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This material is supported by an educational grant from Salix Pharmaceuticals, Inc.

IntroductionThe term diverticular disease encompasses a spectrum ofconditions (diverticulosis, diverticulitis, diverticular bleeding, etc),which share the underlying pathology of acquired diverticula of thecolon. It is believed to occur as a result of outpouching of themucosa and submucosa through weaknesses in the muscular wallof the colon alongside natural openings where arteries (the vasarecta) penetrate the muscularis layer to reach the mucosa andsubmucosa.1 Between 10% and 30% of patients withdiverticulosis, a purely anatomic diagnosis that describes thepresence of ≥1 diverticula, may develop painful diverticulardisease or diverticulitis.2,3 These patients experience a range ofacute and chronic symptoms, including abdominal pain,peritonitis, obstruction, bleeding, fistulization, and abscessformation.4

In some respects, symptomatic diverticular disease shares manyof the features of irritable bowel syndrome (IBS). IBS is a chroniccomplex of gastrointestinal symptoms characterized by significantabdominal pain and disturbed defecation.5 IBS is defined by theRome III criteria as recurrent abdominal pain or discomfort for ≥3days a month in the last 3 months that is associated with at least2 of the following: 1) improvement with defecation, 2) onsetassociated with a change in stool form, or 3) onset associatedwith a change in the frequency of stool.

The symptoms associated with symptomatic diverticular diseaseand IBS overlap significantly; in fact, the concept of “symptomaticdiverticular disorder” has been questioned, with some suggestingthat it represents coincident occurrence of IBS in patients whohappen to have diverticula.6 More recent evidence suggests thatpainful diverticular disease may actually be a distinct entityoccurring as a result of an interaction between an inflammatoryprocess and neuromuscular function in the colon.6

However, the approach to management of these diseases differsconsiderably. It is important to distinguish between these 2disease states consistently to avoid inappropriate treatment,particularly when surgical treatment for diverticulitis is underconsideration. In this monograph, we will explore theepidemiology, etiology, diagnosis, and treatment of diverticulardisease and IBS and then examine pathways that help distinguishthese 2 disease states.

Painful Diverticular Disease or Irritable Bowel Syndrome?

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Learning ObjectivesUpon completion of this activity, the participant will be betterprepared to:

• Describe the pathophysiology, presentation, clinical features, and treatment of painful diverticular disease

• Describe the pathophysiology, presentation, and treatmentof irritable bowel syndrome (IBS)

• Differentiate between painful diverticular disease and IBS in clinical practice

Credit DesignationPurdue University College of Pharmacy designates thisenduring material for a maximum of 1.0 AMA PRA Category1 Credit(s)™. Physicians should claim only the creditcommensurate with the extent of their participation in theactivity.

Physician Accreditation StatementThis activity has been planned and implemented inaccordance with the Essential Areas and Policies of theAccreditation Council for Continuing Medical Education(ACCME) through the joint sponsorship of Purdue UniversityCollege of Pharmacy and the Gi Health Foundation. PurdueUniversity College of Pharmacy, an equal access/equalopportunity institution, is accredited by the ACCME toprovide continuing medical education for physicians.

Disclosure of Conflicts of InterestAll faculty and staff involved in the planning or presentation ofcontinuing education activities sponsored/provided by PurdueUniversity College of Pharmacy are required to disclose to theaudience any real or apparent commercial financial affiliationsrelated to the content of the presentation or enduring material.Full disclosure of all commercial relationships must be made inwriting to the audience prior to the activity. The Gi HealthFoundation staff and Purdue University College of Pharmacystaff have no relationships to disclose.

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DIVERTICULAR DISEASE AND NOMENCLATUREDespite the fact that diverticular disease is one of the mostcommon gastrointestinal diseases in the Western world, muchremains to be learned about it; in fact, confusion exists regardingeven the naming of the various conditions that fall under thediverticular umbrella. The term “diverticulosis” indicates thepresence of colonic diverticula—circumscribed pouches or sacsoccurring due to herniation of the mucous membrane of thegastrointestinal tract—which may or may not be symptomatic.“Diverticular disease,” in contrast, is a term that denotes clinicallysignificant and symptomatic diverticulosis.4 The term “symptomatic(or painful) diverticular disease” is also in common use.7

“Diverticulitis” describes acute or chronic macroscopicinflammation of the colon and may be associated with pain,bleeding, or colonic inflammation or infections.7

