- Email: [email protected]
Cimetidine therapy and duodenal candidiasis
much less edematous, the papilla was found and cannulated, and a benign appearing common duct stricture was diagnosed. Mucosal edema has been associated with portal hypertension in both experimental animals· and humans. 5 In the above case, propranolol appeared to decrease duodenal mucosal edema, making ERCP possible. Propranolol may be a useful adjunct in the preparation of patients with portal hypertension for ERCP.
antagonist therapy are certainly needed to clarify the situation. Eapen Thomas, MD Gastroenterology Quillen-Dishner College of Medicine Veterans Administration Medical Center Johnson City, Tennessee
K. Rajender Reddy, MD Hepato/ogy University of Miami School of Medicine Miami, Florida
Howard K. Gogel, MD Samuel H. Iwata, MD Larry D. Blessing, MD Gastroenterology VA Medical Center University of New Mexico School of Medicine Albuquerque, New Mexico
REFERENCES 1. Lebrec D, Nouel 0, Corbic M, Benhamou J-P. Propranolol-a
2.
3. 4. 5.
medical treatment for portal hypertension? Lancet 1980;2:1802. Lebrec D, Poynard T, Hillon P, Benhamou J-P. Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study. N Engl J Med 1981;305:13714. S~gaard PE. Propranolol in portal hypertension. Lancet 1981;1:1204. Sarfeth IJ, Tarnawski A, Malki A, Mason GR, Mach T, Ivey KJ. Portal hypertension and gastric mucosal injury in rats. Gastroenterology 1983; 84:987-93. Astaldi G, Strosselli E. Peroral biopsy of the intestinal mucosa in hepatic cirrhosis. Am J Dig Dis 1960;5:603-12.
REFERENCES 1. Roy A, McCallum RW. Candidiasis of the duodenum: the role
2. 3. 4. 5. 6.
of continuous cimetidine therapy. Gastrointest Endosc 1984;30:47-8. Thomas E, Reddy KR. Nonhealing duodenal ulceration due to Candida. J Clin Gastroenterol 1983;5:55-8. Stark FR, Ninos N, Hutton J, Katz R, Bullier M. Candida peritonitis and cimetidine (letter). Lancet 1978;2:744. Triger DR, Slater DN, Goepel JR, Underwood JCE. Systemic candidiasis complicating acute hepatic failure in patients treated with cimetidine. Lancet 1982;2:837-8. Teruzzi V, Minoli G, Butti G, Rossini A. Gastric Candida in patients on cimetidine. Lancet 1981;2:1236. Minoli G, Terruzzi V, Ferrara A, et a!. A prospective study of relationships between benign gastric ulcer, Candida, and medical treatment. Am J GastroenteroI1984;79:95-7.
Prognostic importance of visible vessels in hemorrhage of peptic ulcers To the Editor:
Cimetidine therapy and duodenal candidiasis To the Editor: The report by Roy and McCallum 1 in Gastrointestinal Endoscopy on duodenal candidiasis in a patient on longterm cimetidine therapy is interesting. We had reported a case of duodenal ulcer in an elderly diabetic man that did not heal with optimal antacid and cimetidine therapy.2 Endoscopic biopsies revealed Candida involvement of his necrotic ulcer. Healing was achieved with oral mycostatin therapy after discontinuation of cimetidine and antacids. Other complications observed with prolonged cimetidine therapy include Candida peritonitis3 and disseminated candidiasis! Upon literature review we found a predominant involvement of gastric ulcers compared to duodenal ulcers. 2 It has been speculated that cimetidine favors infection by Candida by causing a marked reduction in acid secretion. This assumption, however, should be made with caution because a prospective study has failed to demonstrate that cimetidine therapy favored Candida colonization of the stomach.5 The same authors have further shown by a prospective study that Candida-contaminated gastric ulcers were healed by continued treatment either with cimetidine alone or combined cimetidine-carbenoxolone, without antimycotics. 6 It is difficult to extrapolate the results of these studies to duodenal candidiasis 1 ,2 and the fact that our patient's Candida-involved duodenal ulcer healed with discontinuation of acid-reducing agents and mycostatin therapy. Further studies on duodenal candidiasis and H 2receptor 52
During the last 14 months we performed endoscopy, within 24 hours of admission, in 200 patients admitted to the hospital for acute gastrointestinal hemorrhage. In 110 patients endoscopy revealed peptic ulcers (75 duodenal, 30 gastric, and five stomal). Full examination of the crater was possible in all of them. Visible vessels were identified in 35 (31.8%); other stigmata of recent bleeding (such as oozing from the ulcer crater, an adherent fresh or altered clot, or black slough) were found in 21 (19%); and no stigmata in 54 (49%). Nineteen of 35 patients with visible vessels (54.2%) had rebleeding as compared with three of 21 (14.2%) with other stigmata of recent bleeding (x 2 = 8.8; p < 0.05). No patients with ulcers without visible vessels or other stigmata of recent hemorrhage bled further. Among the patients who rebled an emergency operation was finally performed on 13 of the 19 patients with visible vessels and none of the patients with other stigmata of recent hemorrhage. We conclude that visible vessels are a strong indication of uncontrolled or recurrent gastrointestinal hemorrhage, and in patients where visible vessels are identified physicans should be on the alert in case surgery or endoscopic intervention is necessary. Our findings are in agreement with those of other researchers. 1 Anastasios Emmanuel, MD Theodore Rokkas, MD 2nd Department of Internal Medicine and Gastroenterological Unit 401 Army General Hospital Athens, Greece
GASTROINTESTINAL ENDOSCOPY
antagonist therapy are certainly needed to clarify the situation. Eapen Thomas, MD Gastroenterology Quillen-Dishner College of Medicine Veterans Administration Medical Center Johnson City, Tennessee
K. Rajender Reddy, MD Hepato/ogy University of Miami School of Medicine Miami, Florida
Howard K. Gogel, MD Samuel H. Iwata, MD Larry D. Blessing, MD Gastroenterology VA Medical Center University of New Mexico School of Medicine Albuquerque, New Mexico
REFERENCES 1. Lebrec D, Nouel 0, Corbic M, Benhamou J-P. Propranolol-a
2.
