CASE › Amber S,* a 33-year-old woman who works on the production line at a bread factory, sought care at my health center with a several month history of non-bloody diarrhea that was increasing in frequency and urgency and was accompanied by painful abdominal bloating and cramping. She said that these symptoms were negatively impacting her interpersonal relationships, as well as her productivity at work. She reported that “almost everything” she ate upset her stomach and “goes right through her,” including fruits, vegetables, and meat, as well as greasy fast food. She had researched her symptoms on the Internet and was worried that she might have something serious like inflammatory bowel disease or cancer.

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder (FGID) that negatively impacts the quality of life (QOL) of millions of people worldwide.¹ In fact, one study of 179 people with IBS found that 76% of survey respondents reported some degree of IBS-related impairment in at least 5 domains of daily life: daily activities, comorbid psychiatric diagnoses, symptom severity, QOL, and symptom-specific cognitive affective factors related to IBS.²

Estimating prevalence and incidence is a formidable challenge given various diagnostic criteria, the influence of population selection, inclusion or exclusion of non-GI comorbidities, and various cultural influences.³ That said, it’s estimated that IBS impacts approximately 11% of the world’s population, and approximately 30% of these individuals seek treatment.^1,4 While there are no significant differences in GI symptoms between those who consult physicians and those who do not, those who do seek treatment report higher pain scores, greater levels of anxiety, and a greater reduction in QOL.⁵

All ages affected. IBS has been reported in patients of all ages, including children and the elderly, with no definable difference reported in the frequency of subtypes (diarrhea- or constipation-predominant).

This article reviews the latest explanations, diagnostic criteria, and treatment guidelines for this challenging condition so that you can offer your patients confident care without needless testing or referral.

[polldaddy:9755564]

A lack of consensus among practicing physicians

Historically, IBS has been regarded by many primary care physicians (PCPs) as a diagnosis of exclusion. Lab tests would be ordered, nothing significant would be found, and the patient would be referred to the gastroenterologist for a definitive diagnosis.

Perceptions and misconceptions about IBS continue to abound to this day. Many are neither completely right nor wrong partly because so many triggers for IBS exist and partly because of the heretofore lack of simple, standardized criteria to diagnose the condition. Other factors contributing to the confusion are that the diagnosis of IBS is purely symptom-based and that proposals of its pathophysiology have traditionally been complex.

It is presumed that IBS shares common pathophysiologic mechanisms—including visceral hypersensitivity—with syndromes like functional dyspepsia.For example, a 2006 survey-based study of PCPs and gastroenterologists found that PCPs were less likely than gastroenterologists to believe that IBS was related to prior physical or sexual abuse, previous infection, or learned behavior, but were more likely to associate dietary factors or a linkable genetic etiology with IBS.⁶ Both sets of beliefs, however, may be considered correct.

Similarly, a 2009 qualitative study conducted in the Netherlands found that general practitioners (GPs) considered smoking, caffeine, diet, “hasty lifestyle,” and lack of exercise as potential triggers for IBS symptoms, while PCPs in the United Kingdom considered diet, infection, and travel to be possible triggers.⁷ Again, all play a role.

While GPs reported that patients should take responsibility for managing their IBS and for minimizing its impact on their daily lives, they admitted limited awareness of the extent to which IBS affected their patients’ daily living.⁷

A 2013 survey-based study in England determined that GPs understand the relationship between IBS and psychological symptoms including anxiety and stress, and posited that the majority of patients could be managed within primary care without referral for psychological interventions.⁸ Moreover, they reported that a dedicated risk assessment tool for patients with IBS would be helpful to stratify severity of disease. The study concluded that the reluctance of GPs to refer patients for evidence-based psychological treatments may prevent them from obtaining appropriate services and care.

Newer explanatory model shines light on IBS

A newer explanation that is based on 3 main hypotheses is elucidating the true nature of IBS and providing a pragmatic model for the clinical setting (FIGURE 1).⁹ According to the model, IBS entails the following 3 elements, which combined lead to the symptoms of IBS:

• Altered or abnormal peripheral regulation of gut function (including sensory and secretory mechanisms)
• Altered brain-gut signaling (including visceral hypersensitivity)
• Psychological distress.

It is reasonable to consider that epigenetic changes may underlie the etiology and pathophysiology of IBS and could increase one’s susceptibility to developing the disorder. Additionally, it is presumed that IBS shares common pathophysiologic mechanisms, including visceral hypersensitivity, with other associated functional syndromes, such as functional dyspepsia.

New criteria make diagnosis on symptoms alone easier

In addition to a new explanatory model, clear criteria for diagnosing the disorder now exist, which should make it easier for PCPs to make the diagnosis without additional testing or referral. The 2016 Rome IV criteria³ provide guidelines for diagnosing the various subtypes of IBS including IBS-D (diarrhea predominant), IBS-C (constipation predominant), and IBS-M (mixed subtypes). A laboratory evaluation is really only needed for patients who fall outside the criteria or who have alarm symptoms, which include:

• age >50 years at onset of symptoms,

• new onset of constipation in the elderly,

• rectal bleeding,
• unexplained weight loss or anemia,
• family history of organic GI disease, and
• a palpable abdominal or rectal mass.

These symptoms should prompt referral to a gastroenterologist. Once alarm symptoms have been excluded, the diagnosis of IBS is based upon the presence of characteristic symptoms and changes in stool habits (FIGURE 2^3,10).

Patterns of migration. Over time, patients may migrate between subtypes, most commonly from IBS-C or IBS-D to IBS-M; switching between IBS-C and IBS-D occurs less commonly.¹¹ Patients who meet criteria for IBS but whose bowel habits and symptoms cannot be grouped into any of these 3 categories are considered to have IBS unclassified. The Bristol Stool Form Scale (available at: https://www.niddk.nih.gov/health-information/health-communication-programs/bowel-control-awareness-campaign/Documents/Bristol_Stool_Form_Scale_508.pdf) should be used to gauge and track stool consistency.

A novel diagnostic test for IBS has been validated for differentiating patients with IBS-D from those with inflammatory bowel disease (IBD).¹² The test focused on the beliefs that cytolethal distending toxin B (CdtB) is produced by bacteria that cause acute viral gastroenteritis (eg, norovirus, rotavirus), and that host antibodies to CdtB cross-react with the protein vinculin in the host gut, producing an “IBS-like phenotype.”

Additional treatment options for diarrhea-predominant IBS include antidepressants (tricyclics or SSRIs) and antispasmodics, such as dicyclomine and hyoscyamine.In a 2015 large-scale multicenter trial, both anti-CdtB and anti-vinculin antibodies were found to be significantly elevated in subjects with IBS-D compared to non-IBS subjects,¹² providing evidence to support the long-held belief that viral gastroenteritis is often at the root of IBS.

Treatment aims to decrease symptoms and improve QOL

Treatment of IBS is directed at decreasing symptoms of abdominal pain and discomfort, bloating, diarrhea, and constipation while improving QOL. Therapeutic options for treatment of each symptom are listed in FIGURE 3,^13,14 including several that are commonly used and have moderate efficacy, but are not currently approved by the US Food and Drug Administration for this purpose.

Current evidence-based pharmacologic guidelines from the American Gastroenterological Association (AGA) can be found at: https://www.guideline.gov/summaries/summary/49122?osrc=12. Figure 3^13,14 provides a few additional options not included in the AGA guidelines and presents the information in a simple schematic.

Pharmacologic therapies for IBS-D

Eluxadoline is a novel mixed mu opioid receptor agonist and delta opioid receptor antagonist developed for the treatment of IBS-D. It normalizes GI transit and defecation under conditions of environmental stress or post-inflammatory altered GI function.¹⁵ A 2016 study involving almost 2500 patients found that eluxadoline was significantly better than placebo at decreasing abdominal pain and improving stool consistency on the same day for at least half of a 26-week period.¹³ The most common adverse effects were nausea, constipation, and abdominal pain. Pancreatitis occurred rarely.

Rifaximin. Because GI flora play a central role in the pathophysiology of IBS, researchers have found that rifaximin, a minimally absorbed antibiotic, is a potentially important player in treatment. Two double-blind, placebo-controlled trials (TARGET 1 and TARGET 2) found that after 4 weeks of treatment, patients experienced significant improvement in global IBS symptoms including bloating, abdominal pain, and stool consistency on rifaximin vs placebo (40.7% vs 31.7%; P<.001 in the 2 studies combined).¹⁶ The incidence of adverse effects (headache, upper respiratory infection, nausea, abdominal pain, diarrhea, and urinary tract infection) was comparable to that with placebo.

Alosetron. Research has shown this selective 5-HT3 receptor antagonist to improve all IBS QOL measures, restriction of daily activities, and patient satisfaction significantly more than placebo in women.¹⁷ While initial use of alosetron in 2000 was widespread, the rare serious adverse event of ischemic colitis led to its withdrawal from the US market within a few months.¹⁸ Alosetron returned to the market in 2002 with restricted marketing (to treat only women with severe diarrhea-predominant IBS). (See Lotronex [alosetron hydrochloride] full prescribing information available at: https://lotronex.com/hcp/index.html.) Data from a 9-year risk management program subsequently found a cumulative incidence rate for ischemic colitis of 1.03 cases per 1000 patient/years.¹⁹

Current evidence suggests that targeted carbohydrate and gluten exclusion plays a role in the treatment and symptomatic improvement of patients with IBS.Other possible options include various antidepressants (tricyclics such as amitriptyline, imipramine, and nortriptyline; or selective serotonin reuptake inhibitors [SSRIs] such as citalopram, fluoxetine, and paroxetine) and antispasmodics such as dicyclomine and hyoscyamine.

Pharmacologic therapies for IBS-C

Linaclotide is a guanylate cyclase-C agonist with an indication for treatment of IBS-C. A double-blind, parallel-group, placebo-controlled trial found that the percentage of patients who experienced a decrease in abdominal pain was nearly 25%, with statistically significant improvements in bloating, straining, and stool consistency over a 26-week period.²⁰ In a report on 2 phase 3 trials, researchers found that linaclotide improved global symptom scores and significantly decreased abdominal bloating and fullness, pain, cramping, and discomfort vs placebo. Diarrhea was the most commonly reported adverse event in patients with severe abdominal symptoms (18.8%-21%).²¹

Lubiprostone is a prostaglandin E1 analogue that activates type-2-chloride channels on the apical membrane of epithelial cells in the intestine. In a combined analysis of 2 phase 3 randomized trials, lubiprostone was administered twice daily for 12 weeks vs placebo and patients were asked to describe how they felt after the trial period. Survey responders reported significant improvements in global IBS-C symptoms (17.9% vs 10.1%; P=.001).²² A meta-analysis of studies on lubiprostone found that diarrhea, nausea, and abdominal pain were the most common adverse effects, but their occurrence was not that much greater than with placebo.²³

Diet and probiotics can play a significant role

The role of dietary components in the treatment of IBS is gaining increasing attention. Such components can have a direct effect on gastric and intestinal motility, visceral sensation, immune activation, brain-gut interactions, and the microbiome. Current evidence suggests that targeted carbohydrate and gluten exclusion plays a favorable role in the treatment and symptomatic improvement of patients with IBS.²⁴

A 2014 study conducted in Australia showed that a diet low in FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), which is characterized by avoiding foods containing gluten and those that are high in fructose, reduced overall GI symptom scores (including scores involving abdominal bloating, pain, and flatus) in patients with IBS compared to those consuming a normal Australian diet.²⁵ The International Foundation for Functional Gastrointestinal Disorders’ Web site provides a detailed guide to low FODMAP foods and can be found at: http://www.aboutibs.org/low-fodmap-diet.html.

Probiotics are now commonly used in the symptomatic treatment of many upper and lower GI disorders. While much anecdotal evidence exists to support their benefit, there is a paucity of large-scale and rigorous research to provide substantial outcomes-based evidence. The theory for their use is that they support regulation of the gut microbiome, which in turn improves the imbalance between the intestinal microbiome and a dysfunctional intestinal barrier.

Probiotics are now used in the symptomatic treatment of many upper and lower GI disorders.A 2014 randomized, double-blind, placebo-controlled trial involving multispecies probiotics (a mixture of Bifidobacterium longum, B. bifidum, B. lactis, Lactobacillus acidophilus, L. rhamnosus, and Streptococcus thermophilus) found that patients who received probiotics had significantly reduced symptoms of IBS after 4 weeks compared with placebo, and modest improvement in abdominal pain and discomfort as well as bloating.²⁶ One study involving 122 patients from 2011 found that B. bifidum MIMBb75 reduced the global assessment of IBS symptoms by -88 points (95% CI, -1.07 to -0.69) when compared with only -0.16 (95% CI, -.32 to 0.00) points in the placebo group (P<.0001).²⁷ MIMBb75 also significantly improved the IBS symptoms of pain/discomfort, distension/bloating, urgency, and digestive disorder. And one randomized, double-blind, placebo-controlled study involving 67 patients found that QOL scores improved two-fold when patients took Saccharomyces boulardii (15.4% vs 7.0%; P<.05).²⁸

Dried plums or prunes have been used successfully for decades for the symptomatic treatment of constipation. A single-blinded, randomized, cross-over study compared prunes 50 g/d to psyllium fiber 11 g/d and found that prunes were more efficacious (P<.05) with spontaneous bowel movements and stool consistency scores.²⁹

Peppermint oil has been studied as an alternative therapy for symptoms of IBS, but efficacy and tolerability are concerns. A meta-analysis of randomized controlled trials with a minimum duration of 2 weeks found that compared with placebo, peppermint oil provided improvement in abdominal pain, bloating, and global symptoms, but some patients reported transient heartburn.³⁰ A 4-week, randomized, double-blind, placebo-controlled clinical trial sponsored by IM HealthScience found a novel oral formulation of triple-enteric-coated sustained-release peppermint oil microspheres caused less heartburn than was reported in the previous study, but still significantly improved abdominal symptoms and lessened pain on defecation and fecal urgency.³¹

CASE › Suspecting IBS-D, the FP ordered a complete blood count, tissue transglutaminase antibodies, and a stool culture, all of which were unremarkable. Ms. S has been trying to follow a low FODMAP diet and has been taking some over-the-counter probiotics with only minimal relief of abdominal bloating and cramping and no improvement in stool consistency. Her FP started her on eluxadoline 100 mg twice daily with food. After 12 weeks of therapy, she reports significant improvement in global IBS symptoms and nearly complete resolution of her diarrhea.

