive pulmonary disease, and stroke. Four months earlier, he began taking alendronate (10 mg once per day). Other medications included insulin, furosemide, warfarin, alprazolam, desipramine, diltiazem, and albuterol, all of which had been prescribed for longer than 1 year. He had not taken a prescription or over-thecounter non-steroidal anti-inflammatory drug (NSAID) during the previous year. Orthostasis was present at admission. The Hb level was 8.5 g/dL (normal: 14-17.9 g/dL);
Alendronate-induced colon ulcers: case report of a new clinical entity As the average age of the population of the United States increases, osteoporosis becomes an increasingly important health concern. One in two white, postmenopausal women, and one in 8 older men and women of other racial groups, develop an osteoporotic fracture during their lifetime.1
Reprint requests: Douglas B. Nelson, MD, VA Medical Center (111D), One Veterans Dr., Minneapolis, MN 55417. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(04)02193-5 1024
GASTROINTESTINAL ENDOSCOPY
16.
17.
18.
19.
20.
21.
22.
23.
VOLUME 60, NO. 6, 2004
Brief Reports
Figure 1. Colonoscopic view (Case report 1) of large stellate cecal ulcer. 6 months before admission, the Hb level was 14 g/dL. The international normalized ratio (INR) was 4.0. Treatment included transfusion of packed red blood cells and administration of fresh frozen plasma and vitamin K. Colonoscopy after resuscitation revealed a large, stellate 10-cm ulcer in the cecum (Fig. 1). A visible vessel in the base of the ulcer was bleeding slowly. Hemostasis was achieved by injection of 14 mL of a 1:10,000 solution of epinephrine. Biopsy specimens obtained from the lesion demonstrated ulceration with deposits of fibrin, inflammatory cells, and cellular debris. There was no malignancy, cryptitis, granuloma, or viral inclusions. Viral, fungal, and acid-fast bacilli cultures and stains were negative. Treatment with alendronate was stopped; all other medications were continued. A colonoscopy 1 month later demonstrated marked healing of the cecal ulcer, and colonoscopy 2 years later revealed complete resolution of the ulcer. Case report 2. A healthy 74-year-old man presented to his primary care physician with non-specific bone pain. The alkaline phosphatase was found to be elevated. Standard bone radiographs and radionucleotide bone scintigraphy were suggestive of Paget’s disease. Treatment was started with alendronate (10 mg per day). The patient had hypertension that was well controlled with hydrochlorothiazide and triamterene. He was not taking any other medication. Six months later, a routine screening colonoscopy demonstrated a 4-cm, linear ulcer in the transverse colon (Fig. 2). Biopsy specimens from the lesion revealed granulation tissue with reactive-appearing overlying epithelium. There was no evidence of malignancy or colitis. Viral, fungal, and acid-fast bacilli stains and cultures were negative. Barium contrast radiography of the small bowel, obtained to rule out Crohn’s disease, was normal. Colonoscopy at 3 months after discontinuation of alendronate revealed complete resolution of the colon ulcer. Discussion. Esophageal injury caused by alendronate is well described in numerous case reports and series.3,4 To our knowledge, the present report is the first description of colonic injury associated with alendronate. In both cases, VOLUME 60, NO. 6, 2004
M Sawhney, D Nelson
Figure 2. Colonoscopic view (Case report 2) of linear ulcer in transverse colon.