Epidemiology of Diverticular DiseaseNotably, diverticular disease occurs almost exclusively indeveloped countries; in fact, it has been called a “disease ofWestern civilization.”8 The incidence of diverticular diseasegenerally increases with age; estimates suggest a prevalence of<5% of people aged ≤40 years, increasing to approximately 65%in people aged ≥65 years. In general, approximately 80% of peoplewho present with diverticulitis are aged ≥50 years, although recenttrends suggest a rising prevalence in younger individuals.9

Diverticula are less common among vegetarians and others whoconsume large amounts of dietary fiber. Right-sided disease issignificantly more common among Asians and patients aged ≤60years.5

While diverticulosis is very commonly seen in Western countries,only 10% to 30% of patients with diverticular disease experiencean episode of overt diverticulitis,3 of whom a smaller percentagewill develop significant complications, including abscess formation,fistulas, and hemorrhage.10 Mortality and morbidity from painfuldiverticular disease is significant. In a study conducted in England,more than 500,000 hospital admissions were recorded over a 10-year period; the majority of these admissions were foremergencies.11 Thirty-day mortality was 5% and 1-year mortalitywas 20% in this population. Recent estimates suggest that thehospitalization rates for diverticulitis are increasing, particularlyamong younger people.11

Pathophysiology of Diverticular DiseaseDiverticula are simply small mucosal herniations that protrudethrough the intestinal layers and the smooth muscle, mostcommonly in the sigmoid colon (potentially because of increasedintraluminal pressure in this region), although they can be foundthroughout the large bowel. In most patients, multiple diverticulaare present,1 generally ranging from 5 to 10 mm in diameter,although occasionally exceeding 20 mm. These herniations createsmall pouches lined by the mucosa. The relationship between age

and the prevalence of diverticula can be explained by age-relateddegeneration of the mucosal wall as well as segmental increasesin colon pressure that result in bulging at weak points, typically at the insertion of the vasa recta.4

It is unknown why only a small percentage of patients withdiverticulosis develop symptomatic diverticular disease.Obstruction of the junction between the lumen of the diverticulumand the intestine proper by fecaliths or poorly absorbed foodcomponents may prompt bacterial overgrowth, inflammation,mucosal abrasion, barotrauma, and even microperforations.4 Noconnection has been observed between symptomatic disease andsmoking, caffeine, or alcohol intake, although a lack of exercisemay play an indirect role.1 There is an inverse relationship betweendietary fiber intake and the development of symptomaticdisease;12 in fact, some authors consider diverticulitis a “diseaseof deficiency” like scurvy, in that it is largely avoidable byincreasing fiber intake.8

Painful or symptomatic diverticular disease may also beassociated with fundamental physiologic factors, includingincreased motility index and increased intraluminal pressure.13

Recent evidence suggests that painful diverticular disease may beassociated with ongoing inflammatory changes that affectneuromuscular function in the colon.14-17 In fact, resected tissuesfrom the sigmoid colon of patients with “smouldering” diverticulardisease show chronic inflammatory changes. Moreover, somepatients have a symptomatic response to anti-inflammatory agentssuch as mesalazine.18-21 Both acute and subtle chronic changes inthe colonic microbiota have also been implicated in thepathogenesis of diverticular disease.22

Presentation and Diagnosis of Symptomatic Diverticular DiseaseSymptomatic diverticular disease is, like IBS, a diagnosis ofexclusion. Symptomatic diverticular disease is characterized byacute attacks of localized abdominal pain.9 In general, patientspresent with colicky pain, although the pain may sometimes besteady (Box 1). Pain may be precipitated by eating and is oftenrelieved by passing flatus or having a bowel movement.7 Bloatingand changes in stool form, particularly constipation, may beobserved in some patients. Patients may also have fullness ortenderness in the left lower quadrant or a tender loop of thesigmoid colon, reflecting the propensity of the disease to occur inthe sigmoid colon,8 although as noted previously, Asian patientshave predominantly right-sided diverticula and may manifest right-sided pain. Anorexia, nausea, and vomiting may occur.8 Bowelsounds are often suppressed but may be normal in mild cases.Many of these symptoms overlap with the Rome III criteria for IBS,particularly IBS with constipation (IBS-C) (Box 2).

Painful Diverticular Disease orIrritable Bowel Syndrome?