*Amber S is a real patient in my practice. Her name has been changed to protect her identity.

CORRESPONDENCE
Joel J. Heidelbaugh, MD, FAAFP, FACG, Ypsilanti Health Center, 200 Arnet Suite 200, Ypsilanti, MI 48198; [email protected].

CASE › Amber S,* a 33-year-old woman who works on the production line at a bread factory, sought care at my health center with a several month history of non-bloody diarrhea that was increasing in frequency and urgency and was accompanied by painful abdominal bloating and cramping. She said that these symptoms were negatively impacting her interpersonal relationships, as well as her productivity at work. She reported that “almost everything” she ate upset her stomach and “goes right through her,” including fruits, vegetables, and meat, as well as greasy fast food. She had researched her symptoms on the Internet and was worried that she might have something serious like inflammatory bowel disease or cancer.

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder (FGID) that negatively impacts the quality of life (QOL) of millions of people worldwide.¹ In fact, one study of 179 people with IBS found that 76% of survey respondents reported some degree of IBS-related impairment in at least 5 domains of daily life: daily activities, comorbid psychiatric diagnoses, symptom severity, QOL, and symptom-specific cognitive affective factors related to IBS.²

Estimating prevalence and incidence is a formidable challenge given various diagnostic criteria, the influence of population selection, inclusion or exclusion of non-GI comorbidities, and various cultural influences.³ That said, it’s estimated that IBS impacts approximately 11% of the world’s population, and approximately 30% of these individuals seek treatment.^1,4 While there are no significant differences in GI symptoms between those who consult physicians and those who do not, those who do seek treatment report higher pain scores, greater levels of anxiety, and a greater reduction in QOL.⁵

All ages affected. IBS has been reported in patients of all ages, including children and the elderly, with no definable difference reported in the frequency of subtypes (diarrhea- or constipation-predominant).

This article reviews the latest explanations, diagnostic criteria, and treatment guidelines for this challenging condition so that you can offer your patients confident care without needless testing or referral.

[polldaddy:9755564]

A lack of consensus among practicing physicians

Historically, IBS has been regarded by many primary care physicians (PCPs) as a diagnosis of exclusion. Lab tests would be ordered, nothing significant would be found, and the patient would be referred to the gastroenterologist for a definitive diagnosis.

Perceptions and misconceptions about IBS continue to abound to this day. Many are neither completely right nor wrong partly because so many triggers for IBS exist and partly because of the heretofore lack of simple, standardized criteria to diagnose the condition. Other factors contributing to the confusion are that the diagnosis of IBS is purely symptom-based and that proposals of its pathophysiology have traditionally been complex.

It is presumed that IBS shares common pathophysiologic mechanisms—including visceral hypersensitivity—with syndromes like functional dyspepsia.For example, a 2006 survey-based study of PCPs and gastroenterologists found that PCPs were less likely than gastroenterologists to believe that IBS was related to prior physical or sexual abuse, previous infection, or learned behavior, but were more likely to associate dietary factors or a linkable genetic etiology with IBS.⁶ Both sets of beliefs, however, may be considered correct.

Similarly, a 2009 qualitative study conducted in the Netherlands found that general practitioners (GPs) considered smoking, caffeine, diet, “hasty lifestyle,” and lack of exercise as potential triggers for IBS symptoms, while PCPs in the United Kingdom considered diet, infection, and travel to be possible triggers.⁷ Again, all play a role.

While GPs reported that patients should take responsibility for managing their IBS and for minimizing its impact on their daily lives, they admitted limited awareness of the extent to which IBS affected their patients’ daily living.⁷

A 2013 survey-based study in England determined that GPs understand the relationship between IBS and psychological symptoms including anxiety and stress, and posited that the majority of patients could be managed within primary care without referral for psychological interventions.⁸ Moreover, they reported that a dedicated risk assessment tool for patients with IBS would be helpful to stratify severity of disease. The study concluded that the reluctance of GPs to refer patients for evidence-based psychological treatments may prevent them from obtaining appropriate services and care.

Newer explanatory model shines light on IBS

A newer explanation that is based on 3 main hypotheses is elucidating the true nature of IBS and providing a pragmatic model for the clinical setting (FIGURE 1).⁹ According to the model, IBS entails the following 3 elements, which combined lead to the symptoms of IBS:

• Altered or abnormal peripheral regulation of gut function (including sensory and secretory mechanisms)
• Altered brain-gut signaling (including visceral hypersensitivity)
• Psychological distress.

It is reasonable to consider that epigenetic changes may underlie the etiology and pathophysiology of IBS and could increase one’s susceptibility to developing the disorder. Additionally, it is presumed that IBS shares common pathophysiologic mechanisms, including visceral hypersensitivity, with other associated functional syndromes, such as functional dyspepsia.

New criteria make diagnosis on symptoms alone easier

In addition to a new explanatory model, clear criteria for diagnosing the disorder now exist, which should make it easier for PCPs to make the diagnosis without additional testing or referral. The 2016 Rome IV criteria³ provide guidelines for diagnosing the various subtypes of IBS including IBS-D (diarrhea predominant), IBS-C (constipation predominant), and IBS-M (mixed subtypes). A laboratory evaluation is really only needed for patients who fall outside the criteria or who have alarm symptoms, which include:

• age >50 years at onset of symptoms,

• new onset of constipation in the elderly,

• rectal bleeding,
• unexplained weight loss or anemia,
• family history of organic GI disease, and
• a palpable abdominal or rectal mass.

These symptoms should prompt referral to a gastroenterologist. Once alarm symptoms have been excluded, the diagnosis of IBS is based upon the presence of characteristic symptoms and changes in stool habits (FIGURE 2^3,10).

Patterns of migration. Over time, patients may migrate between subtypes, most commonly from IBS-C or IBS-D to IBS-M; switching between IBS-C and IBS-D occurs less commonly.¹¹ Patients who meet criteria for IBS but whose bowel habits and symptoms cannot be grouped into any of these 3 categories are considered to have IBS unclassified. The Bristol Stool Form Scale (available at: https://www.niddk.nih.gov/health-information/health-communication-programs/bowel-control-awareness-campaign/Documents/Bristol_Stool_Form_Scale_508.pdf) should be used to gauge and track stool consistency.

A novel diagnostic test for IBS has been validated for differentiating patients with IBS-D from those with inflammatory bowel disease (IBD).¹² The test focused on the beliefs that cytolethal distending toxin B (CdtB) is produced by bacteria that cause acute viral gastroenteritis (eg, norovirus, rotavirus), and that host antibodies to CdtB cross-react with the protein vinculin in the host gut, producing an “IBS-like phenotype.”

Additional treatment options for diarrhea-predominant IBS include antidepressants (tricyclics or SSRIs) and antispasmodics, such as dicyclomine and hyoscyamine.In a 2015 large-scale multicenter trial, both anti-CdtB and anti-vinculin antibodies were found to be significantly elevated in subjects with IBS-D compared to non-IBS subjects,¹² providing evidence to support the long-held belief that viral gastroenteritis is often at the root of IBS.

Treatment aims to decrease symptoms and improve QOL

Treatment of IBS is directed at decreasing symptoms of abdominal pain and discomfort, bloating, diarrhea, and constipation while improving QOL. Therapeutic options for treatment of each symptom are listed in FIGURE 3,^13,14 including several that are commonly used and have moderate efficacy, but are not currently approved by the US Food and Drug Administration for this purpose.

Current evidence-based pharmacologic guidelines from the American Gastroenterological Association (AGA) can be found at: https://www.guideline.gov/summaries/summary/49122?osrc=12. Figure 3^13,14 provides a few additional options not included in the AGA guidelines and presents the information in a simple schematic.

Pharmacologic therapies for IBS-D

Eluxadoline is a novel mixed mu opioid receptor agonist and delta opioid receptor antagonist developed for the treatment of IBS-D. It normalizes GI transit and defecation under conditions of environmental stress or post-inflammatory altered GI function.¹⁵ A 2016 study involving almost 2500 patients found that eluxadoline was significantly better than placebo at decreasing abdominal pain and improving stool consistency on the same day for at least half of a 26-week period.¹³ The most common adverse effects were nausea, constipation, and abdominal pain. Pancreatitis occurred rarely.

Rifaximin. Because GI flora play a central role in the pathophysiology of IBS, researchers have found that rifaximin, a minimally absorbed antibiotic, is a potentially important player in treatment. Two double-blind, placebo-controlled trials (TARGET 1 and TARGET 2) found that after 4 weeks of treatment, patients experienced significant improvement in global IBS symptoms including bloating, abdominal pain, and stool consistency on rifaximin vs placebo (40.7% vs 31.7%; P<.001 in the 2 studies combined).¹⁶ The incidence of adverse effects (headache, upper respiratory infection, nausea, abdominal pain, diarrhea, and urinary tract infection) was comparable to that with placebo.

Alosetron. Research has shown this selective 5-HT3 receptor antagonist to improve all IBS QOL measures, restriction of daily activities, and patient satisfaction significantly more than placebo in women.¹⁷ While initial use of alosetron in 2000 was widespread, the rare serious adverse event of ischemic colitis led to its withdrawal from the US market within a few months.¹⁸ Alosetron returned to the market in 2002 with restricted marketing (to treat only women with severe diarrhea-predominant IBS). (See Lotronex [alosetron hydrochloride] full prescribing information available at: https://lotronex.com/hcp/index.html.) Data from a 9-year risk management program subsequently found a cumulative incidence rate for ischemic colitis of 1.03 cases per 1000 patient/years.¹⁹

Current evidence suggests that targeted carbohydrate and gluten exclusion plays a role in the treatment and symptomatic improvement of patients with IBS.Other possible options include various antidepressants (tricyclics such as amitriptyline, imipramine, and nortriptyline; or selective serotonin reuptake inhibitors [SSRIs] such as citalopram, fluoxetine, and paroxetine) and antispasmodics such as dicyclomine and hyoscyamine.

Pharmacologic therapies for IBS-C

Linaclotide is a guanylate cyclase-C agonist with an indication for treatment of IBS-C. A double-blind, parallel-group, placebo-controlled trial found that the percentage of patients who experienced a decrease in abdominal pain was nearly 25%, with statistically significant improvements in bloating, straining, and stool consistency over a 26-week period.²⁰ In a report on 2 phase 3 trials, researchers found that linaclotide improved global symptom scores and significantly decreased abdominal bloating and fullness, pain, cramping, and discomfort vs placebo. Diarrhea was the most commonly reported adverse event in patients with severe abdominal symptoms (18.8%-21%).²¹

Lubiprostone is a prostaglandin E1 analogue that activates type-2-chloride channels on the apical membrane of epithelial cells in the intestine. In a combined analysis of 2 phase 3 randomized trials, lubiprostone was administered twice daily for 12 weeks vs placebo and patients were asked to describe how they felt after the trial period. Survey responders reported significant improvements in global IBS-C symptoms (17.9% vs 10.1%; P=.001).²² A meta-analysis of studies on lubiprostone found that diarrhea, nausea, and abdominal pain were the most common adverse effects, but their occurrence was not that much greater than with placebo.²³

Diet and probiotics can play a significant role

The role of dietary components in the treatment of IBS is gaining increasing attention. Such components can have a direct effect on gastric and intestinal motility, visceral sensation, immune activation, brain-gut interactions, and the microbiome. Current evidence suggests that targeted carbohydrate and gluten exclusion plays a favorable role in the treatment and symptomatic improvement of patients with IBS.²⁴

A 2014 study conducted in Australia showed that a diet low in FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), which is characterized by avoiding foods containing gluten and those that are high in fructose, reduced overall GI symptom scores (including scores involving abdominal bloating, pain, and flatus) in patients with IBS compared to those consuming a normal Australian diet.²⁵ The International Foundation for Functional Gastrointestinal Disorders’ Web site provides a detailed guide to low FODMAP foods and can be found at: http://www.aboutibs.org/low-fodmap-diet.html.

Probiotics are now commonly used in the symptomatic treatment of many upper and lower GI disorders. While much anecdotal evidence exists to support their benefit, there is a paucity of large-scale and rigorous research to provide substantial outcomes-based evidence. The theory for their use is that they support regulation of the gut microbiome, which in turn improves the imbalance between the intestinal microbiome and a dysfunctional intestinal barrier.