treatment with alendronate had been initiated within 6 months of detection of the colonic ulcer. Other known causes of colon ulcers were excluded by histopathologic examination and culture of biopsy specimens. After discontinuation of alendronate, there was complete ulcer healing in both patients. The mechanism of alendronate-induced mucosal toxicity has not been completely elucidated. Experimental evidence suggests that bisphosphonates directly irritate the GI mucosa and may compromise the hydrophobic mucosal phospholipid layer.5,6 Direct irritation of the oropharyngeal mucosa accounted for alendronate-induced palate, tongue, and lower-lip ulcers in two patients described by Gonzales-Moles and Bagan-Sebastian.7 Both patients had upper-dental prostheses that were not removed before drug ingestion, thereby prolonging mucosal contact with the drug. One patient admitted to sucking the alendronate tablet until it dissolved. Parallels can be drawn between the evolution in understanding of NSAID- and alendronate-induced GI injury. Although NSAIDs have been in use for decades, the full extent of NSAID-associated small-bowel and colon injury has been recognized only recently.8 Benign ulcers in the cecum and the sigmoid colon have been attributed to NSAID use.9 Studies that used indium In 111 leukocytes suggest that intestinal inflammation occurs in up to 70% of patients who take NSAIDS for more than 6 months.8 In addition to the esophagus, injury to other segments of the GI tract also is evident with alendronate. In a randomized, blinded, crossover trial, Graham and Malaty10 demonstrated visible gastric mucosal damage in 39% of subjects taking alendronate compared with 13% of those taking a placebo. Also noted was a marked difference in the severity of mucosal damage: no ulcer or large erosion was found in the placebo group, whereas ulcers and erosions up to 8 mm in size were noted in the alendronate group. It is our belief that the temporal course of the colonic ulcers in our two patients relative to the initiation and subsequent cessation of alendronate therapy, the known GASTROINTESTINAL ENDOSCOPY
1025
E Roeb, J Benders, S Matern
Brief Reports
mucosal toxicity of alendronate, and the absence of other apparent causes suggest a causal relationship between alendronate and the observed colonic ulcers. This possible association should be considered when evaluating patients with ‘‘nonspecific’’ colonic ulcers. Mandeep S. Sawhney, MD Douglas B. Nelson, MD Gastroenterology Section Minneapolis VA Medical Center Department of Medicine University of Minnesota Minneapolis, Minnesota REFERENCES 1. Raisz LG, Kream BE, Lorenzo JA. Metabolic bone disease. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, editors. Williams textbook of endocrinology. Philadelphia: Saunders; 2003. p. 1373-410. 2. Altkorn D, Vokes T. Treatment of postmenopausal osteoporosis. JAMA 2001;285:1415-8. 3. de Groen PC, Lubbe DF, Hirsch LJ, Daifotis A, Stephenson W, Freedholm D, et al. Esophagitis associated with the use of alendronate. N Engl J Med 1996;335:1016-21. 4. Levine J, Nelson D. Esophageal stricture associated with alendronate therapy. Am J Med 1997;102:489-91. 5. Ellito SN, McKnight W, Davies NM. Alendronate induces gastric injury and delays ulcer healing in rodents. Life Sci 1998;62:77-91. 6. Lichtenberger LM, Romero JJ, Blank MA. Effects of bisphosphonates (BPS) on the surface hydrophobicity and phosphatidylcholine (PC) concentration of gastric mucosa [abstract]. Gastroenterology 1999;116:A237. 7. Gonzalez-Moles MA, Bagan-Sebastian JV. Alendronaterelated oral mucosa ulcerations. J Oral Pathol Med 2000;29: 514-8. 8. Bjarnason I, Macpherson AJ. Intestinal toxicity of nonsteroidal anti-inflammatory drugs. Pharmacol Ther 1994;62: 145-57. 9. Faucheron J-L. Toxicity of non-steroidal anti-inflammatory drugs in the large bowel. Eur J Gastroenterol Hepatol 1999;11:389-92. 10. Graham DY, Malaty HM. Alendronate gastric ulcers. Aliment Pharmacol Ther 1999;13:515-9.
