LARGE INTESTINE: Edited by Eamonn M.M. Quigley
Colonic disorders, or more accurately, disorders though to originate from the colon represent a considerable component of a gastroenterologist's work-load and a major source of discomfort and distress for the general public. Once regarded as a vestigial organ and readily removed to eliminate the ‘vile humors’ emanating from its sulfurous activities, we now recognize many important contributions of the colon and its microbial inhabitants to homeostasis and health [1▪▪,2,3]. The colon comes with some baggage, however. Colon cancer is the third most common cancer in the United States and its incidence is rising throughout the world and, most dramatically, in developing nations . There is good news. Screening for colon cancer, regardless of its methodology, works and many believe that colonoscopy still maintains its position as the most effective modality [5,6▪]. It is appropriate, therefore, that this volume devotes space to two of the issues that have bedeviled our efforts to eliminate colon cancer through screening colonoscopy – inadequate preparation of the colon and our failure to visualize and remove serrated adenomas. The latter, more prevalent in the right colon and taking a different molecular pathway to carcinoma seem to plot against us to evade our gaze . Indeed, our inability to identify serrated adenomas may well explain reports of different mortality rates for right-sided and left-sided cancer, lower on the left than on the right . No one would argue against the importance to the patient and the colonoscopist of the importance of a well prepared colon; one interesting exception may be the value of the ‘mucus cap’ in a slightly less than perfectly cleansed right colon as a hint that a serrated adenoma may lie beneath.
Eosinophilic esophagitis has emerged as a ‘new’ disease and one that all too frequently gets us out of bed at ungodly hours to remove impacted chicken or steak; investigators at the University of Newcastle (Australia) have been pioneers in expanding the ‘red state’ in to the duodenum (where it seems to be common in functional dyspepsia) and now take us all the way into the colon where eosinophils may be involved in a number of pathological processes [9▪]. As irritable bowel syndrome is increasingly recognized in older individuals, it was inevitable that the question of overlap with diverticulosis would re-emerge. Those of us who have been around for a while will remember the phrase ‘painful diverticular disease’ and the status it once enjoyed as an explanation for abdominal pain, bloating and constipation . Eventually discredited as the ubiquity of diverticula was recognized, the idea that diverticula (diverticulosis) could be associated with a certain symptomatic profile (diverticular disease) has latterly re-emerged and its relationship to irritable bowel syndrome re-examined – the plot thickens but the denouement of this ‘whodunnit’ has yet to be revealed . Another differential diagnosis, that of distinguishing irritable bowel syndrome from inflammatory bowel disease, frequently confronts the clinician, be they, in primary care or specialist practice . At face value, this should be easy, given the vast difference in underlying pathologic findings but there are situations where diagnostic uncertainty prevails – initial presentation (not all patients with colitis have bloody diarrhea!) and when we have, by all available measures, induced clinical remission of Crohn's disease or colitis . In the former, we agonize about missing an inflammatory disease (whose diagnosis is still delayed for far too long); in the latter our concern is inappropriate use of potent and expensive agents when dysfunction and not inflammation is the problem. Although, despite some progress [14▪▪], a universally effective biomarker(s) for irritable bowel syndrome still eludes us, the arrival of sensitive and noninvasive tests for inflammation, such as calprotectin and lactoferrin, offer real promise .
Although we have moved a long way from the Victorian view of the colon as a redundant and potentially malign organ, we also recognize the burden of diseases and disorders associated with this organ; this volume addresses some of the challenging areas in colonic disease and provides considerable optimism for the alleviation of some of these truly colonic ills.
Supported in part by a bequest from the Hughes-Sterling Foundation.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
REFERENCES AND RECOMMENDED READING
Papers of particular interest, published within the annual period of review, have been highlighted as:
- ▪ of special interest
- ▪▪ of outstanding interest
1▪▪. Dinning PG. A new understanding of the physiology and pathophysiology of colonic motility? Neurogastroenterol Motil 2018; 30:e13395.
Provides a nice summary of novel insights into colonic motility in health and disease emphasizing new findings.
2. Greenwood-Van Meerveld B, Johnson AC, Grundy D. Gastrointestinal physiology and function. Handb Exp Pharmacol 2017; 239:1–16.
3. Quigley EM, Abu-Shanab A, Murphy EF, et al. The metabolic role of the microbiome: implications for NAFLD and the metabolic syndrome. Semin Liver Dis 2016; 36:312–316.
4. Irabor DO. Emergence of colorectal cancer in West Africa: accepting the inevitable. Niger Med J 2017; 58:87–91.
5. Issa IA, Noureddine M. Colorectal cancer screening: an updated review of the available options. World J Gastroenterol 2017; 23:5086–5096.
6▪. Zhang J, Cheng Z, Ma Y, et al. Effectiveness of screening modalities in colorectal cancer: a network meta-analysis. Clin Colorectal Cancer 2017; 16:252–263.
A comprehensive analysis of available options.
7. O’Connell B, Hafiz N, Crockett S. The serrated polyp pathway: is it time to alter surveillance guidelines? Curr Gastroenterol Rep 2017; 19:52.
8. Petrelli F, Tomasello G, Borgonovo K, et al. Prognostic survival associated with left-sided vs right-sided colon cancer: a systematic review and meta-analysis. JAMA Oncol 2016; [Epub ahead of print].
9▪. Walker MM, Potter M, Talley NJ. Eosinophilic gastroenteritis and other eosinophilic gut diseases distal to the oesophagus. Lancet Gastroenterol Hepatol 2018; 3:271–280.
A perspective on the possible role of eosinophils in GI disorders from the pioneers in the field.
10. DiSiena MS, Birk JW. Diverticular disease: the old, the new, and the ever-changing view. South Med J 2018; 111:144–150.
11. Rezapour M, Ali S, Stollman N. Diverticular disease: an update on pathogenesis and management. Gut Liver 2018; 12:125–132.
12. Colombel JF, Shin A, Gibson PR. Functional gastrointestinal symptoms in patients with inflammatory bowel disease: a clinical challenge. Clin Gastroenterol Hepatol 2018; [Epub ahead of print].
13. Quigley EM. Overlapping irritable bowel syndrome and inflammatory bowel disease: less to this than meets the eye? Therap Adv Gastroenterol 2016; 9:199–212.
14▪▪. Camilleri M, Halawi H, Oduyebo I. Biomarkers as a diagnostic tool for irritable bowel syndrome: where are we? Expert Rev Gastroenterol Hepatol 2017; 11:303–316.
Biomarkers in IBS critically assessed.
15. Mumolo MG, Bertani L, Ceccarelli L, et al. From bench to bedside: fecal calprotectin in inflammatory bowel diseases clinical setting. World J Gastroenterol 2018; 24:3681–3694.