Probiotics are now used in the symptomatic treatment of many upper and lower GI disorders.A 2014 randomized, double-blind, placebo-controlled trial involving multispecies probiotics (a mixture of Bifidobacterium longum, B. bifidum, B. lactis, Lactobacillus acidophilus, L. rhamnosus, and Streptococcus thermophilus) found that patients who received probiotics had significantly reduced symptoms of IBS after 4 weeks compared with placebo, and modest improvement in abdominal pain and discomfort as well as bloating.²⁶ One study involving 122 patients from 2011 found that B. bifidum MIMBb75 reduced the global assessment of IBS symptoms by -88 points (95% CI, -1.07 to -0.69) when compared with only -0.16 (95% CI, -.32 to 0.00) points in the placebo group (P<.0001).²⁷ MIMBb75 also significantly improved the IBS symptoms of pain/discomfort, distension/bloating, urgency, and digestive disorder. And one randomized, double-blind, placebo-controlled study involving 67 patients found that QOL scores improved two-fold when patients took Saccharomyces boulardii (15.4% vs 7.0%; P<.05).²⁸

Dried plums or prunes have been used successfully for decades for the symptomatic treatment of constipation. A single-blinded, randomized, cross-over study compared prunes 50 g/d to psyllium fiber 11 g/d and found that prunes were more efficacious (P<.05) with spontaneous bowel movements and stool consistency scores.²⁹

Peppermint oil has been studied as an alternative therapy for symptoms of IBS, but efficacy and tolerability are concerns. A meta-analysis of randomized controlled trials with a minimum duration of 2 weeks found that compared with placebo, peppermint oil provided improvement in abdominal pain, bloating, and global symptoms, but some patients reported transient heartburn.³⁰ A 4-week, randomized, double-blind, placebo-controlled clinical trial sponsored by IM HealthScience found a novel oral formulation of triple-enteric-coated sustained-release peppermint oil microspheres caused less heartburn than was reported in the previous study, but still significantly improved abdominal symptoms and lessened pain on defecation and fecal urgency.³¹

CASE › Suspecting IBS-D, the FP ordered a complete blood count, tissue transglutaminase antibodies, and a stool culture, all of which were unremarkable. Ms. S has been trying to follow a low FODMAP diet and has been taking some over-the-counter probiotics with only minimal relief of abdominal bloating and cramping and no improvement in stool consistency. Her FP started her on eluxadoline 100 mg twice daily with food. After 12 weeks of therapy, she reports significant improvement in global IBS symptoms and nearly complete resolution of her diarrhea.

*Amber S is a real patient in my practice. Her name has been changed to protect her identity.

CORRESPONDENCE
Joel J. Heidelbaugh, MD, FAAFP, FACG, Ypsilanti Health Center, 200 Arnet Suite 200, Ypsilanti, MI 48198; [email protected].

CASE › Amber S,* a 33-year-old woman who works on the production line at a bread factory, sought care at my health center with a several month history of non-bloody diarrhea that was increasing in frequency and urgency and was accompanied by painful abdominal bloating and cramping. She said that these symptoms were negatively impacting her interpersonal relationships, as well as her productivity at work. She reported that “almost everything” she ate upset her stomach and “goes right through her,” including fruits, vegetables, and meat, as well as greasy fast food. She had researched her symptoms on the Internet and was worried that she might have something serious like inflammatory bowel disease or cancer.

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder (FGID) that negatively impacts the quality of life (QOL) of millions of people worldwide.¹ In fact, one study of 179 people with IBS found that 76% of survey respondents reported some degree of IBS-related impairment in at least 5 domains of daily life: daily activities, comorbid psychiatric diagnoses, symptom severity, QOL, and symptom-specific cognitive affective factors related to IBS.²

Estimating prevalence and incidence is a formidable challenge given various diagnostic criteria, the influence of population selection, inclusion or exclusion of non-GI comorbidities, and various cultural influences.³ That said, it’s estimated that IBS impacts approximately 11% of the world’s population, and approximately 30% of these individuals seek treatment.^1,4 While there are no significant differences in GI symptoms between those who consult physicians and those who do not, those who do seek treatment report higher pain scores, greater levels of anxiety, and a greater reduction in QOL.⁵

All ages affected. IBS has been reported in patients of all ages, including children and the elderly, with no definable difference reported in the frequency of subtypes (diarrhea- or constipation-predominant).

This article reviews the latest explanations, diagnostic criteria, and treatment guidelines for this challenging condition so that you can offer your patients confident care without needless testing or referral.

[polldaddy:9755564]

A lack of consensus among practicing physicians

Historically, IBS has been regarded by many primary care physicians (PCPs) as a diagnosis of exclusion. Lab tests would be ordered, nothing significant would be found, and the patient would be referred to the gastroenterologist for a definitive diagnosis.

Perceptions and misconceptions about IBS continue to abound to this day. Many are neither completely right nor wrong partly because so many triggers for IBS exist and partly because of the heretofore lack of simple, standardized criteria to diagnose the condition. Other factors contributing to the confusion are that the diagnosis of IBS is purely symptom-based and that proposals of its pathophysiology have traditionally been complex.

It is presumed that IBS shares common pathophysiologic mechanisms—including visceral hypersensitivity—with syndromes like functional dyspepsia.For example, a 2006 survey-based study of PCPs and gastroenterologists found that PCPs were less likely than gastroenterologists to believe that IBS was related to prior physical or sexual abuse, previous infection, or learned behavior, but were more likely to associate dietary factors or a linkable genetic etiology with IBS.⁶ Both sets of beliefs, however, may be considered correct.

Similarly, a 2009 qualitative study conducted in the Netherlands found that general practitioners (GPs) considered smoking, caffeine, diet, “hasty lifestyle,” and lack of exercise as potential triggers for IBS symptoms, while PCPs in the United Kingdom considered diet, infection, and travel to be possible triggers.⁷ Again, all play a role.

While GPs reported that patients should take responsibility for managing their IBS and for minimizing its impact on their daily lives, they admitted limited awareness of the extent to which IBS affected their patients’ daily living.⁷

A 2013 survey-based study in England determined that GPs understand the relationship between IBS and psychological symptoms including anxiety and stress, and posited that the majority of patients could be managed within primary care without referral for psychological interventions.⁸ Moreover, they reported that a dedicated risk assessment tool for patients with IBS would be helpful to stratify severity of disease. The study concluded that the reluctance of GPs to refer patients for evidence-based psychological treatments may prevent them from obtaining appropriate services and care.

Newer explanatory model shines light on IBS

A newer explanation that is based on 3 main hypotheses is elucidating the true nature of IBS and providing a pragmatic model for the clinical setting (FIGURE 1).⁹ According to the model, IBS entails the following 3 elements, which combined lead to the symptoms of IBS:

• Altered or abnormal peripheral regulation of gut function (including sensory and secretory mechanisms)
• Altered brain-gut signaling (including visceral hypersensitivity)
• Psychological distress.

It is reasonable to consider that epigenetic changes may underlie the etiology and pathophysiology of IBS and could increase one’s susceptibility to developing the disorder. Additionally, it is presumed that IBS shares common pathophysiologic mechanisms, including visceral hypersensitivity, with other associated functional syndromes, such as functional dyspepsia.

New criteria make diagnosis on symptoms alone easier

In addition to a new explanatory model, clear criteria for diagnosing the disorder now exist, which should make it easier for PCPs to make the diagnosis without additional testing or referral. The 2016 Rome IV criteria³ provide guidelines for diagnosing the various subtypes of IBS including IBS-D (diarrhea predominant), IBS-C (constipation predominant), and IBS-M (mixed subtypes). A laboratory evaluation is really only needed for patients who fall outside the criteria or who have alarm symptoms, which include:

• age >50 years at onset of symptoms,

• new onset of constipation in the elderly,

• rectal bleeding,
• unexplained weight loss or anemia,
• family history of organic GI disease, and
• a palpable abdominal or rectal mass.

These symptoms should prompt referral to a gastroenterologist. Once alarm symptoms have been excluded, the diagnosis of IBS is based upon the presence of characteristic symptoms and changes in stool habits (FIGURE 2^3,10).

Patterns of migration. Over time, patients may migrate between subtypes, most commonly from IBS-C or IBS-D to IBS-M; switching between IBS-C and IBS-D occurs less commonly.¹¹ Patients who meet criteria for IBS but whose bowel habits and symptoms cannot be grouped into any of these 3 categories are considered to have IBS unclassified. The Bristol Stool Form Scale (available at: https://www.niddk.nih.gov/health-information/health-communication-programs/bowel-control-awareness-campaign/Documents/Bristol_Stool_Form_Scale_508.pdf) should be used to gauge and track stool consistency.

A novel diagnostic test for IBS has been validated for differentiating patients with IBS-D from those with inflammatory bowel disease (IBD).¹² The test focused on the beliefs that cytolethal distending toxin B (CdtB) is produced by bacteria that cause acute viral gastroenteritis (eg, norovirus, rotavirus), and that host antibodies to CdtB cross-react with the protein vinculin in the host gut, producing an “IBS-like phenotype.”

Additional treatment options for diarrhea-predominant IBS include antidepressants (tricyclics or SSRIs) and antispasmodics, such as dicyclomine and hyoscyamine.In a 2015 large-scale multicenter trial, both anti-CdtB and anti-vinculin antibodies were found to be significantly elevated in subjects with IBS-D compared to non-IBS subjects,¹² providing evidence to support the long-held belief that viral gastroenteritis is often at the root of IBS.

Treatment aims to decrease symptoms and improve QOL

Treatment of IBS is directed at decreasing symptoms of abdominal pain and discomfort, bloating, diarrhea, and constipation while improving QOL. Therapeutic options for treatment of each symptom are listed in FIGURE 3,^13,14 including several that are commonly used and have moderate efficacy, but are not currently approved by the US Food and Drug Administration for this purpose.

Current evidence-based pharmacologic guidelines from the American Gastroenterological Association (AGA) can be found at: https://www.guideline.gov/summaries/summary/49122?osrc=12. Figure 3^13,14 provides a few additional options not included in the AGA guidelines and presents the information in a simple schematic.

Pharmacologic therapies for IBS-D

Eluxadoline is a novel mixed mu opioid receptor agonist and delta opioid receptor antagonist developed for the treatment of IBS-D. It normalizes GI transit and defecation under conditions of environmental stress or post-inflammatory altered GI function.¹⁵ A 2016 study involving almost 2500 patients found that eluxadoline was significantly better than placebo at decreasing abdominal pain and improving stool consistency on the same day for at least half of a 26-week period.¹³ The most common adverse effects were nausea, constipation, and abdominal pain. Pancreatitis occurred rarely.

Rifaximin. Because GI flora play a central role in the pathophysiology of IBS, researchers have found that rifaximin, a minimally absorbed antibiotic, is a potentially important player in treatment. Two double-blind, placebo-controlled trials (TARGET 1 and TARGET 2) found that after 4 weeks of treatment, patients experienced significant improvement in global IBS symptoms including bloating, abdominal pain, and stool consistency on rifaximin vs placebo (40.7% vs 31.7%; P<.001 in the 2 studies combined).¹⁶ The incidence of adverse effects (headache, upper respiratory infection, nausea, abdominal pain, diarrhea, and urinary tract infection) was comparable to that with placebo.

Alosetron. Research has shown this selective 5-HT3 receptor antagonist to improve all IBS QOL measures, restriction of daily activities, and patient satisfaction significantly more than placebo in women.¹⁷ While initial use of alosetron in 2000 was widespread, the rare serious adverse event of ischemic colitis led to its withdrawal from the US market within a few months.¹⁸ Alosetron returned to the market in 2002 with restricted marketing (to treat only women with severe diarrhea-predominant IBS). (See Lotronex [alosetron hydrochloride] full prescribing information available at: https://lotronex.com/hcp/index.html.) Data from a 9-year risk management program subsequently found a cumulative incidence rate for ischemic colitis of 1.03 cases per 1000 patient/years.¹⁹

Current evidence suggests that targeted carbohydrate and gluten exclusion plays a role in the treatment and symptomatic improvement of patients with IBS.Other possible options include various antidepressants (tricyclics such as amitriptyline, imipramine, and nortriptyline; or selective serotonin reuptake inhibitors [SSRIs] such as citalopram, fluoxetine, and paroxetine) and antispasmodics such as dicyclomine and hyoscyamine.

Pharmacologic therapies for IBS-C

Linaclotide is a guanylate cyclase-C agonist with an indication for treatment of IBS-C. A double-blind, parallel-group, placebo-controlled trial found that the percentage of patients who experienced a decrease in abdominal pain was nearly 25%, with statistically significant improvements in bloating, straining, and stool consistency over a 26-week period.²⁰ In a report on 2 phase 3 trials, researchers found that linaclotide improved global symptom scores and significantly decreased abdominal bloating and fullness, pain, cramping, and discomfort vs placebo. Diarrhea was the most commonly reported adverse event in patients with severe abdominal symptoms (18.8%-21%).²¹

Lubiprostone is a prostaglandin E1 analogue that activates type-2-chloride channels on the apical membrane of epithelial cells in the intestine. In a combined analysis of 2 phase 3 randomized trials, lubiprostone was administered twice daily for 12 weeks vs placebo and patients were asked to describe how they felt after the trial period. Survey responders reported significant improvements in global IBS-C symptoms (17.9% vs 10.1%; P=.001).²² A meta-analysis of studies on lubiprostone found that diarrhea, nausea, and abdominal pain were the most common adverse effects, but their occurrence was not that much greater than with placebo.²³

Diet and probiotics can play a significant role

The role of dietary components in the treatment of IBS is gaining increasing attention. Such components can have a direct effect on gastric and intestinal motility, visceral sensation, immune activation, brain-gut interactions, and the microbiome. Current evidence suggests that targeted carbohydrate and gluten exclusion plays a favorable role in the treatment and symptomatic improvement of patients with IBS.²⁴

A 2014 study conducted in Australia showed that a diet low in FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), which is characterized by avoiding foods containing gluten and those that are high in fructose, reduced overall GI symptom scores (including scores involving abdominal bloating, pain, and flatus) in patients with IBS compared to those consuming a normal Australian diet.²⁵ The International Foundation for Functional Gastrointestinal Disorders’ Web site provides a detailed guide to low FODMAP foods and can be found at: http://www.aboutibs.org/low-fodmap-diet.html.