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Box 1: Signs and symptoms of symptomatic diverticular disease7

Box 2: Rome III criteria for IBS

Laboratory studies and imaging may be appropriate in somecases to distinguish symptomatic diverticular disease from otherconditions that mimic its symptoms. Common differentialdiagnoses are listed in box 3.1 White blood cell count may beelevated with a predominance of polymorphonuclear cells.1 Anabdominal radiograph series should be obtained in patients withabdominal pain to examine whether macro-perforations haveoccurred. Computerized tomography (CT) with intravenous andoral contrast is the gold standard to confirm a suspecteddiagnosis of diverticulitis.10 Contrast enema examinations areuseful as a complement to CT scanning.3 Ultrasonography mayalso be performed.3 Endoscopy should be avoided in initialevaluations because of the risk for perforation.3 Refer to thetreatment guidelines for a complete discussion of diagnosticmodalities.3

Box 3: Differential diagnoses of symptomatic diverticular diseaseand diverticulitis. Adapted from Salzman 2005.9

Recurrence is common among patients who suffer a symptomaticepisode of diverticular disease; furthermore, increasing evidencesuggests that an acute episode may be followed by chronicsymptoms, possibly as a result of inflammatory changes around diverticula, although exact incidence is unclear.23

Treatment of Symptomatic Diverticular DiseaseHigh-fiber diets are usually recommended to patients withasymptomatic disease in an effort to prevent symptomatic diverticulardisease; however, there are no well-designed, randomized, controlledclinical trials to support this strategy.2,10 Acutely, in patients withsignificant pain, tenderness, or fever, outpatient treatment should beinitiated with broad-spectrum antibiotics; common choices includemetronidazole plus a quinolone, metronidazole plus trimethoprim-sulfamethoxazole, or amoxicillin-clavulanic acid, all for 7 to 10 days.3

Patients should follow a clear liquid diet for 24 to 72 hours, after whichthe diet may cautiously include solids. If the patient is hospitalized, heor she should be placed on bowel rest and treated with intravenousfluids and intravenous antibiotics.3 Between 15% and 20% of patientsmay require surgery during hospital admission due to a lack ofresponse to conservative medical treatment, particularly amongpatients who have been hospitalized previously for ≥1 episodes orbecause of complications of diverticulitis.1,10

As noted previously, symptomatic diverticular disease may be relatedto inflammatory changes in the colon affecting neuromuscularfunction.24 These data suggest that anti-inflammatory agents may havea clinical role in the management of symptomatic diverticular disease.A systematic review of the literature evaluated the efficacy of 5-aminosalicylic acid (5-ASA) in patients with colonic diverticulardisease.21 A total of 6 randomized, controlled clinical trials wereidentified, which enrolled a total of 818 patients (3 in patients withuncomplicated diverticulitis and 3 in patients with symptomaticuncomplicated diverticular disease). The results of these studiesshowed that patients treated with 5-ASA had significantly betteroutcomes and that daily mesalazine was superior to cyclicadministration to prevent relapse of diverticular disease.Given the efficacy of both oral and intravenous antibiotics in themanagement of symptomatic diverticular disease, it is clear that thecolonic microbiota play a role in the pathogenesis andsymptomatology of disease. Nonabsorbable antibiotics such asrifaximin may be a useful treatment in diverticular disease.18,19 Indeed,several studies have examined the combination of acute rifaximin withlong-term mesalazine. In one study of 90 consecutive patients withsymptomatic uncomplicated diverticular disease, patients were treatedwith rifaximin 800 mg/d plus mesalazine 2.4 grams/d for 10 days,followed by mesalazine 1.6 grams/d for 8 weeks.18 Patients wereassessed for constipation, diarrhea, abdominal pain, rectal bleeding,and mucus with stools. Total symptom scores decreased from 1439to 44 (P<.001). The majority of patients were completelyasymptomatic after 8 weeks of treatment.



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Box 1. Signs and Symptoms of symptomatic diverticular disease7

• Localized abdominal pain in the absence of inflammation (eg, fever, leukocytosis, peritoneal signs on examination)• Pain is usually colicky (although may be steady in some patients)• Pain may be precipitated by eating• Pain may be relieved by passing flatus or having a bowel movement• Bloating may be present• Changes in stool form may occur (usually constipation)• Fullness or tenderness in left lower quadrant may be present• A tender loop of the sigmoid colon may be present• Anorexia, nausea, and vomiting may occur• Bowel sounds are typically depressed• Dysuria and urinary frequency may be reported by some patients