Walled-off esophageal perforation as a first manifestation of pulmonary tuberculosis Esophageal involvement is an unusual presentation of tuberculosis; it occurs in 0.15% of patients who die of this disease.1 The clinical and the endoscopic features are variable, diverse, nonspecific, and poorly described. A case is described in which perforated traction diverticula of the
Reprint requests: Prof. Dr. med. Elke Roeb, Department of Medicine III, University Hospital Aachen (UKA), Aachen University (RWTH), Pauwelsstrasse 30, 52057 Aachen, Germany. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(04)02192-3 1026
GASTROINTESTINAL ENDOSCOPY
Figure 1. A, Endoscopic view showing two orifices in mid esophagus at 25 cm. B, Magnified (33) endoscopic view of esophageal orifice. esophagus was the first manifestation of a clinically unapparent tuberculosis. Case report. A 64-year-old Turkish man was hospitalized because of diarrhea, intermittent upper abdominal pain, and fever of 2 weeks’ duration. The patient had a history of severe coronary artery disease and underwent a cardiopulmonary bypass operation 14 months earlier that was complicated by postoperative acute renal failure, as a result of which he was undergoing intermittent dialysis. Temperature at admission was 37.98C. Tenderness to deep palpation was elicited in the upper epigastrium. Laboratory test results included the following: white blood cell count, 12,000/lL (normal: 10,000/lL); and C-reactive protein, 167 mg/L (<5 mg/L). At upper endoscopy, two orifices were present in the mid esophagus at about 25 cm from the frontal dental arch (Fig. 1). Contrast radiography of the esophagus revealed a small ventral eminence at the level of the carina on a lateral view. An anterior-posterior view disclosed a second lumen on the right side of the esophagus, which filled with VOLUME 60, NO. 6, 2004
Brief Reports
strongly considered in the evaluation of patients with portal hypertension and obstructive jaundice when other imaging modalities are unrevealing. REFERENCES
13.
14.
secondary to portal cavernoma. Ital J Gastroenterol Hepatol 1998;30:202-4. Colle I, VanVlierberghe H, Pattyn P, Troisi R, Vogelaers D, deHemptinne B, et al. Cholestasis as presenting symptom of portal cavernoma. Hepatol Res 2003;25:32-7. Mathieu D, Vasile N, Grenier P. Portal thrombosis: dynamic CT features and course. Radiology 1985;154:737-41. West MS, Garra BS, Horii SC, Hayes WS, Cooper C, Silverman PM, et al. Gallbladder varices: imaging findings in patients with portal hypertension. Radiology 1991;179: 179-82. Grimbert S, Vullierme MP, Dahan P, Hammel P, Bernades P. Value of color-Doppler ultrasound in the diagnosis of a diffuse intrahepatic portal cavernoma [French]. Gastroenterol Clin Biol 1993;17:295-7. Chawla A, Dewan R, Sarin SK. The frequency and influence of gallbladder varices on gallbladder functions in patients with portal hypertension. Am J Gastroenterol 1995;90: 2011-4. Condat B, Vilgrain V, Asselah T, O’ Toole D, Rufat P, Zappa M, et al. Portal cavernoma-associated cholangiopathy: a clinical and MR cholangiography coupled with MR portography imaging study. Hepatology 2003;37:1302-8. Petren T. Die extrahepatischen Gallenwegsvenen und ihre pathologischanatomische Bedeutung (The veins of the extrahepatic biliary system and their pathologic anatomic significance) [German]. Verh Anat Ges 1932;41: 139-43. Saint JA. The epicholedochal venous plexus and its importance as a means of identifying the common duct during operations on the extrahepatic biliary tract. Br J Surg 1961; 46:489-98. Gorgul A, Kayhan B, Dogan I, Unal S. Disappearance of the pseudocholangiocarcinoma sign after TIPSS. Am J Gastroenterol 1996;91:150-3. Chaudhary A, Dhar P, Sarin SK, Sachdev A, Agarwal AK, Vij JC, et al. Bile duct obstruction due to portal biliopathy in extrahepatic portal hypertension: surgical management. Br J Surg 1998;85:326-9. Palazzo L, Hochain P, Helmer C, Cuillerier E, Landi B, Roseau G, et al. Biliary varices on endoscopic ultrasonography: clinical presentation and outcome. Endoscopy 2000;32: 520-4.