Probiotics are now commonly used in the symptomatic treatment of many upper and lower GI disorders. While much anecdotal evidence exists to support their benefit, there is a paucity of large-scale and rigorous research to provide substantial outcomes-based evidence. The theory for their use is that they support regulation of the gut microbiome, which in turn improves the imbalance between the intestinal microbiome and a dysfunctional intestinal barrier.

Probiotics are now used in the symptomatic treatment of many upper and lower GI disorders.A 2014 randomized, double-blind, placebo-controlled trial involving multispecies probiotics (a mixture of Bifidobacterium longum, B. bifidum, B. lactis, Lactobacillus acidophilus, L. rhamnosus, and Streptococcus thermophilus) found that patients who received probiotics had significantly reduced symptoms of IBS after 4 weeks compared with placebo, and modest improvement in abdominal pain and discomfort as well as bloating.²⁶ One study involving 122 patients from 2011 found that B. bifidum MIMBb75 reduced the global assessment of IBS symptoms by -88 points (95% CI, -1.07 to -0.69) when compared with only -0.16 (95% CI, -.32 to 0.00) points in the placebo group (P<.0001).²⁷ MIMBb75 also significantly improved the IBS symptoms of pain/discomfort, distension/bloating, urgency, and digestive disorder. And one randomized, double-blind, placebo-controlled study involving 67 patients found that QOL scores improved two-fold when patients took Saccharomyces boulardii (15.4% vs 7.0%; P<.05).²⁸

Dried plums or prunes have been used successfully for decades for the symptomatic treatment of constipation. A single-blinded, randomized, cross-over study compared prunes 50 g/d to psyllium fiber 11 g/d and found that prunes were more efficacious (P<.05) with spontaneous bowel movements and stool consistency scores.²⁹

Peppermint oil has been studied as an alternative therapy for symptoms of IBS, but efficacy and tolerability are concerns. A meta-analysis of randomized controlled trials with a minimum duration of 2 weeks found that compared with placebo, peppermint oil provided improvement in abdominal pain, bloating, and global symptoms, but some patients reported transient heartburn.³⁰ A 4-week, randomized, double-blind, placebo-controlled clinical trial sponsored by IM HealthScience found a novel oral formulation of triple-enteric-coated sustained-release peppermint oil microspheres caused less heartburn than was reported in the previous study, but still significantly improved abdominal symptoms and lessened pain on defecation and fecal urgency.³¹

CASE › Suspecting IBS-D, the FP ordered a complete blood count, tissue transglutaminase antibodies, and a stool culture, all of which were unremarkable. Ms. S has been trying to follow a low FODMAP diet and has been taking some over-the-counter probiotics with only minimal relief of abdominal bloating and cramping and no improvement in stool consistency. Her FP started her on eluxadoline 100 mg twice daily with food. After 12 weeks of therapy, she reports significant improvement in global IBS symptoms and nearly complete resolution of her diarrhea.

*Amber S is a real patient in my practice. Her name has been changed to protect her identity.

CORRESPONDENCE
Joel J. Heidelbaugh, MD, FAAFP, FACG, Ypsilanti Health Center, 200 Arnet Suite 200, Ypsilanti, MI 48198; [email protected].

It’s a whole new biosimilar world. In the April 2012 issue of GI & Hepatology News (GIHN) there was a small article on the issued Food and Drug Administration guidance on how to develop biosimilars. A biosimilar molecule must be structurally similar to the reference or originator product with the expectation that the safety and efficacy will be the same. The European Medicines Agency (EMA) established a legal framework for approving biologics in the European Union in 2003 and guidelines for approval in 2005 to 2006 with the first biosimilar approved in 2006 (somatropin [Omnitrope]).

The first monoclonal antibody biosimilar approved by the EMA was CT-P13 (infliximab-dyyb) in June 2013. There are now over 23 biosimilars approved for use in Europe. In 2012 there were no biosimilars on the market in the United States. This past year (2016) has been the year of the biosimilar with two of the four approved compounds used in inflammatory bowel disease – Inflectra (infliximab-dyyb, Hospira) April 2016 and Amjevita (adalimumab-atto, Amgen) September 2016 appearing.

Kim L. Isaacs, MD, PhD, is professor of medicine in the division of gastroenterology and hepatology at the University of North Carolina at Chapel Hill. She is codirector of the UNC Center for Inflammatory Bowel Disease. She is an Associate Editor for GI and Hepatology News.

It’s a whole new biosimilar world. In the April 2012 issue of GI & Hepatology News (GIHN) there was a small article on the issued Food and Drug Administration guidance on how to develop biosimilars. A biosimilar molecule must be structurally similar to the reference or originator product with the expectation that the safety and efficacy will be the same. The European Medicines Agency (EMA) established a legal framework for approving biologics in the European Union in 2003 and guidelines for approval in 2005 to 2006 with the first biosimilar approved in 2006 (somatropin [Omnitrope]).

The first monoclonal antibody biosimilar approved by the EMA was CT-P13 (infliximab-dyyb) in June 2013. There are now over 23 biosimilars approved for use in Europe. In 2012 there were no biosimilars on the market in the United States. This past year (2016) has been the year of the biosimilar with two of the four approved compounds used in inflammatory bowel disease – Inflectra (infliximab-dyyb, Hospira) April 2016 and Amjevita (adalimumab-atto, Amgen) September 2016 appearing.

Kim L. Isaacs, MD, PhD, is professor of medicine in the division of gastroenterology and hepatology at the University of North Carolina at Chapel Hill. She is codirector of the UNC Center for Inflammatory Bowel Disease. She is an Associate Editor for GI and Hepatology News.

It’s a whole new biosimilar world. In the April 2012 issue of GI & Hepatology News (GIHN) there was a small article on the issued Food and Drug Administration guidance on how to develop biosimilars. A biosimilar molecule must be structurally similar to the reference or originator product with the expectation that the safety and efficacy will be the same. The European Medicines Agency (EMA) established a legal framework for approving biologics in the European Union in 2003 and guidelines for approval in 2005 to 2006 with the first biosimilar approved in 2006 (somatropin [Omnitrope]).

The first monoclonal antibody biosimilar approved by the EMA was CT-P13 (infliximab-dyyb) in June 2013. There are now over 23 biosimilars approved for use in Europe. In 2012 there were no biosimilars on the market in the United States. This past year (2016) has been the year of the biosimilar with two of the four approved compounds used in inflammatory bowel disease – Inflectra (infliximab-dyyb, Hospira) April 2016 and Amjevita (adalimumab-atto, Amgen) September 2016 appearing.

Kim L. Isaacs, MD, PhD, is professor of medicine in the division of gastroenterology and hepatology at the University of North Carolina at Chapel Hill. She is codirector of the UNC Center for Inflammatory Bowel Disease. She is an Associate Editor for GI and Hepatology News.

What led you to pursue a career in medical education?

Believe it or not, I pursued my path in medical education even prior to attending medical school. I was a high school teacher with a master’s in education, working during the summer of 1979 under the auspices of the Student Conservation Association at Grand Canyon National Park. Sitting on the edge of the canyon at sunset, I made the momentous decision to attend medical school, requiring attendance at a postbaccalaureate program at Columbia University. While considering medical schools, I knew that I wanted to combine my interest in education with medicine and I therefore chose to attend Case Western University School of Medicine. Since the mid-1950s, Case had been committed to innovative educational programs with a systems-based approach to the curriculum.

What do you enjoy most about working in medical education?

There are so many aspects of medical education that make work fun and rewarding. Perhaps the most rewarding is the ability to make a difference that affects the learner as well as the patients and communities that they will serve. I also enjoy the diverse experiences and opportunities in education and the ability to work with others in creative endeavors.

What are your responsibilities in a typical week?

One of the great things about a focus in education is that there never is a typical week. In the 32 years since my graduation from medical school, I have had the great fortune to fill many different roles: course director, electives director, fellowship program director, associate dean for student affairs, associate dean for undergraduate medical education, and associate dean for continuing medical education. For the past 6 years, I have been the senior associate dean for education at the University of Connecticut School of Medicine, overseeing undergraduate medical education, graduate medical education, continuing medical education, and the graduate school.

Over time I have had less interaction with students and residents as my administrative responsibilities have grown, but I know it is critical to maintain a presence with learners and I endeavor to do so in limited ways. Since our current priorities are in implementing a new curriculum and in planning for an accreditation visit, there are many days that are filled with meetings, planning, organizing, and writing. To me, the most precious responsibility is shaping a vision and bringing together a team to operationalize that vision in a collaborative and creative way, with learners, teachers, and administrators working together.
 

What are the different career options available for early-career GIs who are interested in medical education?

There are so many options in medical education for early-career gastroenterologists. For those working in private, group, or community practices, there are opportunities to precept students, residents, and fellows. For those working in an academic setting, opportunities abound. It is often a good idea to start within the division: get involved in teaching fellows in a clinical setting, or creating a new simulation experience or case workshop for fellows. There are opportunities to teach and supervise students. One of my first opportunities was in teaching in the physical diagnosis course. There are options to be involved in curriculum committees, admissions, CME, and to engage in educational initiatives at your institution.

The Association of American Medical Colleges has defined five areas of scholarship in education, and it is possible to get promoted to full professor – and even to attain academic tenure, as I have – if you fulfill the requirements for promotion at your institution. These areas include teaching, curriculum development, assessment, mentorship/advising, and leadership. There are also many ways to get involved in the AGA (http://www.gastro.org/trainees) and other organizations.^1,2

Are there advanced training options available for those interested in medical education?

The AGA Academy of Educators (http://www.gastro.org/about/initiatives/aga-academy-of-educators)³ is a wonderful resource for networking. It has a competitive process for educational project grants as well as faculty development sessions and networking events at DDW^®. There are also national leadership academies in medicine that have a focus in medical education. The Harvard Macy Institute is one such opportunity. Many medical schools have their own academies to support educators and teachers. I have been privileged to be one of the co-leaders of the AGA Future Leaders Program (http://www.gastro.org/about/initiatives/aga-future-leaders-program) and those with a niche interest in education can benefit and pursue related projects.⁴ One group was successful in publishing an educational article after completing the Future Leaders program.⁵ There are also several master’s programs for further education and training in educational theory. Some of these programs are available online or largely online, with limited requirements for onsite classes.

How do you go about finding a job in medical education?

First of all, you have to do your “day job.” In order to be a credible medical clinician-educator you must have clinical experience in patient care. It is important for the first years of your career to make sure that you have at least 70% clinical roles that can be reduced over time to accommodate advancing educational responsibilities. Get involved in teaching fellows. If you are in a practice, reach out to your local medical school or hospital to see how you might participate in educational programs. If you are in an academic setting, meet with the deans in education to express your interest and look for opportunities to get involved in an area of interest. If you are in academia, you have to make your work “count twice:” being productive in a scholarly way is not only important as a role model for learners, but it is important for you as a faculty member to grow and advance in your professional career.

It is always wise to think about when to say “yes” and when to say “no.” An important point is not to overextend yourself. Your reputation of completing tasks not only well, but on time, and thoroughly, is critical to your success. This includes making sure your learner evaluations are submitted on time, that you complete the administrative work in order to participate in CME programs, and that you honor your commitments by attending committee meetings.
 

What are the resources available to early-career GIs interested in medical education?

It is easy to find resources within your practice, your institution, or externally. The AGA has many resources available with a good start being the AGA Academy of Educators. Opportunities for creativity are numerous and with new advances in team-based learning, simulation, and interprofessional learning, there are new areas for involvement evolving all the time.^6,7

Finally, pursuing a career in education is exciting, fun, and fulfilling. Having the opportunity to influence learners, which in turn will impact patient care, is an awesome privilege.
 

Dr. Rose is a professor of medicine and senior associate dean for education at the University of Connecticut School of Medicine.

References

1. Gusic M, et al. MedEdPORTAL; 2013. Available from: http://www.mededportal.org/publication/9313.

2. Gusic ME, et al. Acad Med. 2014;89(7):1006-11.

3. Pfeil SA, et al. Gastroenterology 2015;149(6):1309-14.

4. Cryer B, Rose S. Gastroenterology 2015;149:246-8.

5. Shah BJ, et al. Gastroenterology 2016;151(2):218-21.

6. Shah BJ, Rose S. Gastroenterology 2012;142:684-9.

7. Shah BJ, Rose S. AGA Perspectives 2012;April-May:20-21.
 

What led you to pursue a career in medical education?

Believe it or not, I pursued my path in medical education even prior to attending medical school. I was a high school teacher with a master’s in education, working during the summer of 1979 under the auspices of the Student Conservation Association at Grand Canyon National Park. Sitting on the edge of the canyon at sunset, I made the momentous decision to attend medical school, requiring attendance at a postbaccalaureate program at Columbia University. While considering medical schools, I knew that I wanted to combine my interest in education with medicine and I therefore chose to attend Case Western University School of Medicine. Since the mid-1950s, Case had been committed to innovative educational programs with a systems-based approach to the curriculum.

What do you enjoy most about working in medical education?

There are so many aspects of medical education that make work fun and rewarding. Perhaps the most rewarding is the ability to make a difference that affects the learner as well as the patients and communities that they will serve. I also enjoy the diverse experiences and opportunities in education and the ability to work with others in creative endeavors.

What are your responsibilities in a typical week?

