Letters to the Editor
membrane TNF␣ and activates immune effector functions. Cytokine 1995;7:251–3. Plevy SE, Landers CJ, Prehn J, et al. A role for TNF␣ and mucosal T helper-1 cytokines in the pathogenesis of Crohn’s disease. J Immunol 1997;159:6276 – 82. Baert FJ, D’Haens GR, Peeters M, et al. Tumor necrosis factor ␣ antibody (infliximab) therapy profoundly down-regulates the inflammation in Crohn’s ileocolitis. Gastroenterology 1999;116:22– 8. D’Haens G, Van Deventer S, Van Hogezand R, et al. Endoscopic and histological healing with infliximab anti-tumor necrosis factor antibodies in Crohn’s disease: A European multicenter trial. Gastroenterology 1999;116:1029 –34. American Thoracic Society/CDC. Diagnostic standards and classification of tuberculosis. Am Rev Respir Dis 1990;142: 725–35. Screening for tuberculosis, and tuberculosis infection in highrisk populations. Recomendations of the Advisory Council for the Elimination of Tuberculosis. MMWR 1995;44:19 –34.
Reprint requests and correspondence: Oscar Nu´n˜ez Martı´nez, H.G.U. Gregorio Maran˜o´n, Servicio de Aparato Digestivo, C/Doctor Esquerdo No. 46, CP: 28007, Madrid, Spain. Received Jan. 3, 2001; accepted Jan. 16, 2001.
AJG – Vol. 96, No. 5, 2001
fluid. She underwent an uneventful laparoscopic cholecystectomy and was discharged. Perforation and bleeding are well-known complications of colonoscopy (1). When abdominal pain, vomiting, and/or fever occur in the immediate postcolonoscopy period, perforation should be considered and promptly ruled out. To our knowledge, there have been no previous reports of acute cholecystitis after colonoscopy. Because all patients need to take a preparation before colonoscopy, perhaps it is the relative dehydration that makes them more susceptible to developing cholecystitis. The bile may become more lithogenic, with diminished bile flow and gallbladder distention (2). There is now fertile ground for an inflammatory process to erupt. The mechanical manipulation of the colon associated with bacterial translocation might also play a role. The diagnosis of colonoscopic perforation was first entertained in our two patients. Our experience teaches us to consider cholecystitis in the differential diagnosis of postcolonoscopy abdominal pain, vomiting, and/or fever, and to obtain additional imaging studies as indicated. Perry J. Milman, M.D. Steven P. Goldenberg, M.D. Lake Success, New York
Colonoscopy Cholecystitis TO THE EDITOR: Complications secondary to colonoscopy are uncommon. We report two cases of acute cholecystitis after colonoscopy. A 58-yr-old woman, with a history of well-differentiated adenocarcinoma in an ascending colon polyp and other previous polyps, underwent colonoscopy. She also had a history of dyspepsia, substernal chest pain, Helicobacter pylori–positive duodenal ulcer, and gallstones. Colonoscopy revealed two small sessile polyps that were removed with the biopsy forceps. She tolerated the procedure well and was discharged. Later that afternoon, she developed epigastric and substernal pain, induced vomiting, and presented to the emergency room. She had a fever of 101°F and elevated liver enzymes. Sonogram revealed gallstones and a thickwalled gallbladder consistent with acute cholecystitis. Two hours later, a hepatobiliary scan failed to demonstrate radionuclide in the gallbladder or small bowel. She underwent laparoscopic cholecystectomy with an intraoperative cholangiogram that revealed a choledochocele. Endoscopic sphincterotomy was done for persistent liver enzyme elevation. She made an uneventful recovery and has done well. A 49-yr-old woman underwent colonoscopy because of frequent stool, borborygmi, and increased gas, only partially relieved by antispasmodics and antidiarrheals. Colonoscopy was normal, but random biopsies revealed collagenous colitis. Eight hours after the procedure, she noted epigastric pain radiating to the back and recurrent emesis. Her symptoms spontaneously resolved, but recurred 5 days later. Abdominal CT scan revealed a thick-walled gallbladder containing a solitary stone with debris and pericholecystic
REFERENCES 1. Waye JD, Kahn O, Auerbach ME. Complications of colonoscopy and flexible sigmoidoscopy. Gastrointest Endosc Clin North Am 1996;6:343–77. 2. Bennion LJ, Grundy SM. Risk factors for the development of cholelithiasis in man. N Engl J Med 1979;299:1161–7, 1221–7. Reprint requests and correspondence: Perry J. Milman, M.D., 2001 Marcus Avenue, Suite N18, Lake Success, NY 11042. Received Jan. 8, 2001; accepted Jan. 16, 2001.
