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Why Do Symptoms Persist After Acute Diverticulitis?
Clinical Gastroenterology and Hepatology 2014;-:1
LETTERS TO THE EDITOR Readers are encouraged to write letters to the editor concerning articles that have been published in Clinical Gastroenterology and Hepatology. Short, general comments are also considered, but use of the Letters to the Editor section for publication of original data in preliminary form is not encouraged. Letters should be typewritten and submitted electronically to http://www. editorialmanager.com/cgh.
Why Do Symptoms Persist After Acute Diverticulitis? Dear Editor: In their recent article, Cohen et al1 evaluated the yield of functional outcomes after acute diverticulitis. They found that cases were 4.7-fold more likely to develop irritable bowel syndrome (IBS) than controls. These results are in line with those recently reported by Levack et al,2 who found that one-fifth of patients reported significant complaints after surgery for diverticulitis, ranging from fecal urgency to incomplete emptying. The study by Cohen et al1 opens several questions for clinical practice. First, why do symptoms persist after acute diverticulitis? Authors reported a strong relation with IBS. Although an overlap between IBS and diverticular disease is still considered an important cause of symptoms in diverticular disease, patients with previous diagnosis of IBS were excluded from the final evaluation in the study by Cohen et al, and therefore it cannot be considered a confounding factor. Moreover, although patients undoubtedly share features with IBS, strictly speaking, they cannot have IBS because the definition of IBS specifically excludes “organic or structural lesions likely to be responsible for symptoms.”3 In this way, it seems to be appropriate to speak of IBS-like symptoms rather than IBS. Cohen et al1 postulate that these patients may develop IBS as consequence of the injury represented by diverticulitis, similar to that in post-infective IBS. But we know that post-infective IBS is characterized by altered cytokine expression, compared with general IBS population; also, a low-grade inflammation may be detected in the colonic mucosa of these patients.4 Thus, factors other than simple IBS should be considered in explaining why symptoms persist after acute diverticulitis. Clues could arise from the recent studies on diverticular disease physiopathology. Recent observations suggest that the natural history of the disease has many similarities to that of chronic inflammatory bowel disease. For example, enhanced expression of tumor necrosis factor alpha has been found in diverticular disease. Furthermore, persistence of endoscopic/histologic low-grade inflammation may be detected after acute diverticulitis.5 As in inflammatory bowel disease, postinflammatory damage to the enteric nervous system can be found after recent diverticulitis and is strongly associated with symptom persistence.6 Finally, patients with a history of acute diverticulitis have significant attenuation
in serotonin-transporter levels, a primary trigger of gut motility, likely as a result of previous inflammation. These findings may explain the persistence of pain and the altered motility often observed in patients with diverticulitis after recovery from the acute inflammatory response, as well as persistence of symptoms after acute attack. We should therefore talk of persistent smoldering inflammation or altered motility rather than “postdiverticulitis IBS-like symptoms.” The second question for clinical practice is how we can prevent persistence/occurrence of abdominal complaints after acute diverticulitis. Elective surgery may be a therapeutic option in patients with persistent symptoms, but this approach does not eliminate the risk to develop abdominal symptoms. But if we consider the hypothesis of persistent smoldering inflammation as cause of symptom persistence/ occurrence, long-term therapy controlling inflammation may be a promising choice. Mesalazine is currently under active investigation. Two recent placebo-controlled trials found mesalazine significantly better than placebo in controlling symptoms after acute diverticulitis.7,8 Thus, it is probable that mesalazine plays a similar role in controlling symptoms to that after acute attack of inflammatory bowel disease. However, if we consider a significant reduction of serotonin-transporter level as cause of some abdominal complaint, it is a reasonable, testable approach to treat those patients with the new agent prucalopride, which appears to be highly selective for the serotonin 5-HT4 receptor and is therefore a potent stimulator of gut motility. ANTONIO TURSI, MD Servizio di Gastroenterologia Territoriale ASL BAT Andria (BT), Italy
References 1.
Cohen E, et al. Clin Gastroenterol Hepatol 2013;11:1614–1619.
2. 3.
Levack MM, et al. Dis Colon Rectum 2012;55:10–17. Drossman DA, et al. McLean: Degnon Associates, 2006.
4.
Spiller R, et al. J Neurogastroenterol Motil 2012;18:258–268.
5.
Tursi A, et al. J Gastrointest Liver Dis 2013;22:12–17.
6.
Simpson J, et al. Neurogastroenterol Motil 2009;21:847–858.
7.
Stollman N, et al. J Clin Gastroenterol 2013;47:621–629.
8.
Parente F, et al. Int J Colorectal Dis 2013;28:1423–1431.