One of the great things about a focus in education is that there never is a typical week. In the 32 years since my graduation from medical school, I have had the great fortune to fill many different roles: course director, electives director, fellowship program director, associate dean for student affairs, associate dean for undergraduate medical education, and associate dean for continuing medical education. For the past 6 years, I have been the senior associate dean for education at the University of Connecticut School of Medicine, overseeing undergraduate medical education, graduate medical education, continuing medical education, and the graduate school.

Over time I have had less interaction with students and residents as my administrative responsibilities have grown, but I know it is critical to maintain a presence with learners and I endeavor to do so in limited ways. Since our current priorities are in implementing a new curriculum and in planning for an accreditation visit, there are many days that are filled with meetings, planning, organizing, and writing. To me, the most precious responsibility is shaping a vision and bringing together a team to operationalize that vision in a collaborative and creative way, with learners, teachers, and administrators working together.
 

What are the different career options available for early-career GIs who are interested in medical education?

There are so many options in medical education for early-career gastroenterologists. For those working in private, group, or community practices, there are opportunities to precept students, residents, and fellows. For those working in an academic setting, opportunities abound. It is often a good idea to start within the division: get involved in teaching fellows in a clinical setting, or creating a new simulation experience or case workshop for fellows. There are opportunities to teach and supervise students. One of my first opportunities was in teaching in the physical diagnosis course. There are options to be involved in curriculum committees, admissions, CME, and to engage in educational initiatives at your institution.

The Association of American Medical Colleges has defined five areas of scholarship in education, and it is possible to get promoted to full professor – and even to attain academic tenure, as I have – if you fulfill the requirements for promotion at your institution. These areas include teaching, curriculum development, assessment, mentorship/advising, and leadership. There are also many ways to get involved in the AGA (http://www.gastro.org/trainees) and other organizations.^1,2

Are there advanced training options available for those interested in medical education?

The AGA Academy of Educators (http://www.gastro.org/about/initiatives/aga-academy-of-educators)³ is a wonderful resource for networking. It has a competitive process for educational project grants as well as faculty development sessions and networking events at DDW^®. There are also national leadership academies in medicine that have a focus in medical education. The Harvard Macy Institute is one such opportunity. Many medical schools have their own academies to support educators and teachers. I have been privileged to be one of the co-leaders of the AGA Future Leaders Program (http://www.gastro.org/about/initiatives/aga-future-leaders-program) and those with a niche interest in education can benefit and pursue related projects.⁴ One group was successful in publishing an educational article after completing the Future Leaders program.⁵ There are also several master’s programs for further education and training in educational theory. Some of these programs are available online or largely online, with limited requirements for onsite classes.

How do you go about finding a job in medical education?

First of all, you have to do your “day job.” In order to be a credible medical clinician-educator you must have clinical experience in patient care. It is important for the first years of your career to make sure that you have at least 70% clinical roles that can be reduced over time to accommodate advancing educational responsibilities. Get involved in teaching fellows. If you are in a practice, reach out to your local medical school or hospital to see how you might participate in educational programs. If you are in an academic setting, meet with the deans in education to express your interest and look for opportunities to get involved in an area of interest. If you are in academia, you have to make your work “count twice:” being productive in a scholarly way is not only important as a role model for learners, but it is important for you as a faculty member to grow and advance in your professional career.

It is always wise to think about when to say “yes” and when to say “no.” An important point is not to overextend yourself. Your reputation of completing tasks not only well, but on time, and thoroughly, is critical to your success. This includes making sure your learner evaluations are submitted on time, that you complete the administrative work in order to participate in CME programs, and that you honor your commitments by attending committee meetings.
 

What are the resources available to early-career GIs interested in medical education?

It is easy to find resources within your practice, your institution, or externally. The AGA has many resources available with a good start being the AGA Academy of Educators. Opportunities for creativity are numerous and with new advances in team-based learning, simulation, and interprofessional learning, there are new areas for involvement evolving all the time.^6,7

Finally, pursuing a career in education is exciting, fun, and fulfilling. Having the opportunity to influence learners, which in turn will impact patient care, is an awesome privilege.
 

Dr. Rose is a professor of medicine and senior associate dean for education at the University of Connecticut School of Medicine.

References

1. Gusic M, et al. MedEdPORTAL; 2013. Available from: http://www.mededportal.org/publication/9313.

2. Gusic ME, et al. Acad Med. 2014;89(7):1006-11.

3. Pfeil SA, et al. Gastroenterology 2015;149(6):1309-14.

4. Cryer B, Rose S. Gastroenterology 2015;149:246-8.

5. Shah BJ, et al. Gastroenterology 2016;151(2):218-21.

6. Shah BJ, Rose S. Gastroenterology 2012;142:684-9.

7. Shah BJ, Rose S. AGA Perspectives 2012;April-May:20-21.
 

What led you to pursue a career in medical education?

Believe it or not, I pursued my path in medical education even prior to attending medical school. I was a high school teacher with a master’s in education, working during the summer of 1979 under the auspices of the Student Conservation Association at Grand Canyon National Park. Sitting on the edge of the canyon at sunset, I made the momentous decision to attend medical school, requiring attendance at a postbaccalaureate program at Columbia University. While considering medical schools, I knew that I wanted to combine my interest in education with medicine and I therefore chose to attend Case Western University School of Medicine. Since the mid-1950s, Case had been committed to innovative educational programs with a systems-based approach to the curriculum.

What do you enjoy most about working in medical education?

There are so many aspects of medical education that make work fun and rewarding. Perhaps the most rewarding is the ability to make a difference that affects the learner as well as the patients and communities that they will serve. I also enjoy the diverse experiences and opportunities in education and the ability to work with others in creative endeavors.

What are your responsibilities in a typical week?

One of the great things about a focus in education is that there never is a typical week. In the 32 years since my graduation from medical school, I have had the great fortune to fill many different roles: course director, electives director, fellowship program director, associate dean for student affairs, associate dean for undergraduate medical education, and associate dean for continuing medical education. For the past 6 years, I have been the senior associate dean for education at the University of Connecticut School of Medicine, overseeing undergraduate medical education, graduate medical education, continuing medical education, and the graduate school.

Over time I have had less interaction with students and residents as my administrative responsibilities have grown, but I know it is critical to maintain a presence with learners and I endeavor to do so in limited ways. Since our current priorities are in implementing a new curriculum and in planning for an accreditation visit, there are many days that are filled with meetings, planning, organizing, and writing. To me, the most precious responsibility is shaping a vision and bringing together a team to operationalize that vision in a collaborative and creative way, with learners, teachers, and administrators working together.
 

What are the different career options available for early-career GIs who are interested in medical education?

There are so many options in medical education for early-career gastroenterologists. For those working in private, group, or community practices, there are opportunities to precept students, residents, and fellows. For those working in an academic setting, opportunities abound. It is often a good idea to start within the division: get involved in teaching fellows in a clinical setting, or creating a new simulation experience or case workshop for fellows. There are opportunities to teach and supervise students. One of my first opportunities was in teaching in the physical diagnosis course. There are options to be involved in curriculum committees, admissions, CME, and to engage in educational initiatives at your institution.

The Association of American Medical Colleges has defined five areas of scholarship in education, and it is possible to get promoted to full professor – and even to attain academic tenure, as I have – if you fulfill the requirements for promotion at your institution. These areas include teaching, curriculum development, assessment, mentorship/advising, and leadership. There are also many ways to get involved in the AGA (http://www.gastro.org/trainees) and other organizations.^1,2

Are there advanced training options available for those interested in medical education?

The AGA Academy of Educators (http://www.gastro.org/about/initiatives/aga-academy-of-educators)³ is a wonderful resource for networking. It has a competitive process for educational project grants as well as faculty development sessions and networking events at DDW^®. There are also national leadership academies in medicine that have a focus in medical education. The Harvard Macy Institute is one such opportunity. Many medical schools have their own academies to support educators and teachers. I have been privileged to be one of the co-leaders of the AGA Future Leaders Program (http://www.gastro.org/about/initiatives/aga-future-leaders-program) and those with a niche interest in education can benefit and pursue related projects.⁴ One group was successful in publishing an educational article after completing the Future Leaders program.⁵ There are also several master’s programs for further education and training in educational theory. Some of these programs are available online or largely online, with limited requirements for onsite classes.

How do you go about finding a job in medical education?

First of all, you have to do your “day job.” In order to be a credible medical clinician-educator you must have clinical experience in patient care. It is important for the first years of your career to make sure that you have at least 70% clinical roles that can be reduced over time to accommodate advancing educational responsibilities. Get involved in teaching fellows. If you are in a practice, reach out to your local medical school or hospital to see how you might participate in educational programs. If you are in an academic setting, meet with the deans in education to express your interest and look for opportunities to get involved in an area of interest. If you are in academia, you have to make your work “count twice:” being productive in a scholarly way is not only important as a role model for learners, but it is important for you as a faculty member to grow and advance in your professional career.

It is always wise to think about when to say “yes” and when to say “no.” An important point is not to overextend yourself. Your reputation of completing tasks not only well, but on time, and thoroughly, is critical to your success. This includes making sure your learner evaluations are submitted on time, that you complete the administrative work in order to participate in CME programs, and that you honor your commitments by attending committee meetings.
 

What are the resources available to early-career GIs interested in medical education?

It is easy to find resources within your practice, your institution, or externally. The AGA has many resources available with a good start being the AGA Academy of Educators. Opportunities for creativity are numerous and with new advances in team-based learning, simulation, and interprofessional learning, there are new areas for involvement evolving all the time.^6,7

Finally, pursuing a career in education is exciting, fun, and fulfilling. Having the opportunity to influence learners, which in turn will impact patient care, is an awesome privilege.
 

Dr. Rose is a professor of medicine and senior associate dean for education at the University of Connecticut School of Medicine.

References

1. Gusic M, et al. MedEdPORTAL; 2013. Available from: http://www.mededportal.org/publication/9313.

2. Gusic ME, et al. Acad Med. 2014;89(7):1006-11.

3. Pfeil SA, et al. Gastroenterology 2015;149(6):1309-14.

4. Cryer B, Rose S. Gastroenterology 2015;149:246-8.

5. Shah BJ, et al. Gastroenterology 2016;151(2):218-21.

6. Shah BJ, Rose S. Gastroenterology 2012;142:684-9.

7. Shah BJ, Rose S. AGA Perspectives 2012;April-May:20-21.
 

An unfortunate fact for many physicians practicing in the United States is that they will contend with medical malpractice suits at some point in their careers. While data specific to gastroenterology malpractice claims is difficult to find,¹ the Physician Insurers Association of America has reported that out of the 28 specialty fields of medicine analyzed from 1985 to 2004, gastroenterology ranked 21st in the number of claims reported², representing about 2% of the total overall number of claims.

JAMA

Professional liability

Patients can allege or establish malpractice liability against a doctor based on a number of things; we will discuss a few of the most common types of liability, offer suggestions as to how you might minimize your risk of being sued, and how best to cope when you are sued.

Negligence: One of the most common theories you may be sued under is negligence. To state a negligence claim against a physician, a plaintiff must show that the doctor owed the patient a duty recognized by law, that the physician breached that duty, that the alleged breach resulted in injury to the patient, and that the patient sustained legally recognized damages as a result. In a lawsuit brought on the basis of claimed medical negligence, a patient claims that a physician, in the course of rendering treatment, failed to meet the applicable standard of care.

Contractual liability of doctor to patient: Physicians and patients can enter into express written contracts regarding the care provided. These contracts can include various treatment plans, the likelihood of success, and even the physician’s promise to cure. Traditionally, courts have respected a physician’s freedom to contract as he or she chooses. However, once a contract is formed, a plaintiff may have a cause of action for breach of contract if the outcome of the treatment is not what was promised.
 

Minimizing risk

Another opportunity to decrease your chances of being sued is to keep informed about recent developments in your field. Make a point to read pertinent literature, attend seminars, and do whatever is necessary to stay aware of, and to incorporate into your practice, current methods of treatment and diagnosis.

Physicians should also be cognizant of contractual liability. When discussing treatment, never guarantee results. Additionally, once a physician-patient relationship is established, you cannot withdraw from the relationship without providing adequate notice to the patient in time to obtain alternative care. Terminating the relationship without such is called abandonment, and can result in professional discipline and civil liability.

Conclusion

Before a lawsuit, and as a regular part of your practice, it is important that you thoroughly and legibly document all aspects of care provided, stay current with medical advances, and take the time to create a relationship with your patients involving quality communication. It is impossible for us to provide you with enough information to adequately prepare you for the day on which you may be sued. We nevertheless hope that following the aforementioned suggestions will be of some help.

References

1. Medical Malpractice Claims and Risk Management in Gastroenterology and Gastrointestinal Endoscopy. American Society for Gastrointestinal Endoscopy, 2017. <www.asge.org>.

2. Physician Insurers Association of America. PIAA Claim Trend Analysis: Gastroenterology, iv. Lawrenceville, N.J.: PIAA, 2004. <http://www.piaa.us>.

3. Kane C., Policy Research Perspective: Medical Liability Claim Frequency: 2007-2008 Snapshot of Physicians, American Medical Association, 2010.

4. Schaffer A.C., et al. JAMA Internal Med. 2017;177(5):710-8.

5. Dodge A.M. Wilsonville, Ore. Book Partners, Inc. 2001.

An unfortunate fact for many physicians practicing in the United States is that they will contend with medical malpractice suits at some point in their careers. While data specific to gastroenterology malpractice claims is difficult to find,¹ the Physician Insurers Association of America has reported that out of the 28 specialty fields of medicine analyzed from 1985 to 2004, gastroenterology ranked 21st in the number of claims reported², representing about 2% of the total overall number of claims.