3. 4. 5.
medical treatment for portal hypertension? Lancet 1980;2:1802. Lebrec D, Poynard T, Hillon P, Benhamou J-P. Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study. N Engl J Med 1981;305:13714. S~gaard PE. Propranolol in portal hypertension. Lancet 1981;1:1204. Sarfeth IJ, Tarnawski A, Malki A, Mason GR, Mach T, Ivey KJ. Portal hypertension and gastric mucosal injury in rats. Gastroenterology 1983; 84:987-93. Astaldi G, Strosselli E. Peroral biopsy of the intestinal mucosa in hepatic cirrhosis. Am J Dig Dis 1960;5:603-12.
REFERENCES 1. Roy A, McCallum RW. Candidiasis of the duodenum: the role
2. 3. 4. 5. 6.
of continuous cimetidine therapy. Gastrointest Endosc 1984;30:47-8. Thomas E, Reddy KR. Nonhealing duodenal ulceration due to Candida. J Clin Gastroenterol 1983;5:55-8. Stark FR, Ninos N, Hutton J, Katz R, Bullier M. Candida peritonitis and cimetidine (letter). Lancet 1978;2:744. Triger DR, Slater DN, Goepel JR, Underwood JCE. Systemic candidiasis complicating acute hepatic failure in patients treated with cimetidine. Lancet 1982;2:837-8. Teruzzi V, Minoli G, Butti G, Rossini A. Gastric Candida in patients on cimetidine. Lancet 1981;2:1236. Minoli G, Terruzzi V, Ferrara A, et a!. A prospective study of relationships between benign gastric ulcer, Candida, and medical treatment. Am J GastroenteroI1984;79:95-7.
Prognostic importance of visible vessels in hemorrhage of peptic ulcers To the Editor:
Cimetidine therapy and duodenal candidiasis To the Editor: The report by Roy and McCallum 1 in Gastrointestinal Endoscopy on duodenal candidiasis in a patient on longterm cimetidine therapy is interesting. We had reported a case of duodenal ulcer in an elderly diabetic man that did not heal with optimal antacid and cimetidine therapy.2 Endoscopic biopsies revealed Candida involvement of his necrotic ulcer. Healing was achieved with oral mycostatin therapy after discontinuation of cimetidine and antacids. Other complications observed with prolonged cimetidine therapy include Candida peritonitis3 and disseminated candidiasis! Upon literature review we found a predominant involvement of gastric ulcers compared to duodenal ulcers. 2 It has been speculated that cimetidine favors infection by Candida by causing a marked reduction in acid secretion. This assumption, however, should be made with caution because a prospective study has failed to demonstrate that cimetidine therapy favored Candida colonization of the stomach.5 The same authors have further shown by a prospective study that Candida-contaminated gastric ulcers were healed by continued treatment either with cimetidine alone or combined cimetidine-carbenoxolone, without antimycotics. 6 It is difficult to extrapolate the results of these studies to duodenal candidiasis 1 ,2 and the fact that our patient's Candida-involved duodenal ulcer healed with discontinuation of acid-reducing agents and mycostatin therapy. Further studies on duodenal candidiasis and H 2receptor 52
During the last 14 months we performed endoscopy, within 24 hours of admission, in 200 patients admitted to the hospital for acute gastrointestinal hemorrhage. In 110 patients endoscopy revealed peptic ulcers (75 duodenal, 30 gastric, and five stomal). Full examination of the crater was possible in all of them. Visible vessels were identified in 35 (31.8%); other stigmata of recent bleeding (such as oozing from the ulcer crater, an adherent fresh or altered clot, or black slough) were found in 21 (19%); and no stigmata in 54 (49%). Nineteen of 35 patients with visible vessels (54.2%) had rebleeding as compared with three of 21 (14.2%) with other stigmata of recent bleeding (x 2 = 8.8; p < 0.05). No patients with ulcers without visible vessels or other stigmata of recent hemorrhage bled further. Among the patients who rebled an emergency operation was finally performed on 13 of the 19 patients with visible vessels and none of the patients with other stigmata of recent hemorrhage. We conclude that visible vessels are a strong indication of uncontrolled or recurrent gastrointestinal hemorrhage, and in patients where visible vessels are identified physicans should be on the alert in case surgery or endoscopic intervention is necessary. Our findings are in agreement with those of other researchers. 1 Anastasios Emmanuel, MD Theodore Rokkas, MD 2nd Department of Internal Medicine and Gastroenterological Unit 401 Army General Hospital Athens, Greece
GASTROINTESTINAL ENDOSCOPY