Box 2. Rome III criteria for IBS• IBS: Recurrent abdominal pain/discomfort ≥3 days/month for the past 3 months, associated with ≥2 of the following: - Improvement with defecation - Onset associated with change in stool frequency - Onset associated with change in stool form• Subtyped by predominant stool pattern - IBS-C: hard or lumpy stools ≥25% of defecations; loose or watery stools <25% of defecations

Box 3. Differential diagnoses of symptomatic diverticular disease and diverticulitis. Adapted from Salzman 2005.9

• Acute appendicitis

• Colorectal cancer

• Complicated ulcer disease

• Crohn’s disease

• Cystitis

• Ectopic pregnancy

• Gallbladder disease

• Incarcerated hernia

• Irritable bowel syndrome

• Ischemic colitis

• Mesenteric infarction

• Ovarian cyst, abscess, or neoplasm

• Ovarian torsion

• Pancreatic disease

• Pelvic inflammatory disease

• Peritonitis

• Pseudomembranous colitis

• Renal disease

• Small bowel obstruction

• Ulcerative colitis

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Probiotics, with and without 5-ASA, have been examined in theprevention of symptomatic diverticular disease recurrence.25 In amulticenter, prospective, randomized, controlled study, Tursi andcolleagues treated patients with symptomatic uncomplicateddiverticular disease to remission with rifaximin 800 mg/d plusmesalazine 2.4 grams/d for 10 days, followed by mesalazine 1.6grams/d for 8 weeks. Patients were subsequently randomized tolong-term treatment with mesalazine 1.6 grams/d, Lactobacilluscasei probiotic, or the combination of the 2 treatments. Notably,76.7% of the monotherapy groups and 96% of the combinationtherapy group remained recurrence-free at 12 months.

IBSIBS is a chronic complex of gastrointestinal symptoms characterizedby significant abdominal pain and disturbed defecation. IBS is definedby the Rome criteria as recurrent abdominal pain or discomfort for≥3 days a month in the last 3 months that is associated with at least2 of the following: 1) improvement with defecation, 2) onsetassociated with a change in stool form, or 3) onset associated with achange in the frequency of stool (Box 2).5 It is most commonlyclassified into 3 subtypes depending on predominant stool form: IBSwith constipation (IBS-C), IBS with diarrhea (IBS-D), and IBS with bothdiarrhea and constipation (IBS-M). Other subtypes used in theliterature include IBS-A (alternating diarrheal/constipation pattern) andIBS-U, which describes IBS without a predominant stool form orpattern. As noted above, there is considerable overlap between thesymptoms of symptomatic diverticular disease and IBS (particularlyIBS-C). Given that the appropriate management paradigms for these2 disease states differ, particularly with regard to surgicalapproaches to treatment, it is critical to distinguish them consistently.

Epidemiology of IBSIBS represents a major burden in terms of patient quality of life, workproductivity, and health care costs.26 In North America, IBS iscommon, with prevalence estimates ranging from 1% to over 20%;27

when defined using the most stringent criteria, pooled analysesindicate that between 7% and 10% of people have IBS worldwide.27-29

Notably, the actual number of patients suffering from IBS is likely tobe greater than the reported prevalence, as most patients fail to seekmedical attention.30-32

IBS is one of the most commonly diagnosed gastrointestinalconditions in clinical practice and has historically been the primarymotivating factor in between 25% and 50% of all referrals togastroenterologists.33 IBS also accounts for a significant number ofvisits to primary care physicians. On the individual level, IBS has atremendous impact on the patient in terms of physical andpsychological wellbeing, the ability to interact socially, and the abilityto work. In fact, studies consistently demonstrate that health-relatedquality of life is consistently lower among patients with IBS thanamong those with depression or gastroesophageal reflux disease andsimilar to that seen in patients with diabetes.24,34 IBS is associatedwith significant incremental health care costs, with some studies

suggesting annual direct and indirect costs of up to $30 billion,22 muchof which arises from sequential diagnostic tests, invasive procedures,and abdominal operations, despite data suggesting that IBSsymptoms almost invariably persist following surgery.35

Pathophysiology of IBSThe precise cause(s) of IBS is (are) not known; however, it is likely thatthere are multiple underlying etiologies (eg, altered gastrointestinalmotility, visceral hypersensitivity, infection and inflammation, stress,bile acid modulation) that ultimately result in similar symptoms. Ofparticular note, recent data suggest a role of immune activationand/or low-grade inflammatory processes in the pathogenesis ofIBS.36 For these reasons, IBS remains an area of very active clinicalresearch.