JAMA

Professional liability

Patients can allege or establish malpractice liability against a doctor based on a number of things; we will discuss a few of the most common types of liability, offer suggestions as to how you might minimize your risk of being sued, and how best to cope when you are sued.

Negligence: One of the most common theories you may be sued under is negligence. To state a negligence claim against a physician, a plaintiff must show that the doctor owed the patient a duty recognized by law, that the physician breached that duty, that the alleged breach resulted in injury to the patient, and that the patient sustained legally recognized damages as a result. In a lawsuit brought on the basis of claimed medical negligence, a patient claims that a physician, in the course of rendering treatment, failed to meet the applicable standard of care.

Contractual liability of doctor to patient: Physicians and patients can enter into express written contracts regarding the care provided. These contracts can include various treatment plans, the likelihood of success, and even the physician’s promise to cure. Traditionally, courts have respected a physician’s freedom to contract as he or she chooses. However, once a contract is formed, a plaintiff may have a cause of action for breach of contract if the outcome of the treatment is not what was promised.
 

Minimizing risk

Another opportunity to decrease your chances of being sued is to keep informed about recent developments in your field. Make a point to read pertinent literature, attend seminars, and do whatever is necessary to stay aware of, and to incorporate into your practice, current methods of treatment and diagnosis.

Physicians should also be cognizant of contractual liability. When discussing treatment, never guarantee results. Additionally, once a physician-patient relationship is established, you cannot withdraw from the relationship without providing adequate notice to the patient in time to obtain alternative care. Terminating the relationship without such is called abandonment, and can result in professional discipline and civil liability.

Conclusion

Before a lawsuit, and as a regular part of your practice, it is important that you thoroughly and legibly document all aspects of care provided, stay current with medical advances, and take the time to create a relationship with your patients involving quality communication. It is impossible for us to provide you with enough information to adequately prepare you for the day on which you may be sued. We nevertheless hope that following the aforementioned suggestions will be of some help.

References

1. Medical Malpractice Claims and Risk Management in Gastroenterology and Gastrointestinal Endoscopy. American Society for Gastrointestinal Endoscopy, 2017. <www.asge.org>.

2. Physician Insurers Association of America. PIAA Claim Trend Analysis: Gastroenterology, iv. Lawrenceville, N.J.: PIAA, 2004. <http://www.piaa.us>.

3. Kane C., Policy Research Perspective: Medical Liability Claim Frequency: 2007-2008 Snapshot of Physicians, American Medical Association, 2010.

4. Schaffer A.C., et al. JAMA Internal Med. 2017;177(5):710-8.

5. Dodge A.M. Wilsonville, Ore. Book Partners, Inc. 2001.

An unfortunate fact for many physicians practicing in the United States is that they will contend with medical malpractice suits at some point in their careers. While data specific to gastroenterology malpractice claims is difficult to find,¹ the Physician Insurers Association of America has reported that out of the 28 specialty fields of medicine analyzed from 1985 to 2004, gastroenterology ranked 21st in the number of claims reported², representing about 2% of the total overall number of claims.

JAMA

Professional liability

Patients can allege or establish malpractice liability against a doctor based on a number of things; we will discuss a few of the most common types of liability, offer suggestions as to how you might minimize your risk of being sued, and how best to cope when you are sued.

Negligence: One of the most common theories you may be sued under is negligence. To state a negligence claim against a physician, a plaintiff must show that the doctor owed the patient a duty recognized by law, that the physician breached that duty, that the alleged breach resulted in injury to the patient, and that the patient sustained legally recognized damages as a result. In a lawsuit brought on the basis of claimed medical negligence, a patient claims that a physician, in the course of rendering treatment, failed to meet the applicable standard of care.

Contractual liability of doctor to patient: Physicians and patients can enter into express written contracts regarding the care provided. These contracts can include various treatment plans, the likelihood of success, and even the physician’s promise to cure. Traditionally, courts have respected a physician’s freedom to contract as he or she chooses. However, once a contract is formed, a plaintiff may have a cause of action for breach of contract if the outcome of the treatment is not what was promised.
 

Minimizing risk

Another opportunity to decrease your chances of being sued is to keep informed about recent developments in your field. Make a point to read pertinent literature, attend seminars, and do whatever is necessary to stay aware of, and to incorporate into your practice, current methods of treatment and diagnosis.

Physicians should also be cognizant of contractual liability. When discussing treatment, never guarantee results. Additionally, once a physician-patient relationship is established, you cannot withdraw from the relationship without providing adequate notice to the patient in time to obtain alternative care. Terminating the relationship without such is called abandonment, and can result in professional discipline and civil liability.

Conclusion

Before a lawsuit, and as a regular part of your practice, it is important that you thoroughly and legibly document all aspects of care provided, stay current with medical advances, and take the time to create a relationship with your patients involving quality communication. It is impossible for us to provide you with enough information to adequately prepare you for the day on which you may be sued. We nevertheless hope that following the aforementioned suggestions will be of some help.

References

1. Medical Malpractice Claims and Risk Management in Gastroenterology and Gastrointestinal Endoscopy. American Society for Gastrointestinal Endoscopy, 2017. <www.asge.org>.

2. Physician Insurers Association of America. PIAA Claim Trend Analysis: Gastroenterology, iv. Lawrenceville, N.J.: PIAA, 2004. <http://www.piaa.us>.

3. Kane C., Policy Research Perspective: Medical Liability Claim Frequency: 2007-2008 Snapshot of Physicians, American Medical Association, 2010.

4. Schaffer A.C., et al. JAMA Internal Med. 2017;177(5):710-8.

5. Dodge A.M. Wilsonville, Ore. Book Partners, Inc. 2001.

The 2017 AGA Women’s Leadership Conference brought together 38 women from across the United States and Mexico for an inspiring and productive meeting. The group included 21 early-career and 17 experienced track women in GI. Among the attendees were 3 PhDs, 9 private practitioners, 1 pediatric gastroenterologist, and 25 academic gastroenterologists. We were particularly fortunate to benefit from the strong representation of AGA leadership, including Marcia Cruz-Correa, MD, PhD, AGAF (At-Large Councillor) and Deborah Proctor, MD, AGAF (Education and Training Councillor), as well as Ellen Zimmermann, MD, AGAF (Chair of the Women’s Committee) and Sheila Crowe, MD, AGAF (President, AGA Institute Governing Board).

The AGA leaders in attendance shared inspiring stories of their own paths to leadership. These paths were not linear and it was reassuring to discover common themes of finding and developing personal strengths, identifying passions, and building areas of expertise. We learned, how once identified, strengths and passions can be connected to areas of need within a home institution or an organization such as the AGA. Dr. Zimmermann offered moving commentary about her own journey as a clinician, scientist, and mother. She encouraged those in attendance with small children to take the time to be present at home, knowing that there will be opportunities to assume leadership roles in the future. Of course, for others, the time to assume leadership roles may be now, and the Women’s Leadership Conference offered the chance to network and forge new connections within the AGA.

Dr. Garman is an assistant professor of medicine in the division of gastroenterology at Duke University, Durham, N.C. Dr. Alaparthi is managing partner of Gastroenterology Center of Connecticut and assistant clinical professor of medicine at Yale School of Medicine, Conn., and Frank Netter School of Medicine, Conn.

The 2017 AGA Women’s Leadership Conference brought together 38 women from across the United States and Mexico for an inspiring and productive meeting. The group included 21 early-career and 17 experienced track women in GI. Among the attendees were 3 PhDs, 9 private practitioners, 1 pediatric gastroenterologist, and 25 academic gastroenterologists. We were particularly fortunate to benefit from the strong representation of AGA leadership, including Marcia Cruz-Correa, MD, PhD, AGAF (At-Large Councillor) and Deborah Proctor, MD, AGAF (Education and Training Councillor), as well as Ellen Zimmermann, MD, AGAF (Chair of the Women’s Committee) and Sheila Crowe, MD, AGAF (President, AGA Institute Governing Board).

The AGA leaders in attendance shared inspiring stories of their own paths to leadership. These paths were not linear and it was reassuring to discover common themes of finding and developing personal strengths, identifying passions, and building areas of expertise. We learned, how once identified, strengths and passions can be connected to areas of need within a home institution or an organization such as the AGA. Dr. Zimmermann offered moving commentary about her own journey as a clinician, scientist, and mother. She encouraged those in attendance with small children to take the time to be present at home, knowing that there will be opportunities to assume leadership roles in the future. Of course, for others, the time to assume leadership roles may be now, and the Women’s Leadership Conference offered the chance to network and forge new connections within the AGA.

Dr. Garman is an assistant professor of medicine in the division of gastroenterology at Duke University, Durham, N.C. Dr. Alaparthi is managing partner of Gastroenterology Center of Connecticut and assistant clinical professor of medicine at Yale School of Medicine, Conn., and Frank Netter School of Medicine, Conn.

The 2017 AGA Women’s Leadership Conference brought together 38 women from across the United States and Mexico for an inspiring and productive meeting. The group included 21 early-career and 17 experienced track women in GI. Among the attendees were 3 PhDs, 9 private practitioners, 1 pediatric gastroenterologist, and 25 academic gastroenterologists. We were particularly fortunate to benefit from the strong representation of AGA leadership, including Marcia Cruz-Correa, MD, PhD, AGAF (At-Large Councillor) and Deborah Proctor, MD, AGAF (Education and Training Councillor), as well as Ellen Zimmermann, MD, AGAF (Chair of the Women’s Committee) and Sheila Crowe, MD, AGAF (President, AGA Institute Governing Board).

The AGA leaders in attendance shared inspiring stories of their own paths to leadership. These paths were not linear and it was reassuring to discover common themes of finding and developing personal strengths, identifying passions, and building areas of expertise. We learned, how once identified, strengths and passions can be connected to areas of need within a home institution or an organization such as the AGA. Dr. Zimmermann offered moving commentary about her own journey as a clinician, scientist, and mother. She encouraged those in attendance with small children to take the time to be present at home, knowing that there will be opportunities to assume leadership roles in the future. Of course, for others, the time to assume leadership roles may be now, and the Women’s Leadership Conference offered the chance to network and forge new connections within the AGA.

Dr. Garman is an assistant professor of medicine in the division of gastroenterology at Duke University, Durham, N.C. Dr. Alaparthi is managing partner of Gastroenterology Center of Connecticut and assistant clinical professor of medicine at Yale School of Medicine, Conn., and Frank Netter School of Medicine, Conn.

Introduction

Chronic esophageal symptoms attributed to gastroesophageal reflux disease (GERD) are common presenting symptoms in gastroenterology, leading to high healthcare costs and adverse quality of life globally.^1,2 The clinical diagnosis of GERD hinges on the presence of “troublesome” compatible typical symptoms (heartburn, acid regurgitation) or evidence of mucosal injury on endoscopy (esophagitis, Barrett’s esophagus, peptic stricture).³ With the growing availability of proton pump inhibitors (PPIs), patients and clinicians often utilize an empiric therapeutic trial of PPI as an initial test, with symptom improvement in the absence of alarm symptoms indicating a high likelihood of GERD.⁴ A meta-analysis of studies that used objective measures of GERD (in this case, 24-hour pH monitoring) showed that the “PPI test” has a sensitivity of 78%, but a specificity of only 54%, as a diagnostic approach to GERD symptoms.⁵ Apart from noncardiac chest pain, the diagnostic yield is even lower for atypical and extra-esophageal symptoms such as cough or laryngeal symptoms.⁶

The “nuts and bolts” of reflux testing

Ambulatory reflux testing assesses esophageal reflux burden and symptom-reflux association (SRA). Individual reflux events are identified as either a drop in esophageal pH to less than 4 (acid reflux events), or a sharp decrease in esophageal impedance measurements in a retrograde fashion (impedance-detected reflux events), with subsequent recovery to the baseline in each instance. Ambulatory reflux testing affords insight into three areas: 1) measurement of esophageal acid exposure time (AET); the cumulative time duration when distal esophageal pH is less than 4 at the recording site, reported as a percentage of the recording period; 2) measurement of the number of reflux events both acidic (from pH monitoring) and weakly acidic/alkaline (from impedance monitoring); and 3) quantitative evaluation of the association between reported symptom episodes and reflux events.

Copyright Elsevier/AGA

Testing on or off PPI?

For symptoms attributable to GERD that persist despite properly administered PPI therapy, the 2013 American College of Gastroenterology guidelines suggest upper endoscopy with esophageal biopsies for typical symptoms and appropriate referrals for atypical symptoms.²⁴ However, if these evaluations are unremarkable, reflux monitoring is recommended, with PPI status for testing guided by the pre-test probability of GERD: with a low pre-test probability of GERD, reflux testing is best performed off PPI with either pH or combined pH-impedance testing. In contrast, with a high pre-test probability of GERD, testing is best performed on PPI with combined pH-impedance testing. A similar concept is proposed in the Rome IV approach (Figure 2)²³ and on GERD consensus guidelines:⁷ when heartburn or chest pain persists despite PPI therapy and endoscopy and esophageal biopsies are normal, evidence for GERD (past esophagitis, Barrett’s esophagus, peptic stricture, or prior positive reflux testing) prompts pH-impedance monitoring on PPI therapy (i.e., proven GERD). Those without this evidence for proven GERD (i.e., unproven GERD) are best tested off PPI, and the test utilized can be either pH alone or combined pH-impedance.