Conflicts of interest The author discloses no conflicts. http://dx.doi.org/10.1016/j.cgh.2013.12.017
LETTERS TO THE EDITOR Readers are encouraged to write letters to the editor concerning articles that have been published in Clinical Gastroenterology and Hepatology. Short, general comments are also considered, but use of the Letters to the Editor section for publication of original data in preliminary form is not encouraged. Letters should be typewritten and submitted electronically to http://www. editorialmanager.com/cgh.
Why Do Symptoms Persist After Acute Diverticulitis? Dear Editor: In their recent article, Cohen et al1 evaluated the yield of functional outcomes after acute diverticulitis. They found that cases were 4.7-fold more likely to develop irritable bowel syndrome (IBS) than controls. These results are in line with those recently reported by Levack et al,2 who found that one-fifth of patients reported significant complaints after surgery for diverticulitis, ranging from fecal urgency to incomplete emptying. The study by Cohen et al1 opens several questions for clinical practice. First, why do symptoms persist after acute diverticulitis? Authors reported a strong relation with IBS. Although an overlap between IBS and diverticular disease is still considered an important cause of symptoms in diverticular disease, patients with previous diagnosis of IBS were excluded from the final evaluation in the study by Cohen et al, and therefore it cannot be considered a confounding factor. Moreover, although patients undoubtedly share features with IBS, strictly speaking, they cannot have IBS because the definition of IBS specifically excludes “organic or structural lesions likely to be responsible for symptoms.”3 In this way, it seems to be appropriate to speak of IBS-like symptoms rather than IBS. Cohen et al1 postulate that these patients may develop IBS as consequence of the injury represented by diverticulitis, similar to that in post-infective IBS. But we know that post-infective IBS is characterized by altered cytokine expression, compared with general IBS population; also, a low-grade inflammation may be detected in the colonic mucosa of these patients.4 Thus, factors other than simple IBS should be considered in explaining why symptoms persist after acute diverticulitis. Clues could arise from the recent studies on diverticular disease physiopathology. Recent observations suggest that the natural history of the disease has many similarities to that of chronic inflammatory bowel disease. For example, enhanced expression of tumor necrosis factor alpha has been found in diverticular disease. Furthermore, persistence of endoscopic/histologic low-grade inflammation may be detected after acute diverticulitis.5 As in inflammatory bowel disease, postinflammatory damage to the enteric nervous system can be found after recent diverticulitis and is strongly associated with symptom persistence.6 Finally, patients with a history of acute diverticulitis have significant attenuation
in serotonin-transporter levels, a primary trigger of gut motility, likely as a result of previous inflammation. These findings may explain the persistence of pain and the altered motility often observed in patients with diverticulitis after recovery from the acute inflammatory response, as well as persistence of symptoms after acute attack. We should therefore talk of persistent smoldering inflammation or altered motility rather than “postdiverticulitis IBS-like symptoms.” The second question for clinical practice is how we can prevent persistence/occurrence of abdominal complaints after acute diverticulitis. Elective surgery may be a therapeutic option in patients with persistent symptoms, but this approach does not eliminate the risk to develop abdominal symptoms. But if we consider the hypothesis of persistent smoldering inflammation as cause of symptom persistence/ occurrence, long-term therapy controlling inflammation may be a promising choice. Mesalazine is currently under active investigation. Two recent placebo-controlled trials found mesalazine significantly better than placebo in controlling symptoms after acute diverticulitis.7,8 Thus, it is probable that mesalazine plays a similar role in controlling symptoms to that after acute attack of inflammatory bowel disease. However, if we consider a significant reduction of serotonin-transporter level as cause of some abdominal complaint, it is a reasonable, testable approach to treat those patients with the new agent prucalopride, which appears to be highly selective for the serotonin 5-HT4 receptor and is therefore a potent stimulator of gut motility. ANTONIO TURSI, MD Servizio di Gastroenterologia Territoriale ASL BAT Andria (BT), Italy
References 1.
Cohen E, et al. Clin Gastroenterol Hepatol 2013;11:1614–1619.
2. 3.
Levack MM, et al. Dis Colon Rectum 2012;55:10–17. Drossman DA, et al. McLean: Degnon Associates, 2006.
4.
Spiller R, et al. J Neurogastroenterol Motil 2012;18:258–268.
5.
Tursi A, et al. J Gastrointest Liver Dis 2013;22:12–17.
6.
Simpson J, et al. Neurogastroenterol Motil 2009;21:847–858.
7.
Stollman N, et al. J Clin Gastroenterol 2013;47:621–629.
8.
Parente F, et al. Int J Colorectal Dis 2013;28:1423–1431.
Conflicts of interest The author discloses no conflicts. http://dx.doi.org/10.1016/j.cgh.2013.12.017