Diagnosis of IBS-CLike diverticular disease, IBS is largely a disease of exclusion. Althoughthe exact definition of IBS remains controversial, IBS is currentlydefined by abdominal pain or discomfort that occurs in associationwith altered bowel habits over a period of at least 3 months.37

Individual symptoms have limited accuracy for diagnosing IBS, andtherefore, the disorder should be considered a symptom complex.Alarm features (eg, anemia, weight loss, family history of colorectalcancer, inflammatory bowel disease, celiac sprue), offer littlediscriminative value in separating patients with IBS from those withorganic diseases. For this reason, in patients who fulfill symptom-based criteria for IBS in the absence of alarm features are usuallyconsidered to have IBS.37

Routine diagnostic testing with a complete blood count, serumchemistries, thyroid function studies, stool for ova and parasites, andabdominal imaging is generally not recommended for patients withtypical IBS symptoms and no alarm features because of a lowlikelihood of uncovering organic disease. Routine screening for celiacsprue should be considered in patients with IBS-D or IBS-M but not inthose with IBS-C, and lactulose breath testing should be considered inpatients in whom lactose maldigestion remains a concern despitedietary modification. The value of breath testing for small bowelbacterial overgrowth remains an area of considerable controversy,although recent meta-analyses suggest that this test has diagnosticvalue.38

Managing IBS-CAlthough the symptoms of diverticular disease and IBS-C can overlapsignificantly, the pharmacologic management paradigm, aside fromincreasing fiber intake, differs significantly. Often, the symptomaticoverlap between these 2 disease states can be a source ofconsiderable frustration for both health care providers and patients.Fiber, laxatives, antidepressants, lubiprostone, and linaclotide all offerpharmacologic options for the management of IBS; probiotics and diethave also been shown to be effective.

In general, fiber is effective for relieving global IBS symptoms, but



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there is little evidence that it is effective for relief of abdominal pain.Soluble and insoluble fiber had different effects on global IBSsymptoms. Soluble fiber (eg, psyllium, ispaghula, calciumpolycarbophil) has been associated with significant improvements inglobal symptoms (relative risk of symptoms not improving, 1.55; 95%CI, 1.35-1.78). In contrast, insoluble fiber (eg, corn, wheat bran) wasno better than placebo (relative risk, 0.89; 95% CI, 0.72-1.11) and, infact, may be associated with worse outcomes. A systematic reviewconducted for the ACG guidelines identified 12 randomized, controlledtrials evaluating fiber in patients with IBS, most of which were old, hadsuboptimal design, or failed to differentiate between IBS-C and IBS-Dpatients.39 Overall, the relative risk of IBS symptoms not improving withwheat bran was 1.02 (95% CI, 0.82-1.27). In contrast, global IBSsymptoms were improved in 4 of 6 studies with psyllium. The relativerisk of IBS symptoms not improving with psyllium was 0.78 (95% CI,0.63-0.96) and the number needed to treat was 6 (95% CI, 3-50).Thus, fiber probably provides only marginal benefits in patients withIBS. As importantly, these data suggest that the various available fibersupplements should not be considered a homogenous class; indeed, iffiber is used at all in IBS-C, it should be soluble.

Few well-designed clinical trials have evaluated the overall efficacy ofosmotic laxatives (eg, lactulose, PEG-3350, magnesium hydroxide,milk of magnesia) in patients with IBS, although they are commonlyused. Three randomized, double-blind, placebo-controlled studiescompared lactulose with placebo in patients with chronic constipation;lactulose was superior to placebo in improving stool consistency andthe number of bowel movements per day in all 3 studies.40 A single,small, sequential study in patients with IBS-C compared symptomsbefore and after PEG treatment in adolescents with IBS-C.41 In thisstudy, PEG resulted in a significant improvement in the frequency ofbowel movements (P<.05) but was not associated with a significantimprovement in pain.

Stimulant laxatives (eg, senna, bisacodyl, cascara) are another optionfor the management of constipation in patients with IBS. Two recentrandomized trials have been conducted evaluating these agents forchronic constipation. In the first,42 patients with chronic constipation,as defined by Rome III criteria, were randomly allocated to treatmentwith 10 mg bisacodyl (n=247) or placebo (n=121) once daily for 4weeks; the primary endpoint was the number of completespontaneous bowel movements (CSBMs) per week during thetreatment period. The mean number of CSBMs increased from 1.1 ±0.1 in both groups to 5.2 ± 0.3 in the bisacodyl group and 1.1 ± 0.1in the placebo group (P<.0001). All secondary endpoints evaluated inthis trial (number of CSBMs/week, number of spontaneous bowelmovements (SBMs), and constipation-associated symptoms) improvedsignificantly with bisacodyl. A separate study43 evaluated the effects ofsodium picosulfate in patients with chronic constipation. In this study(n=367), the mean number of CSBMs/week increased from 0.9 ± 0.1to 3.4 ± 0.2 in the sodium picosulfate group and from 1.1 ± 0.1 to1.7 ± 0.1 in the placebo group (P<.0001).