GERD phenotypes and management

The presence or absence of the two core metrics on ambulatory reflux monitoring – abnormal AET and positive SRA – can stratify symptomatic GERD patients into phenotypes that predict symptomatic improvement with antireflux therapy and guide management of symptoms (Figure 3).^25,26 The presence of both abnormal AET and positive SRA suggests “strong” evidence for GERD, for which symptom improvement is likely with maximization of antireflux therapy, which can include BID PPI, baclofen (to decrease transient LES relaxations), alginates (such as Gaviscon), and consideration of endosopic or surgical antireflux procedures such as fundoplication or magnetic sphincter augmentation. Abnormal AET but negative SRA is regarded as “good” evidence for GERD, for which similar antireflux therapies can be advocated. Normal AET but positive SRA is designated as “reflux hypersensitivity,”²³ with increasing proportions of patients meeting this phenotype when tested with combined pH-impedance and off PPI therapy.²⁷ Both normal AET and negative SRA suggest equivocal evidence for GERD and the likely presence of a functional esophageal disorder, such as functional heartburn.²³ For reflux hypersensitivity and especially functional esophageal disorders, antireflux therapy is unlikely to be as effective and management can include pharmacologic neuromodulation (such as tricyclic antidepressants administered at bedtime) as well as adjunctive nonpharmacologic approaches (such as stress reduction, relaxation, hypnosis, or cognitive-behavioral therapy).

The future of reflux diagnostics

Conclusions

For esophageal symptoms potentially attributable to GERD that persist despite optimized PPI therapy, esophageal testing should be undertaken, starting with endoscopy and biopsies and proceeding to ambulatory reflux monitoring with HRM. The decisions between pH testing alone versus combined pH-impedance monitoring, and between testing on or off PPI therapy, can be guided either by the pre-test probability of GERD or whether GERD has been proven or unproven in prior evaluations (Figure 2). Elevated AET and positive SRA with impedance-detected reflux events can predict the likelihood of successful management outcomes from antireflux therapy. These two core metrics can be utilized to phenotype GERD and guide management approaches for persisting symptoms (Figure 3). Novel impedance metrics (baseline mucosal impedance, postreflux swallow-induced peristaltic wave index) and markers for esophageal mucosal damage continue to be studied as potential markers for evidence of longitudinal reflux exposure.

Dr. Patel is assistant professor of medicine, division of gastroenterology, Duke University School of Medicine and the Durham Veterans Affairs Medical Center, Durham, N.C. Dr. Gyawali is professor of medicine, division of gastroenterology, Washington University School of Medicine, St. Louis, Mo.

References

1. Shaheen N.J., et al. Am J Gastroenterol. 2006;101:2128-38.

2. Patel A., Gyawali C.P.. Switzerland: Springer International, 2016.

3. Vakil N., et al. Am J Gastroenterol. 2006;101:1900-20; quiz 1943.

4. Fass R., et al. Arch Intern Med. 1999;159:2161-8.

5. Numans M.E., et al. Ann Intern Med. 2004;140:518-27.

6. Shaheen N.J., et al. Aliment Pharmacol Ther. 2011;33:225-34.

7. Roman S., et al. Neurogastroenterol Motil Mar 31. doi: 10.1111/nmo.13067. [Epub ahead of print] 2017.

8. Dellon E.S., et al. Am J Gastroenterol. 2013;108:679-92; quiz 693.

9. Pandolfino JE, Vela MF. Gastrointest Endosc. 2009;69:917-30, 930 e1.

10. Shay S., et al. Am J Gastroenterol. 2004;99:1037-43.

11. Zerbib F., et al. Clin Gastroenterol Hepatol. 2013;11:366-72.

12. Wiener G.J., et al. Am J Gastroenterol 1988;83:358-61.

13. Weusten B.L., et al. Gastroenterology. 1994;107:1741-5.

14. Ghillebert G., et al. Gut 1990;31:738-44.

15. Kushnir V.M., et al. Aliment Pharmacol Ther. 2012;35(9):1080-7.

16. Bredenoord A.J., et al. Am J Gastroenterol. 2006;101:453-9.

17. Patel A., et al. Clin Gastroenterol Hepatol. 2015;13:884-91.

18. Slaughter J.C., et al. Clin Gastroenterol Hepatol. 2011;9:868-74.

19. Kavitt R.T., et al. Am J Gastroenterol. 2012;107:1826-32.

20. Kahrilas P.J., et al. Gastroenterology 2008;135:1383-91, 1391 e1-5.

21. Kessing B.F., et al. Clin Gastroenterol Hepatol. 2011;9:1020-4.

22. Kahrilas P.J., et al. Neurogastroenterol Motil. 2015;27:160-74.

23. Aziz A, et al. Esophageal disorders. Gastroenterology 2016;150:1368-79.

24. Katz P.O., et al. Am J Gastroenterol. 2013;108:308-28; quiz 329.

25. Boeckxstaens G., et al. Gut 2014;63:1185-93.

26. Patel A., et al. Neurogastroenterol Motil. 2016;28:513-21.

27. Patel A., et al. Neurogastroenterol Motil. 2016;28:1382-90.

28. Martinucci I., et al. Neurogastroenterol Motil. 2014;26:546-55.

29. Ates F., et al. Gastroenterology 2015;148:334-43.

30. Kessing B.F., et al. Am J Gastroenterol. 2011;106:2093-7.

31. Patel A., et al. Aliment Pharmacol Ther. 2016;44:890-8.

32. Frazzoni M., et al. Neurogastroenterol Motil. 2016.

33. Frazzoni M., et al. Neurogastroenterol Motil. 2013;25:399-406, e295.

34. Vela M.F., et al. Am J Gastroenterol. 2011;106:844-50.
 

Introduction

Chronic esophageal symptoms attributed to gastroesophageal reflux disease (GERD) are common presenting symptoms in gastroenterology, leading to high healthcare costs and adverse quality of life globally.^1,2 The clinical diagnosis of GERD hinges on the presence of “troublesome” compatible typical symptoms (heartburn, acid regurgitation) or evidence of mucosal injury on endoscopy (esophagitis, Barrett’s esophagus, peptic stricture).³ With the growing availability of proton pump inhibitors (PPIs), patients and clinicians often utilize an empiric therapeutic trial of PPI as an initial test, with symptom improvement in the absence of alarm symptoms indicating a high likelihood of GERD.⁴ A meta-analysis of studies that used objective measures of GERD (in this case, 24-hour pH monitoring) showed that the “PPI test” has a sensitivity of 78%, but a specificity of only 54%, as a diagnostic approach to GERD symptoms.⁵ Apart from noncardiac chest pain, the diagnostic yield is even lower for atypical and extra-esophageal symptoms such as cough or laryngeal symptoms.⁶

The “nuts and bolts” of reflux testing

Ambulatory reflux testing assesses esophageal reflux burden and symptom-reflux association (SRA). Individual reflux events are identified as either a drop in esophageal pH to less than 4 (acid reflux events), or a sharp decrease in esophageal impedance measurements in a retrograde fashion (impedance-detected reflux events), with subsequent recovery to the baseline in each instance. Ambulatory reflux testing affords insight into three areas: 1) measurement of esophageal acid exposure time (AET); the cumulative time duration when distal esophageal pH is less than 4 at the recording site, reported as a percentage of the recording period; 2) measurement of the number of reflux events both acidic (from pH monitoring) and weakly acidic/alkaline (from impedance monitoring); and 3) quantitative evaluation of the association between reported symptom episodes and reflux events.

Copyright Elsevier/AGA

Testing on or off PPI?

For symptoms attributable to GERD that persist despite properly administered PPI therapy, the 2013 American College of Gastroenterology guidelines suggest upper endoscopy with esophageal biopsies for typical symptoms and appropriate referrals for atypical symptoms.²⁴ However, if these evaluations are unremarkable, reflux monitoring is recommended, with PPI status for testing guided by the pre-test probability of GERD: with a low pre-test probability of GERD, reflux testing is best performed off PPI with either pH or combined pH-impedance testing. In contrast, with a high pre-test probability of GERD, testing is best performed on PPI with combined pH-impedance testing. A similar concept is proposed in the Rome IV approach (Figure 2)²³ and on GERD consensus guidelines:⁷ when heartburn or chest pain persists despite PPI therapy and endoscopy and esophageal biopsies are normal, evidence for GERD (past esophagitis, Barrett’s esophagus, peptic stricture, or prior positive reflux testing) prompts pH-impedance monitoring on PPI therapy (i.e., proven GERD). Those without this evidence for proven GERD (i.e., unproven GERD) are best tested off PPI, and the test utilized can be either pH alone or combined pH-impedance.

GERD phenotypes and management

The presence or absence of the two core metrics on ambulatory reflux monitoring – abnormal AET and positive SRA – can stratify symptomatic GERD patients into phenotypes that predict symptomatic improvement with antireflux therapy and guide management of symptoms (Figure 3).^25,26 The presence of both abnormal AET and positive SRA suggests “strong” evidence for GERD, for which symptom improvement is likely with maximization of antireflux therapy, which can include BID PPI, baclofen (to decrease transient LES relaxations), alginates (such as Gaviscon), and consideration of endosopic or surgical antireflux procedures such as fundoplication or magnetic sphincter augmentation. Abnormal AET but negative SRA is regarded as “good” evidence for GERD, for which similar antireflux therapies can be advocated. Normal AET but positive SRA is designated as “reflux hypersensitivity,”²³ with increasing proportions of patients meeting this phenotype when tested with combined pH-impedance and off PPI therapy.²⁷ Both normal AET and negative SRA suggest equivocal evidence for GERD and the likely presence of a functional esophageal disorder, such as functional heartburn.²³ For reflux hypersensitivity and especially functional esophageal disorders, antireflux therapy is unlikely to be as effective and management can include pharmacologic neuromodulation (such as tricyclic antidepressants administered at bedtime) as well as adjunctive nonpharmacologic approaches (such as stress reduction, relaxation, hypnosis, or cognitive-behavioral therapy).

The future of reflux diagnostics

Conclusions

For esophageal symptoms potentially attributable to GERD that persist despite optimized PPI therapy, esophageal testing should be undertaken, starting with endoscopy and biopsies and proceeding to ambulatory reflux monitoring with HRM. The decisions between pH testing alone versus combined pH-impedance monitoring, and between testing on or off PPI therapy, can be guided either by the pre-test probability of GERD or whether GERD has been proven or unproven in prior evaluations (Figure 2). Elevated AET and positive SRA with impedance-detected reflux events can predict the likelihood of successful management outcomes from antireflux therapy. These two core metrics can be utilized to phenotype GERD and guide management approaches for persisting symptoms (Figure 3). Novel impedance metrics (baseline mucosal impedance, postreflux swallow-induced peristaltic wave index) and markers for esophageal mucosal damage continue to be studied as potential markers for evidence of longitudinal reflux exposure.

Dr. Patel is assistant professor of medicine, division of gastroenterology, Duke University School of Medicine and the Durham Veterans Affairs Medical Center, Durham, N.C. Dr. Gyawali is professor of medicine, division of gastroenterology, Washington University School of Medicine, St. Louis, Mo.

References

1. Shaheen N.J., et al. Am J Gastroenterol. 2006;101:2128-38.

2. Patel A., Gyawali C.P.. Switzerland: Springer International, 2016.

3. Vakil N., et al. Am J Gastroenterol. 2006;101:1900-20; quiz 1943.

4. Fass R., et al. Arch Intern Med. 1999;159:2161-8.

5. Numans M.E., et al. Ann Intern Med. 2004;140:518-27.

6. Shaheen N.J., et al. Aliment Pharmacol Ther. 2011;33:225-34.

7. Roman S., et al. Neurogastroenterol Motil Mar 31. doi: 10.1111/nmo.13067. [Epub ahead of print] 2017.

8. Dellon E.S., et al. Am J Gastroenterol. 2013;108:679-92; quiz 693.

9. Pandolfino JE, Vela MF. Gastrointest Endosc. 2009;69:917-30, 930 e1.

10. Shay S., et al. Am J Gastroenterol. 2004;99:1037-43.

11. Zerbib F., et al. Clin Gastroenterol Hepatol. 2013;11:366-72.

12. Wiener G.J., et al. Am J Gastroenterol 1988;83:358-61.

13. Weusten B.L., et al. Gastroenterology. 1994;107:1741-5.

14. Ghillebert G., et al. Gut 1990;31:738-44.

15. Kushnir V.M., et al. Aliment Pharmacol Ther. 2012;35(9):1080-7.

16. Bredenoord A.J., et al. Am J Gastroenterol. 2006;101:453-9.

17. Patel A., et al. Clin Gastroenterol Hepatol. 2015;13:884-91.

18. Slaughter J.C., et al. Clin Gastroenterol Hepatol. 2011;9:868-74.

19. Kavitt R.T., et al. Am J Gastroenterol. 2012;107:1826-32.

20. Kahrilas P.J., et al. Gastroenterology 2008;135:1383-91, 1391 e1-5.

21. Kessing B.F., et al. Clin Gastroenterol Hepatol. 2011;9:1020-4.

22. Kahrilas P.J., et al. Neurogastroenterol Motil. 2015;27:160-74.

23. Aziz A, et al. Esophageal disorders. Gastroenterology 2016;150:1368-79.

24. Katz P.O., et al. Am J Gastroenterol. 2013;108:308-28; quiz 329.

25. Boeckxstaens G., et al. Gut 2014;63:1185-93.

26. Patel A., et al. Neurogastroenterol Motil. 2016;28:513-21.

27. Patel A., et al. Neurogastroenterol Motil. 2016;28:1382-90.

28. Martinucci I., et al. Neurogastroenterol Motil. 2014;26:546-55.

29. Ates F., et al. Gastroenterology 2015;148:334-43.

30. Kessing B.F., et al. Am J Gastroenterol. 2011;106:2093-7.

31. Patel A., et al. Aliment Pharmacol Ther. 2016;44:890-8.

32. Frazzoni M., et al. Neurogastroenterol Motil. 2016.

33. Frazzoni M., et al. Neurogastroenterol Motil. 2013;25:399-406, e295.

34. Vela M.F., et al. Am J Gastroenterol. 2011;106:844-50.
 

Introduction

Chronic esophageal symptoms attributed to gastroesophageal reflux disease (GERD) are common presenting symptoms in gastroenterology, leading to high healthcare costs and adverse quality of life globally.^1,2 The clinical diagnosis of GERD hinges on the presence of “troublesome” compatible typical symptoms (heartburn, acid regurgitation) or evidence of mucosal injury on endoscopy (esophagitis, Barrett’s esophagus, peptic stricture).³ With the growing availability of proton pump inhibitors (PPIs), patients and clinicians often utilize an empiric therapeutic trial of PPI as an initial test, with symptom improvement in the absence of alarm symptoms indicating a high likelihood of GERD.⁴ A meta-analysis of studies that used objective measures of GERD (in this case, 24-hour pH monitoring) showed that the “PPI test” has a sensitivity of 78%, but a specificity of only 54%, as a diagnostic approach to GERD symptoms.⁵ Apart from noncardiac chest pain, the diagnostic yield is even lower for atypical and extra-esophageal symptoms such as cough or laryngeal symptoms.⁶

The “nuts and bolts” of reflux testing

Ambulatory reflux testing assesses esophageal reflux burden and symptom-reflux association (SRA). Individual reflux events are identified as either a drop in esophageal pH to less than 4 (acid reflux events), or a sharp decrease in esophageal impedance measurements in a retrograde fashion (impedance-detected reflux events), with subsequent recovery to the baseline in each instance. Ambulatory reflux testing affords insight into three areas: 1) measurement of esophageal acid exposure time (AET); the cumulative time duration when distal esophageal pH is less than 4 at the recording site, reported as a percentage of the recording period; 2) measurement of the number of reflux events both acidic (from pH monitoring) and weakly acidic/alkaline (from impedance monitoring); and 3) quantitative evaluation of the association between reported symptom episodes and reflux events.