1. Sarin SK, Bhatia V, Makwane U. Portal biliopathy in extra hepatic portal vein obstruction [abstract]. Indian J Gastroenterol 1992;2:A82. 2. Khuroo MS, Yattoo GN, Zargar SA, Javid G, Dar MY, Khan BA, et al. Biliary abnormalities associated with extrahepatic portal venous obstruction. Hepatology 1993;17: 807-13. 3. Chandra R, Kapoor D, Tharakan A, Chaudhary A, Sarin SK. Portal biliopathy: review. J Gastroenterol Hepatol 2001;16: 1086-92. 4. Chandra R, Tharakan A, Kapoor D, Sarin SK. Comparative study of portal biliopathy in patients with portal hypertension due to different etiologies [abstract]. Indian J Gastroenterol 1997;15(Suppl 2):A59. 5. Malkan GH, Bhatia SJ, Bashir K, Khemani R, Abraham P, Gandhi MS, et al. Cholangiopathy associated with portal hypertension: diagnostic evaluation and clinical implications. Gastrointest Endosc 1999;49:344-8. 6. Dhiman RK, Puri P, Chawla Y, Minz M, Bapuraj JR, Gupta S, et al. Biliary changes in extrahepatic portal venous obstruction: compression by collaterals or ischemic? Gastrointest Endosc 1999;50:646-52. 7. Dilawari JB, Chawla YK. Pseudosclerosing cholangitis in extrahepatic portal venous obstruction. Gut 1992;33:272-6. 8. Gibson JP, Johnston GW, Fulton TT. Extrahepatic portal vein obstruction. Br J Surg 1965;52:129-39. 9. Kim S, Chew FS. Choledochal varices. AJR Am J Roentgenol 1988;150:578-80. 10. Thervet L, Faulques B, Pissas A, Bremondy A, Monges B, Salducci J, et al. Endoscopic management of obstructive jaundice due to portal cavernoma. Endoscopy 1993;25:423-5. 11. Perlemuter G, Bejanin H, Fritsch J, Prat F, Gaudric M, Chaussade S, et al. Biliary obstruction caused by portal cavernoma: a study of 8 cases. J Hepatol 1996;25:58-63. 12. Solmi L, Rossi A, Conigliaro R, Sassatelli R, Gandolfi L. Endoscopic treatment of a case of obstructive jaundice
15.
BRIEF REPORTS
Thus, there is increasing use of bisphosphonates to prevent and to treat osteoporosis. These agents decrease bone resorption and increase bone mass, resulting in a decreased incidence of fractures.2 Esophageal injury caused by alendronate is well characterized, but there are no reports of injury to the colon. Two patients with colonic ulceration related to the use of alendronate are presented. Case report 1. A 62-year-old man presented to the emergency department with hematochezia. The medical history included severe osteoporosis, diabetes, chronic obstructive pulmonary disease, and stroke. Four months earlier, he began taking alendronate (10 mg once per day). Other medications included insulin, furosemide, warfarin, alprazolam, desipramine, diltiazem, and albuterol, all of which had been prescribed for longer than 1 year. He had not taken a prescription or over-thecounter non-steroidal anti-inflammatory drug (NSAID) during the previous year. Orthostasis was present at admission. The Hb level was 8.5 g/dL (normal: 14-17.9 g/dL);
Alendronate-induced colon ulcers: case report of a new clinical entity As the average age of the population of the United States increases, osteoporosis becomes an increasingly important health concern. One in two white, postmenopausal women, and one in 8 older men and women of other racial groups, develop an osteoporotic fracture during their lifetime.1
Reprint requests: Douglas B. Nelson, MD, VA Medical Center (111D), One Veterans Dr., Minneapolis, MN 55417. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(04)02193-5 1024
GASTROINTESTINAL ENDOSCOPY
16.
17.
18.
19.
20.
21.
22.
23.