Antidepressants are another option for the management of IBS-C,particularly among those who fail to respond to peripherally acting

agents and those in whom abdominal pain is a prominent symptom.While individual clinical trials of antidepressants have failed to show aprominent benefit, meta-analysis suggests that these agents can beeffective in patients with IBS.44 A meta-analysis of 13 randomized,controlled trials that evaluated either TCAs or SSRIs (N=789) foundthat global symptoms were significantly more likely to improve inpatients taking an antidepressant, regardless of type (relative risk ofIBS symptoms not improving, 0.66; 95% CI, 0.57-0.78). Among thosetaking TCAs (9 trials; N=575), the relative risk of IBS not improvingwas 0.68 (95% CI, 0.56-0.83; NNT=4.0); among those taking SSRIs(5 trials; n=230) the relative risk of IBS not improving was 0.62 (95%CI, 0.45-0.87; NNT=3.5).

Lubiprostone is a locally acting, bicyclic functional fatty acid derivedfrom prostaglandin E1 that acts by specifically activating CIC-2chloride channels on the apical aspect of gastrointestinal cells, elicitinga chloride-rich fluid secretion.45 Lubiprostone was assessed in ananalysis of 1171 patients with IBS-C;46 the primary efficacy endpointwas the percentage of overall responders (moderate or significantrelief for at least 2 of the 3 months of the study). The percentage ofoverall responders with the lubiprostone group was 17.9% vs 10.1% inthe placebo group (P=.001). The mean improvement from baseline inabdominal discomfort and pain was also significantly greater amongpatients who received lubiprostone compared with placebo-treatedpatients (-0.43 vs -0.35; P=.039).

Linaclotide is approved for chronic constipation and IBS-C.47-50 Arandomized, double-blind, placebo-controlled Phase 3 trial examinedthe efficacy and safety of linaclotide at a once daily dosage of 290 μg(n=407) versus placebo (n=397) for 12 weeks.49 In this study, IBS-Cpatients with an average of <3 CSBMs/week, ≤5 SBMs/week, andabdominal pain ≥3 (0-10 scale) during a 2-week baseline period wererandomized to linaclotide 290 μg or placebo for 12 weeks.Significantly more linaclotide patients met the 4 primary and 10secondary endpoints over the 12-week duration of the trial. In asecond study of approximately 800 patients, improvements amonglinaclotide patients were sustained through 26 weeks of treatment.50

Overall, linaclotide demonstrated statistically significant improvementcompared with placebo at each of the 26 weeks of treatment forabdominal pain as well as for abdominal discomfort, bloating,straining, stool consistency, CSBMs, and SBMs.50 Diarrhea was themost common adverse event, resulting in the discontinuation of 4% oflinaclotide and 0.2% of placebo patients.49,50

CONCLUSIONSAs shown in this monograph, there is considerable overlap betweendiverticular disease and IBS and there are few objective methods fordistinguishing among the 2 disease states in clinical practice. Ingeneral, IBS is more often seen in younger patients and women,whereas diverticular disease should be more strongly suspected inolder male or female patients. Diverticular disease is usually episodic,short-lived, and often responds to treatment with fiber, laxatives,antibiotics, or surgical removal of the diverticular segment. In contrast,IBS is usually chronic and recurrent.



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33. Everhart JE, Renault PF. Irritable bowel syndrome in office-based practice in the United States. Gastroenterology. 1991;100:998-1005.

34. El-Serag HB, Olden K, Bjorkman D. Health-related quality of life among persons with irritable bowel syndrome: a systematic review. Aliment Pharmacol Ther. 2002;16:1171-1185.

35. Longstreth GF, Wilson A, Knight K, et al. Irritable bowel syndrome, health care use, and costs: a U.S. managed care perspective. Am J Gastroenterol. 2003;98:600-607.

36. Ford AC, Talley NJ. Mucosal inflammation as a potential etiological factor in irritable bowel syndrome: a systematic review. J Gastroenterol. 2011;46:421-431.