Copyright Elsevier/AGA

Testing on or off PPI?

For symptoms attributable to GERD that persist despite properly administered PPI therapy, the 2013 American College of Gastroenterology guidelines suggest upper endoscopy with esophageal biopsies for typical symptoms and appropriate referrals for atypical symptoms.²⁴ However, if these evaluations are unremarkable, reflux monitoring is recommended, with PPI status for testing guided by the pre-test probability of GERD: with a low pre-test probability of GERD, reflux testing is best performed off PPI with either pH or combined pH-impedance testing. In contrast, with a high pre-test probability of GERD, testing is best performed on PPI with combined pH-impedance testing. A similar concept is proposed in the Rome IV approach (Figure 2)²³ and on GERD consensus guidelines:⁷ when heartburn or chest pain persists despite PPI therapy and endoscopy and esophageal biopsies are normal, evidence for GERD (past esophagitis, Barrett’s esophagus, peptic stricture, or prior positive reflux testing) prompts pH-impedance monitoring on PPI therapy (i.e., proven GERD). Those without this evidence for proven GERD (i.e., unproven GERD) are best tested off PPI, and the test utilized can be either pH alone or combined pH-impedance.

GERD phenotypes and management

The presence or absence of the two core metrics on ambulatory reflux monitoring – abnormal AET and positive SRA – can stratify symptomatic GERD patients into phenotypes that predict symptomatic improvement with antireflux therapy and guide management of symptoms (Figure 3).^25,26 The presence of both abnormal AET and positive SRA suggests “strong” evidence for GERD, for which symptom improvement is likely with maximization of antireflux therapy, which can include BID PPI, baclofen (to decrease transient LES relaxations), alginates (such as Gaviscon), and consideration of endosopic or surgical antireflux procedures such as fundoplication or magnetic sphincter augmentation. Abnormal AET but negative SRA is regarded as “good” evidence for GERD, for which similar antireflux therapies can be advocated. Normal AET but positive SRA is designated as “reflux hypersensitivity,”²³ with increasing proportions of patients meeting this phenotype when tested with combined pH-impedance and off PPI therapy.²⁷ Both normal AET and negative SRA suggest equivocal evidence for GERD and the likely presence of a functional esophageal disorder, such as functional heartburn.²³ For reflux hypersensitivity and especially functional esophageal disorders, antireflux therapy is unlikely to be as effective and management can include pharmacologic neuromodulation (such as tricyclic antidepressants administered at bedtime) as well as adjunctive nonpharmacologic approaches (such as stress reduction, relaxation, hypnosis, or cognitive-behavioral therapy).

The future of reflux diagnostics

Conclusions

For esophageal symptoms potentially attributable to GERD that persist despite optimized PPI therapy, esophageal testing should be undertaken, starting with endoscopy and biopsies and proceeding to ambulatory reflux monitoring with HRM. The decisions between pH testing alone versus combined pH-impedance monitoring, and between testing on or off PPI therapy, can be guided either by the pre-test probability of GERD or whether GERD has been proven or unproven in prior evaluations (Figure 2). Elevated AET and positive SRA with impedance-detected reflux events can predict the likelihood of successful management outcomes from antireflux therapy. These two core metrics can be utilized to phenotype GERD and guide management approaches for persisting symptoms (Figure 3). Novel impedance metrics (baseline mucosal impedance, postreflux swallow-induced peristaltic wave index) and markers for esophageal mucosal damage continue to be studied as potential markers for evidence of longitudinal reflux exposure.

Dr. Patel is assistant professor of medicine, division of gastroenterology, Duke University School of Medicine and the Durham Veterans Affairs Medical Center, Durham, N.C. Dr. Gyawali is professor of medicine, division of gastroenterology, Washington University School of Medicine, St. Louis, Mo.

References

1. Shaheen N.J., et al. Am J Gastroenterol. 2006;101:2128-38.

2. Patel A., Gyawali C.P.. Switzerland: Springer International, 2016.

3. Vakil N., et al. Am J Gastroenterol. 2006;101:1900-20; quiz 1943.

4. Fass R., et al. Arch Intern Med. 1999;159:2161-8.

5. Numans M.E., et al. Ann Intern Med. 2004;140:518-27.

6. Shaheen N.J., et al. Aliment Pharmacol Ther. 2011;33:225-34.

7. Roman S., et al. Neurogastroenterol Motil Mar 31. doi: 10.1111/nmo.13067. [Epub ahead of print] 2017.

8. Dellon E.S., et al. Am J Gastroenterol. 2013;108:679-92; quiz 693.

9. Pandolfino JE, Vela MF. Gastrointest Endosc. 2009;69:917-30, 930 e1.

10. Shay S., et al. Am J Gastroenterol. 2004;99:1037-43.

11. Zerbib F., et al. Clin Gastroenterol Hepatol. 2013;11:366-72.

12. Wiener G.J., et al. Am J Gastroenterol 1988;83:358-61.

13. Weusten B.L., et al. Gastroenterology. 1994;107:1741-5.

14. Ghillebert G., et al. Gut 1990;31:738-44.

15. Kushnir V.M., et al. Aliment Pharmacol Ther. 2012;35(9):1080-7.

16. Bredenoord A.J., et al. Am J Gastroenterol. 2006;101:453-9.

17. Patel A., et al. Clin Gastroenterol Hepatol. 2015;13:884-91.

18. Slaughter J.C., et al. Clin Gastroenterol Hepatol. 2011;9:868-74.

19. Kavitt R.T., et al. Am J Gastroenterol. 2012;107:1826-32.

20. Kahrilas P.J., et al. Gastroenterology 2008;135:1383-91, 1391 e1-5.

21. Kessing B.F., et al. Clin Gastroenterol Hepatol. 2011;9:1020-4.

22. Kahrilas P.J., et al. Neurogastroenterol Motil. 2015;27:160-74.

23. Aziz A, et al. Esophageal disorders. Gastroenterology 2016;150:1368-79.

24. Katz P.O., et al. Am J Gastroenterol. 2013;108:308-28; quiz 329.

25. Boeckxstaens G., et al. Gut 2014;63:1185-93.

26. Patel A., et al. Neurogastroenterol Motil. 2016;28:513-21.

27. Patel A., et al. Neurogastroenterol Motil. 2016;28:1382-90.

28. Martinucci I., et al. Neurogastroenterol Motil. 2014;26:546-55.

29. Ates F., et al. Gastroenterology 2015;148:334-43.

30. Kessing B.F., et al. Am J Gastroenterol. 2011;106:2093-7.

31. Patel A., et al. Aliment Pharmacol Ther. 2016;44:890-8.

32. Frazzoni M., et al. Neurogastroenterol Motil. 2016.

33. Frazzoni M., et al. Neurogastroenterol Motil. 2013;25:399-406, e295.

34. Vela M.F., et al. Am J Gastroenterol. 2011;106:844-50.
 

Dear Trainees and Early-Career GIs,

As I begin my time as President of AGA, I am reflecting on other new beginnings in my career. Though time has passed, I vividly recall the excitement and uncertainty of beginning training and, subsequently, my career. It’s a career that I’ve enjoyed immensely and I hope that you will as well.

AGA Institute

Dear Trainees and Early-Career GIs,

As I begin my time as President of AGA, I am reflecting on other new beginnings in my career. Though time has passed, I vividly recall the excitement and uncertainty of beginning training and, subsequently, my career. It’s a career that I’ve enjoyed immensely and I hope that you will as well.

AGA Institute

Dear Trainees and Early-Career GIs,

As I begin my time as President of AGA, I am reflecting on other new beginnings in my career. Though time has passed, I vividly recall the excitement and uncertainty of beginning training and, subsequently, my career. It’s a career that I’ve enjoyed immensely and I hope that you will as well.

AGA Institute

Dear Colleagues,

Congratulations to the new gastroenterology fellows who have just begun their fellowships and also to those who have just finished and are starting their careers. It is certainly an exciting time of year for so many! A letter from AGA President Sheila Crowe, included in this issue, details the benefits and opportunities our organization offers GIs entering practice and academia.

Sincerely,

Bryson W. Katona, MD, PhD

Editor in Chief

Dr. Bryson W. Katona is an instructor of medicine in the division of gastroenterology at the University of Pennsylvania.

Dear Colleagues,

Congratulations to the new gastroenterology fellows who have just begun their fellowships and also to those who have just finished and are starting their careers. It is certainly an exciting time of year for so many! A letter from AGA President Sheila Crowe, included in this issue, details the benefits and opportunities our organization offers GIs entering practice and academia.

Sincerely,

Bryson W. Katona, MD, PhD

Editor in Chief

Dr. Bryson W. Katona is an instructor of medicine in the division of gastroenterology at the University of Pennsylvania.

Dear Colleagues,

Congratulations to the new gastroenterology fellows who have just begun their fellowships and also to those who have just finished and are starting their careers. It is certainly an exciting time of year for so many! A letter from AGA President Sheila Crowe, included in this issue, details the benefits and opportunities our organization offers GIs entering practice and academia.

Sincerely,

Bryson W. Katona, MD, PhD

Editor in Chief

Dr. Bryson W. Katona is an instructor of medicine in the division of gastroenterology at the University of Pennsylvania.

Minocycline, an antibiotic that has immune-modulating properties and crosses the blood-brain barrier, appears to delay conversion to multiple sclerosis in patients who have an initial focal demyelinating event, according to a report published online June 1 in the New England Journal of Medicine.

Two small clinical trials involving patients with relapsing-remitting multiple sclerosis (MS) recently showed that minocycline reduces the number of lesions detected on MRI with gadolinium enhancement. So researchers led by Luanne M. Metz, MD, of the Cumming School of Medicine and the Hotchkiss Brain Institute, Calgary, Alta., conducted a randomized, double-blind, placebo-controlled trial at 12 Canadian MS clinics to determine whether the drug might delay conversion to MS after a first, clinically isolated demyelinating event, such as optic neuritis or a brainstem, cerebral, cerebellar, or myelopathy syndrome.

copyright Zerbor/Thinkstock

Minocycline, an antibiotic that has immune-modulating properties and crosses the blood-brain barrier, appears to delay conversion to multiple sclerosis in patients who have an initial focal demyelinating event, according to a report published online June 1 in the New England Journal of Medicine.

Two small clinical trials involving patients with relapsing-remitting multiple sclerosis (MS) recently showed that minocycline reduces the number of lesions detected on MRI with gadolinium enhancement. So researchers led by Luanne M. Metz, MD, of the Cumming School of Medicine and the Hotchkiss Brain Institute, Calgary, Alta., conducted a randomized, double-blind, placebo-controlled trial at 12 Canadian MS clinics to determine whether the drug might delay conversion to MS after a first, clinically isolated demyelinating event, such as optic neuritis or a brainstem, cerebral, cerebellar, or myelopathy syndrome.

copyright Zerbor/Thinkstock

Minocycline, an antibiotic that has immune-modulating properties and crosses the blood-brain barrier, appears to delay conversion to multiple sclerosis in patients who have an initial focal demyelinating event, according to a report published online June 1 in the New England Journal of Medicine.

Two small clinical trials involving patients with relapsing-remitting multiple sclerosis (MS) recently showed that minocycline reduces the number of lesions detected on MRI with gadolinium enhancement. So researchers led by Luanne M. Metz, MD, of the Cumming School of Medicine and the Hotchkiss Brain Institute, Calgary, Alta., conducted a randomized, double-blind, placebo-controlled trial at 12 Canadian MS clinics to determine whether the drug might delay conversion to MS after a first, clinically isolated demyelinating event, such as optic neuritis or a brainstem, cerebral, cerebellar, or myelopathy syndrome.

copyright Zerbor/Thinkstock