VOLUME 60, NO. 6, 2004
Brief Reports
Figure 1. Colonoscopic view (Case report 1) of large stellate cecal ulcer. 6 months before admission, the Hb level was 14 g/dL. The international normalized ratio (INR) was 4.0. Treatment included transfusion of packed red blood cells and administration of fresh frozen plasma and vitamin K. Colonoscopy after resuscitation revealed a large, stellate 10-cm ulcer in the cecum (Fig. 1). A visible vessel in the base of the ulcer was bleeding slowly. Hemostasis was achieved by injection of 14 mL of a 1:10,000 solution of epinephrine. Biopsy specimens obtained from the lesion demonstrated ulceration with deposits of fibrin, inflammatory cells, and cellular debris. There was no malignancy, cryptitis, granuloma, or viral inclusions. Viral, fungal, and acid-fast bacilli cultures and stains were negative. Treatment with alendronate was stopped; all other medications were continued. A colonoscopy 1 month later demonstrated marked healing of the cecal ulcer, and colonoscopy 2 years later revealed complete resolution of the ulcer. Case report 2. A healthy 74-year-old man presented to his primary care physician with non-specific bone pain. The alkaline phosphatase was found to be elevated. Standard bone radiographs and radionucleotide bone scintigraphy were suggestive of Paget’s disease. Treatment was started with alendronate (10 mg per day). The patient had hypertension that was well controlled with hydrochlorothiazide and triamterene. He was not taking any other medication. Six months later, a routine screening colonoscopy demonstrated a 4-cm, linear ulcer in the transverse colon (Fig. 2). Biopsy specimens from the lesion revealed granulation tissue with reactive-appearing overlying epithelium. There was no evidence of malignancy or colitis. Viral, fungal, and acid-fast bacilli stains and cultures were negative. Barium contrast radiography of the small bowel, obtained to rule out Crohn’s disease, was normal. Colonoscopy at 3 months after discontinuation of alendronate revealed complete resolution of the colon ulcer. Discussion. Esophageal injury caused by alendronate is well described in numerous case reports and series.3,4 To our knowledge, the present report is the first description of colonic injury associated with alendronate. In both cases, VOLUME 60, NO. 6, 2004
M Sawhney, D Nelson
Figure 2. Colonoscopic view (Case report 2) of linear ulcer in transverse colon.
treatment with alendronate had been initiated within 6 months of detection of the colonic ulcer. Other known causes of colon ulcers were excluded by histopathologic examination and culture of biopsy specimens. After discontinuation of alendronate, there was complete ulcer healing in both patients. The mechanism of alendronate-induced mucosal toxicity has not been completely elucidated. Experimental evidence suggests that bisphosphonates directly irritate the GI mucosa and may compromise the hydrophobic mucosal phospholipid layer.5,6 Direct irritation of the oropharyngeal mucosa accounted for alendronate-induced palate, tongue, and lower-lip ulcers in two patients described by Gonzales-Moles and Bagan-Sebastian.7 Both patients had upper-dental prostheses that were not removed before drug ingestion, thereby prolonging mucosal contact with the drug. One patient admitted to sucking the alendronate tablet until it dissolved. Parallels can be drawn between the evolution in understanding of NSAID- and alendronate-induced GI injury. Although NSAIDs have been in use for decades, the full extent of NSAID-associated small-bowel and colon injury has been recognized only recently.8 Benign ulcers in the cecum and the sigmoid colon have been attributed to NSAID use.9 Studies that used indium In 111 leukocytes suggest that intestinal inflammation occurs in up to 70% of patients who take NSAIDS for more than 6 months.8 In addition to the esophagus, injury to other segments of the GI tract also is evident with alendronate. In a randomized, blinded, crossover trial, Graham and Malaty10 demonstrated visible gastric mucosal damage in 39% of subjects taking alendronate compared with 13% of those taking a placebo. Also noted was a marked difference in the severity of mucosal damage: no ulcer or large erosion was found in the placebo group, whereas ulcers and erosions up to 8 mm in size were noted in the alendronate group. It is our belief that the temporal course of the colonic ulcers in our two patients relative to the initiation and subsequent cessation of alendronate therapy, the known GASTROINTESTINAL ENDOSCOPY