37. Brandt LJ, Chey WD, Foxx-Orenstein AE, et al. An evidence-based position statement on the management of irritable bowel syndrome. Am J Gastroenterol. 2009;104Suppl 1:S1-35.

38. Shah ED, Basseri RJ, Chong K, Pimentel M. Abnormal breath testing in IBS: a meta-analysis. Dig Dis Sci. 2010;55:2441-2449.

39. Ford AC, Talley NJ, Spiegel BM, et al. Effect of fibre, antispasmodics, and peppermint oil in the treatment of irritable bowel syndrome: systematic review and meta-analysis. BMJ. 2008;337:a2313.

40. Brandt LJ, Prather CM, Quigley EM, Schiller LR, Schoenfeld P, Talley NJ. Systematic review on the management of chronic constipation in North America. Am J Gastroenterol. 2005;100 Suppl 1:S5-S21.

41. Khoshoo V, Armstead C, Landry L. Effect of a laxative with and without tegaserod in adolescents with constipation predominant irritable bowel syndrome. Aliment Pharmacol Ther. 2006;23:191-196.

42. Kamm MA, Mueller-Lissner S, Wald A, Richter E, Swallow R, Gessner U. Oral bisacodyl is effective and well-tolerated in patients with chronic constipation. Clin Gastroenterol Hepatol. 2011;9:577-583.

43. Mueller-Lissner S, Kamm MA, Wald A, et al. Multicenter, 4-week, double-blind, randomized, placebo-controlled trial of sodium picosulfate in patients with chronic constipation. Am J Gastroenterol. 2010;105:897-903.

44. Ford AC, Talley NJ, Schoenfeld PS, Quigley EM, Moayyedi P. Efficacy of antidepressants and psychological therapies in irritable bowel syndrome: systematic review and meta-analysis. Gut. 2009;58:367-378.

45. Camilleri M, Bharucha AE, Ueno R, et al. Effect of a selective chloride channel activator, lubiprostone, on gastrointestinal transit, gastric sensory, and motor functions in healthy volunteers. Am J Physiol Gastrointest Liver Physiol. 2006;290:G942-947.

46. Drossman DA, Chey WD, Johanson JF, et al. Clinical trial: lubiprostone in patients with constipation-associated irritable bowel syndrome--results of two randomized, placebo-controlled studies. Aliment Pharmacol Ther. 2009;29:329-341.

47. Lembo AJ, Kurtz CB, Macdougall JE, et al. Efficacy of linaclotide for patients with chronicconstipation. Gastroenterology. 2010;138:886-895.

48. Lembo AJ, Schneier HA, Shiff SJ, et al. Two randomized trials of linaclotide for chronic constipation. N Engl J Med. 2011;365:527-536.

49. Rao S, Lembo A, Shiff SJ. Efficacy and safety of once daily linaclotide in patients with irritable bowel syndrome with constipation: a 12-week, randomized, double-blind, placebo-controlled Phase 3 trial followed by a 4-week randomized withdrawal period. Gastroenterology. 2011;140:S138.

50. Chey WD, Lembo A, MacDougall JE. Efficacy and safety of once-daily linaclotide administered orally for 26 weeks in patients with IBS-C: results from a randomized, double-blind, placebo-controlled Phase 3 trial. Gastroenterology. 2011;140:S135.

References


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Please select the one best answer by circling the appropriate letter.

1. The term “diverticulitis” describes:

a. The presence of colonic diverticula

b. Clinically significant and symptomatic disease

c. Acute or chronic macroscopic inflammation of the colon

d. Segmental colitis

2. Which of the following has been hypothesized to be a mechanism for symptomatic diverticular disease?

a. Increased production of flatus

b. Chronic inflammatory changes

c. Functional constipation

d. Functional diarrhea

3. The relationship between diverticular disease and fiber intake is:

a. Inverse

b. Direct

c. Direct in patients aged <50; inverse in patients aged ≥50

d. Diverticular disease is unaffected by fiber intake

4. Which of the following is the only demographic factor that has been shown to be related to the development of diverticular disease?

a. Smoking

b. Alcohol

c. Lack of exercise

d. Caffeine

5. What percentage of patients with diverticulosis develop diverticulitis?

a. 10% to 30%

b. 20% to 40%

c. 30% to 50%

d. 40% to 60%

6. The term “diverticulosis” refers to:

a. The presence of colonic diverticula

b. Clinically significant and symptomatic disease

c. Acute or chronic macroscopic inflammation of the colon

d. Segmental colitis

If you wish to receive acknowledgement of participation for this activity, please completethe post test, evaluation form, and request for credit and fax pages 7-11 to 973-867-3684.