Re: Percutaneous Endoscopic Gastrostomy TO THE EDITOR: Since its inception in the late 1970s and publication of reports about it in 1980, percutaneous endoscopic gastrostomy has become a standard procedure performed by many gastroenterologists and surgeons (1, 2). However, not all patients requiring enteral support are acceptable candidates for gastrostomy tube placement. When a jejunal feeding tube is passed through a gastrostomy, it has been incorrectly called a percutaneous endoscopic jejunostomy (PEJ). Recently, the journal has continued this error with the article by Lien et al. (3). Although informative and well done, this study has nothing to do with jejunostomy: not one patient in the study had a jejunostomy and all patients had feeding tubes placed through a gastrostomy. A more appropriate designation for feeding tubes placed through a gastrostomy and passed into the small bowel is
AJG – May, 2001
Letters to the Editor
JETPEG (jejunal enteral tube placed through a percutaneous endoscopic gastrostomy). This term has been proposed by Shike et al. (4). Jejunostomy should refer only to direct access through the skin and into the jejunal lumen. Endoscopists have successfully placed PEJ tubes (4 – 6). However, some have reported difficulty with a percutaneous approach (7, 8). Using enteroscopy, Shike et al. (4) reported a 96% success rate in direct PEJ placement in patients with prior esophageal or gastric surgery. With the increase in enteroscopy, and the likely increase in endoscopic jejunostomy, we should call these procedures what they are and not continue to use outdated and incorrect terms. Michael A. Shetzline, M.D. Division of Gastroenterology Duke University Medical Center Durham, North Carolina
REFERENCES 1. Gauderer MW, Ponsky JL, Izant RJ Jr. Gastrostomy without laparotomy: A percutaneous endoscopic technique. J Pediatr Surg 1980;15:872–5. 2. Gauderer M. Twenty years of percutaneous endoscopic gastrostomy: Origin and evolution of a concept and its expanded applications. Gastrointest Endosc 1999;50:879 – 83. 3. Lien H-C, Chang C-S, Chen G-H. Can percutaneous endoscopic jejunostomy prevent gastroesophageal reflux in patients with preexisting esophagitis? Am J Gastroenterol 2000;95: 3439 – 43. 4. Shike M, Latkany L, Gerdes H, Bloch AS. Direct percutaneous endoscopic jejunostomies for enteral feeding. Gastrointest Endosc 1996;44:536 – 40. 5. Shike M, Latkany L. Direct percutaneous endoscopic jejunostomy. Gastrointest Endosc Clin North Am 1998;8:569 – 80. 6. Rumalla A, Baron TH. Results of direct percutaneous endoscopic jejunostomy, an alternative method for providing jejunal feeding. Mayo Clin Proc 2000;75:807–10. 7. Kaplan DS, Murthy UK, Linscheer WG. Percutaneous endoscopic jejunostomy: Long-term follow-up of 23 patients. Gastrointest Endosc 1989;35:403– 6. 8. DiSario JA, Foutch PG, Sanowski RA. Poor results with percutaneous endoscopic jejunostomy. Gastrointest Endosc 1990; 36:257– 60.
thirds of bulimics show abnormalities in esophageal motility (2). Other work has demonstrated that most anorexics suffer from abnormal gastric emptying of solids (3) and prolonged small intestinal transit time (4). Anorexics and bulimics who surreptitiously abuse laxatives show a plethora of physical and endoscopic findings including colonic dilation, hypokalemia, rebound edema after diuretic discontinuation, and Melanosis coli (5). Although all of these studies have been performed to document the incidence of these various abnormalities in patients with anorexia and bulimia nervosa, thus far no one has determined at what point during the course of these illnesses patients present to physicians with complaints involving the upper or lower GI tract. Do patients present to their primary care physician with complaints of reflux or stomachaches before ever seeking treatment for anorexia or bulimia? Or do patients seek help for their GI complaints after successful treatment of the eating disorder has prompted self-care? This study was designed to examine GI histories in anorexic and bulimic patients and to determine the incidence of their having sought help for GI complaints. Over a 1-month period, 13 inpatients on an eating disorders unit were interviewed with regard to their personal disease history and history of abuse of laxatives (Fig. 1). A directed history was taken that concentrated on GI problems, GI medications, family history of GI problems, and reflux. Of 15 patients, one was excluded because she was profoundly depressed and incapable of participating, and one patient refused to take part in the survey.
Reprint requests and correspondence: Michael A. Shetzline, M.D., Division of Gastroenterology, Box 3083 Medical Center, Duke University Medical Center, Durham, NC 27710. Received Jan. 12, 2001; accepted Jan. 16, 2001.
Frequency of Physician Visits for GI Complaints by Anorexic and Bulimic Patients TO THE EDITOR: It comes as no surprise that anorexics and bulimics suffer from a variety of upper and lower GI ailments as a result of their pathological behaviors. Studies have shown that about one-third of bulimics have esophageal inflammation or erosions on endoscopy (1), and two-
Figure 1. Questionnaire.