1025
E Roeb, J Benders, S Matern
Brief Reports
mucosal toxicity of alendronate, and the absence of other apparent causes suggest a causal relationship between alendronate and the observed colonic ulcers. This possible association should be considered when evaluating patients with ‘‘nonspecific’’ colonic ulcers. Mandeep S. Sawhney, MD Douglas B. Nelson, MD Gastroenterology Section Minneapolis VA Medical Center Department of Medicine University of Minnesota Minneapolis, Minnesota REFERENCES 1. Raisz LG, Kream BE, Lorenzo JA. Metabolic bone disease. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, editors. Williams textbook of endocrinology. Philadelphia: Saunders; 2003. p. 1373-410. 2. Altkorn D, Vokes T. Treatment of postmenopausal osteoporosis. JAMA 2001;285:1415-8. 3. de Groen PC, Lubbe DF, Hirsch LJ, Daifotis A, Stephenson W, Freedholm D, et al. Esophagitis associated with the use of alendronate. N Engl J Med 1996;335:1016-21. 4. Levine J, Nelson D. Esophageal stricture associated with alendronate therapy. Am J Med 1997;102:489-91. 5. Ellito SN, McKnight W, Davies NM. Alendronate induces gastric injury and delays ulcer healing in rodents. Life Sci 1998;62:77-91. 6. Lichtenberger LM, Romero JJ, Blank MA. Effects of bisphosphonates (BPS) on the surface hydrophobicity and phosphatidylcholine (PC) concentration of gastric mucosa [abstract]. Gastroenterology 1999;116:A237. 7. Gonzalez-Moles MA, Bagan-Sebastian JV. Alendronaterelated oral mucosa ulcerations. J Oral Pathol Med 2000;29: 514-8. 8. Bjarnason I, Macpherson AJ. Intestinal toxicity of nonsteroidal anti-inflammatory drugs. Pharmacol Ther 1994;62: 145-57. 9. Faucheron J-L. Toxicity of non-steroidal anti-inflammatory drugs in the large bowel. Eur J Gastroenterol Hepatol 1999;11:389-92. 10. Graham DY, Malaty HM. Alendronate gastric ulcers. Aliment Pharmacol Ther 1999;13:515-9.
Walled-off esophageal perforation as a first manifestation of pulmonary tuberculosis Esophageal involvement is an unusual presentation of tuberculosis; it occurs in 0.15% of patients who die of this disease.1 The clinical and the endoscopic features are variable, diverse, nonspecific, and poorly described. A case is described in which perforated traction diverticula of the
Reprint requests: Prof. Dr. med. Elke Roeb, Department of Medicine III, University Hospital Aachen (UKA), Aachen University (RWTH), Pauwelsstrasse 30, 52057 Aachen, Germany. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(04)02192-3 1026
GASTROINTESTINAL ENDOSCOPY
Figure 1. A, Endoscopic view showing two orifices in mid esophagus at 25 cm. B, Magnified (33) endoscopic view of esophageal orifice. esophagus was the first manifestation of a clinically unapparent tuberculosis. Case report. A 64-year-old Turkish man was hospitalized because of diarrhea, intermittent upper abdominal pain, and fever of 2 weeks’ duration. The patient had a history of severe coronary artery disease and underwent a cardiopulmonary bypass operation 14 months earlier that was complicated by postoperative acute renal failure, as a result of which he was undergoing intermittent dialysis. Temperature at admission was 37.98C. Tenderness to deep palpation was elicited in the upper epigastrium. Laboratory test results included the following: white blood cell count, 12,000/lL (normal: 10,000/lL); and C-reactive protein, 167 mg/L (<5 mg/L). At upper endoscopy, two orifices were present in the mid esophagus at about 25 cm from the frontal dental arch (Fig. 1). Contrast radiography of the esophagus revealed a small ventral eminence at the level of the carina on a lateral view. An anterior-posterior view disclosed a second lumen on the right side of the esophagus, which filled with VOLUME 60, NO. 6, 2004