Post Test

Painful Diverticular Disease or Irritable Bowel Syndrome?Project ID: 12-0013

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7. What percentage of patients who present with diverticulitis are aged ≥50 years?

a. 40%

b. 50%

c. 70%

d. 80%

8. True or false: daily 5-ASA is superior to cyclic administration of 5-ASA to prevent relapse of diverticular disease?

a. True

b. False

9. Rifaximin treatment resulted in asymptomatic disease in the majority of patients with diverticular disease after ____ weeks of treatment.

a. 2

b. 4

c. 6

d. 8

10. What is the relative risk of symptoms not improving in patients with IBS who receive soluble fiber?

a. 1.25

b. 1.55

c. 1.95

d. 2.05

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Evaluation

Purdue University College of Pharmacy respects and appreciates your opinions. To assist us in evaluating the effectiveness of thisactivity and to make recommendations for future educational offerings, please take a few minutes to complete this evaluation form.

This learning objective did (or will) increase/ improve my:

HighImpact

ModerateImpact

NoImpact

NotApplicable

• Describe the pathophysiology, presentation, clinicalfeatures, and treatment of painful diverticular disease

• Describe the pathophysiology, presentation, andtreatment of irritable bowel syndrome (IBS)

• Differentiate between painful diverticular disease andIBS in clinical practice

Knowledge ................................... qCompetence ................................. qPerformance ................................. qPatient Outcomes .......................... q

q q qq q qq q qq q q





• The content of this activity matched my current (or potential) scope of practice.

q No

q Yes, please explain

• Was this activity scientifically sound and free of commercial bias* or influence?

q Yes

q No, please explain

* Commercial bias is defined as a personal judgment in favor of a specific product or service of a commercial interest.

Impact of the Activity• Please indicate which of the following American Board of Medical Specialties/Institute of Medicine core competencies were addressed by this educational activity (select all that apply):

q Patient care or patient-centered care

q Practice-based learning and improvement

q Interpersonal and communication skills

q Employ evidence-based practice

q Interdisciplinary teams

q Professionalism

q Quality improvement

q Medical knowledge

q System-based practice

q Utilize informatics

q None of the above



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How well did this activity meet thefollowing learning objectives?

10

Evaluation

q Lack of experience

q Lack of resources (equipment)

q Lack of time to assess/counsel patients

q Lack of consensus of professional guidelines

q Lack of opportunity (patients)

q Lack of administrative support

q Reimbursement/insurance issues

q Patient compliance issues

q No barriers

q Cost

q Other __________________________________________

_________________________________________________

• How will you change your practice as a result of participating in this activity (select all that apply)?

q Create/revise protocols, policies, and/or procedures

q Change the management and/or treatment of my patients

q This activity validated my current practice

q I will not make any changes to my practice

q Other, please specify: ______________________________

_________________________________________________

• Please indicate any barriers you perceive in implementing these changes.

• What new information did you learn during this activity?

StronglyAgree

Agree Disagree StronglyDisagree

NotApplicable

q q q q q

q q q q q

• The educational activity has enhanced my professional effectiveness in treating patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

• The educational activity will result in a change in my practice behavior . . . . . . . .

____________________________________________________________________________________________________________________________________

To assist with future planning,please attest to time spent on activity:

I spent ______ hours on this program.

• If you indicated any barriers, how will you address these barriers in order to implement changes in your knowledge, competency, performance, and/or patients’ outcomes?

• Comments to help improve this activity?

• Recommendations for future CME/CPE topics.

____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________



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REQUEST FOR CREDIT

If you wish to receive acknowledgement of participation for this activity, please complete this request for credit and fax to 973-867-3684.

– –– –

Please do not use abbreviations.We need current and complete information to assure delivery of participation acknowledgement.

q MD/DO q PharmD/RPh q NP q PA q RN q Other

Degree (please mark appropriate box and circle appropriate degree):

Signature: Date:

Attestation to time spent on activity is required.

q I participated in the entire activity and q I participated in only part of the activity and claim _______ credits.claim 1.0 AMA PRA Category 1 Credit(s)™.

Signature is required to receive statement of credit.

Purdue University College of Pharmacy designates this enduring material for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.


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