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Figure 1. Endoscopic pictures demonstrate closure of the anastomotic leak with hemoclips (a–c). Endoscopic views of the colorectal anastomosis 11 weeks later (d–f).
CONFLICT OF INTEREST
The authors declare no conflict of interest. REFERENCES 1. Carlson E, Schlichting E, Guldvog I et al. Effect of introduction of total mesorectal excision for the treatment of rectal cancer. Br J Surg 1998;85:526–8. 2. Wang J. Principle and complications of anuspreserving operation for low rectal cancer. J Clin Surg 2005;13:678–9. 3. Cong ZJ, Fu CG, Wang HT et al. Influencing factors of symptomatic anastomotic leakage after anterior resection of the rectum for cancer. World J Surg 2009;33:1292–7. 4. Pera M, Delgado S, García-Valdecasas JC et al. The management of leaking rectal anastomoses by minimally invasive techniques. Surg Endosc 2002;16:603–6. 5. Testi W, Vernillo R, Spagnulo M et al. Endoscopic treatment of intestinal anastomotic leakage in low anterior resection of the rectum by using fibrin adhesive. Our experience. Minerva Chir 2002;57:683–8. 6. Weidenhagen R, Gruetzner KU, Wiecken T et al. Endoscopic vacuum-assisted closure of anastomotic leakage following anterior resection of the rectum: a new method. Surg Endosc 2008;22:1818–25. 7. Merrifield BF, Lautz D, Thompson CC. Endoscopic repair of gastric leaks after Roux-en-Y gastric bypass: a less invasive approach. Gastrointest Endosc 2006;63:710–4. 8. Gumbs AA, Duffy AJ, Bell RL. Management of gastrogastric fistula after laparoscopic Roux-en-Y gastric bypass. Surg Obes Relat Dis 2006;2:117–21.
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Department of Gastroenterology, Turkiye Yuksek Ihtisas Teaching and Research Hospital, Ankara,
The American Journal of GASTROENTEROLOGY
Turkey. Correspondence: Mevlut Kurt, MD, Department of Gastroenterology, Turkiye Yuksek Ihtisas Teaching and Research Hospital, Kýzýlay Sk. No. 2, Ankara, Sýhhiye 06100, Turkey. E-mail:
[email protected]
Endoscopic Hemorrhoid Ligation Is Simple, Safe, and Effective Ming-Yao Su, MD1 and Cheng-Tang Chiu, MD1 doi:10.1038/ajg.2010.135
To the Editor: We read with interest the paper by Jutabha et al. (1) in the August 2009 issue of the American Journal of Gastroenterology, which compared endoscopic rubber band ligation (RBL) and bipolar coagulation for chronically bleeding internal hemorrhoid. The authors concluded that the success rate was significantly higher with RBL than with bipolar coagulation, but the cases of severe pain during treatment were also more. The authors did not mention the number of bands ligated per session. The more frequent painful sensation in the RBL group
(8% vs. 0%) may be related to the number of ligated bands used per session. Our previous study (2) showed that the deployment of up to three bands per session is safe and tolerable; a number more than this will induce tenesmus sensation and pain. The rectal prolapsed patients were excluded from this study. They included patients with grade II and III bleeding internal hemorrhoid. By the definition of Goligher’s classification (3), internal hemorrhoids can be classified into 4 grades: grade I, hemorrhoids with bleeding; grade II, hemorrhoids with bleeding and protrusion, with spontaneous reduction; grade III, hemorrhoids with bleeding and protrusion that require manual reduction; grade IV, prolapsed hemorrhoids that cannot be replaced. There seemed to be no criterion available to exclude patients with the grade II and III hemorrhoid, especially grade III, usually combined with prolapsed symptoms. In our experience, RBL is an effective treatment not only for bleeding hemorrhoid but also prolapsed hemorrhoid (2,3). In our series, the bleeding symptom was controlled in 95.4% of the patients, and the success rate for control of prolapsed hemorrhoids was 91.99%. There were no severe complications (such as perirectal abscess, anal fissure, or rectal stenosis) during this study. An excellent result was obtained, but this could be attributed to the small sample size used in this study. In our experience relating to a series of 576 patients who received RBL, 85 patients experienced mild anal pain that was resolved by using non-steroidal anti-inflammatory drugs, 37 had mild bleeding that stopped spontaneously or was controlled by local injection of diluted epinephrine solution (4), 4 developed external hemorrhoidal thromboses, and 1 had peri-anal abscess that received further surgical management. In conclusion of our study and the paper, endoscopic hemorrhoid ligation (EHL) is an important advancement in the treatment of patients with symptoms caused by internal hemorrhoids, not only bleeding but also prolapsed. EHL is simple, safe, and effective. CONFLICT OF INTEREST
The authors declare no conflict of interest. VOLUME 105 | JUNE 2010 www.amjgastro.com
Letters to the Editor
REFERENCES 1. Jutabha R, Jensen DM, Chavalitdhamrong D. Randomized prospective study of endoscopic rubber band ligation compared with bipolar coagulation for chronically bleeding internal hemorrhoids. Am J Gastroenterol 2009;104:2057–64. 2. Su MY, Chiu CT, Wu CS et al. Endoscopic hemorrhoidal ligation of symptomatic internal hemorrhoids. Gastrointest Endosc 2003;68:871–4. 3. Schrock TR. Hemorrhoids: nonoperative and interventional management. In: Barkin J, O’Phelan CA (eds). Advanced Therapeutic Endoscopy. Raven Press: New York, 1991. 4. Su MY, Tung SY, Wu CS et al. A long term result of endoscopic hemorrhoidal ligation-two different devices with similar results. Endoscopy 2003;35:416–20. 1 Department of Gastroenterology and Hepatology, Chang Gung University College of Medicine, Linkou Chang Gung Memorial Hospital, Taipei, Taiwan, ROC. Correspondence: Ming-Yao Su, MD, Department of Gastroenterology and Hepatology, Chang Gung University College of Medicine, Linkou Chang Gung Memorial Hospital, 5, Fushin Street, Kweishan, Taoyuan, Taipei 333 Taiwan, ROC. E-mail:
[email protected]
Elevated Serotonin Associated With Collagenous Colitis 1
Michael Docherty, MD doi:10.1038/ajg.2010.90
To the Editor: A 59-year-old woman with a history of rheumatoid arthritis and ankylosing spondylitis presented with a 5-week history of profuse, watery, nonbloody diarrhea with 15–20 bowel movements per day. The diarrhea was associated with crampy lower abdominal pain. She had already been seen in the emergency department twice for dehydration. There had been no travel or sick contacts and no family history of gastrointestinal disease. Physical examination was normal with no abdominal tenderness. Her complete blood count and metabolic panel were normal. Clostridium difficile toxin testing and stool cultures were negative. Stools were negative for ova and parasites on three separate occasions. There were no fecal leukocytes, and the Giardia direct fluorescent antibody and celiac testing were negative. © 2010 by the American College of Gastroenterology
The serotonin level was markedly elevated at 877 ng/ml (ref. range 50–200 ng/ml). A repeat blood test confirmed this. The 24-h urine 5-hydroxyindoleacetic acid test was normal (3 mg/day) and the chromogranin-A level was mildly elevated at 60 ng/ml (ref. range 0–50 ng/ml). A computed tomography scan of the abdomen/pelvis and an octreotide scan were normal. Colonoscopy was normal with normal biopsies of the terminal ileum. Colonic biopsies showed increased intraepithelial lymphocytes and a thickened subepithelial collagen table consistent with collagenous colitis. The patient was started on Entocort and symptoms resolved within 2 days. Symptoms recurred after stopping the medication, and hence she remains on a low dose of Entocort. The serotonin level decreased to 237 ng/ml and chromogranin-A level decreased to 13 ng/ml. Collagenous colitis is a relatively common cause of chronic diarrhea, especially in an older female such as in this case (1). There have been no reports of elevated serotonin levels associated with this disease. Most of the body’s serotonin is produced by enterochromaffin cells in the intestine. The serotonin detected by blood tests is virtually all a result of this “overflow ” from enterochromaffin cells (2). The fact that this patient’s levels dropped with treatment and symptom relief also supports an intestinal source. Recently, serotonin has been shown to have an important role in experimental colitis (3). Serotonin-deficient mice were protected from developing colitis, while replenishing serotonin induced more severe colitis. Similarly, a serotonin receptor antagonist was shown to protect against the development of colitis in mice (4). Interestingly, selective serotonin reuptake inhibitors are a common cause of microscopic colitis (5). This raises the question of whether serotonin has a role in microscopic colitis. If so, it would open the door for a better understanding of this disease and perhaps for new therapeutic options. CONFLICT OF INTEREST The author declares no conflict of interest.
REFERENCES 1. Pardi D, Smyrk T, Tremaine W et al. Microscopic colitis: a review. Am J Gastroenterol 2002;97:794–802. 2. Gershon M, Tack J. The serotonin signaling system: from basic understanding to drug development for functional GI disorders. Gastroenterology 2007;132:397–414. 3. Ghia J, Li N, Wang H et al. Serotonin has a key role in pathogenesis of experimental colitis. Gastroenterology 2009;137:1649–60. 4. Mousavizadeh K, Rahimian R, Fakhfouri G et al. Anti-inflammatory effects of 5-HT receptor antagonist, tropisetron on experimental colitis in rats. Eur J Clin Invest 2009;39:375–83. 5. Fernández-Bañares F, Esteve M, Espinós J et al. Drug consumption and the risk of microscopic colitis. Am J Gastroenterol 2007;102:324–30. 1
Division of Gastroenterology, Department of Internal Medicine, University of California, San Diego, San Diego, California, USA. Correspondence: Michael Docherty, MD, Division of Gastroenterology, Department of Internal Medicine, University of California, San Diego, 200 W. Arbor Drive, San Diego, California 92103, USA. E-mail:
[email protected]
Comment on ACG Guidelines—Management of Alcoholic Liver Disease Ashwani K. Singal, MD1 doi:10.1038/ajg.2010.144
To the Editor: We read with great interest the article by O’Shea et al. (1) in the January issue of the American Journal of Gastroenterology regarding the ACG guidelines on alcoholic liver disease. The article is well written and informative. However, we would like to bring some points to your kind attention, which may be of interest to physicians, gastroenterologists, and hepatologists. In Table 2, the authors described how to calculate the quantity of alcohol in a standard drink. This is an important piece of information when taking the history of alcohol intake from the patients. However, what constitutes one drink should also be described, as patients describe their history of alcohol intake in terms of the amount (in ml) of wine, beer, or hard liquor. It is defined that 12 ounces of beer (360 ml), 4 ounces of wine (120 ml), and 1.5 ounce of hard liquor (45 ml) constitute one drink (2). The American Journal of GASTROENTEROLOGY
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