Low FODMAPs Versus Traditional Dietary Advice for Treatment of Irritable Bowel SyndromeVisceral hypersensitivity, abnormal gastrointestinal motility, altered brain–gut communication, and altered gut microbiota, among other mechanisms, are thought to be factors in the pathophysiology of irritable bowel syndrome (IBS), yet there are few effective treatment options for patients suffering from this common functional gastrointestinal disorder. The majority of patients with IBS identify certain foods as triggers of their symptoms and, consequently, many dietary interventions have been proposed in the management of IBS, despite the absence of a large number of controlled clinical trials and concerns about the long-term safety of overly restricted diets. For example, a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs), has been advocated recently based on clinical trials demonstrating benefit in patients with IBS. However, there have been no randomized controlled trials comparing a low FODMAP diet with traditional dietary recommendations, such as maintaining regular meal patterns, avoiding large meals, reducing fat intake, avoiding excessive insoluble fiber intake, reducing caffeine, and avoiding foods that produce intestinal gas. In this issue of Gastroenterology, Böhn et al describe a single-blind randomized controlled study, involving 3 centers in Sweden, of 67 outpatients meeting Rome III criteria for IBS, comparing the effect of 4 weeks of a low FODMAP diet with traditional dietary advice on symptoms of IBS. Female patients predominated (n = 56) and all patients had medium to severe symptoms based on an IBS Symptom Severity Score (IBS-SSS) of ≥175. Symptom severity was reduced in both groups compared with baseline, with significant improvement in abdominal pain frequency, severity of abdominal distention, and life interference in both groups and reduction in the number of bowel movements per day in the low FODMAP diet group (Figure 1). A similar number of patients were defined as responders (IBS-SSS reduction of >50) in both treatment groups (19 in the FODMAP diet group and 17 in the traditional IBS diet group). Responders in the low FODMAP diet group had lower intake of FODMAPs at baseline, were older, and were almost exclusively female. Although IBS subtype did not affect the likelihood of response in the low FODMAP diet group, responders in the traditional IBS diet group were less likely to be patients with constipation-predominant IBS. These findings, using an active comparator with a low FODMAP diet, suggest that providing dietary advice to patients with IBS in the outpatient setting improves symptoms, regardless of whether that dietary advice is a low FODMAP or a traditional IBS diet.See page 1399.Genetics of Lynch Syndrome and IBD in African AmericansAlthough the prevalence of inflammatory bowel disease (IBD) is less in African Americans (AA) compared with Caucasian Americans, AAs have the highest incidence of and mortality from colorectal cancer (CRC) in the United States. However, little is known about the molecular genetic susceptibility of AAs, an admixed population with recent introduction of European genetic lineages into a West African–derived population, to these 2 major gastrointestinal disorders. In this issue of Gastroenterology, 2 studies begin to address this deficiency by examining the genetic susceptibility of AAs to Lynch syndrome, or hereditary nonpolyposis CRC, the most common inherited CRC syndrome, known to be caused by mutations in the DNA mismatch repair (MMR) genes, MLH1, MSH2, MSH6, PMS2 and EPCAM, and to IBD.Guindalini et al performed a retrospective study of MMR gene mutations in 920 members of 51 AA families from 13 US referral centers. Thirty-one families had MLH1 mutations, 11 had MSH2 mutations, 3 had MSH6 mutations, and 6 had PMS2 mutations. Of 39 distinctive mutations, 11 had not been described previously, including 6 in MLH1 and 2 in PMS2. The predominance of mutations in MLH1 was distinct from the mutation spectrum previously reported in individuals of European descent, where MSH2 mutations predominate. For all MMR gene mutation carriers combined, the cumulative risk of CRC to 80 years was estimated to be 36.2% for male carriers and 29.7% for female carriers. For MLH1 and MSH2 mutation carriers, the cumulative risk of CRC was even higher; 53.9% for male carriers and 45.6% for female carriers (Figure 2).Figure 2Percentage of cumulative risks (unbroken lines) and corresponding 95% confidence intervals (dotted lines) of colorectal cancer for African American carriers of (A) all MMR gene mutations and (B) mutations in MLH1 and MSH2 and AA SEER population-based data (dashed lines). Blue and red represent males and females, respectively. SEER, Surveillance, Epidemiology and End Results database.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Huang et al, using the Immunochip genotyping array, which has identified 163 susceptibility loci for IBD in Caucasians, performed a genetic mapping study, of 1088 AA patients with Crohn’s disease, 361 with ulcerative colitis, 62 with unknown IBD-type, and 1797 controls. Although established Caucasian associations were replicated in AAs, loci and variants were observed that had not previously been associated with IBD. The high frequency of genes associated with infectious diseases in both AAs and Caucasians with IBD supports the hypothesis that genetic susceptibility to IBD across populations may be the result of evolutionary adaptation to geographically distinct human pathogens.See pages 1446 and 1575; editorial on page 1323.Use of Clinical and Molecular Features to Classify Pancreatic CystsLargely owing to their improved resolving power and increased utility, the incidence of pancreatic cysts continues to increase. Pancreatic cysts are classified according to pathological criteria as either serous cystadenomas, solid pseudopapillary neoplasms, mucinous cystic neoplasms, or intraductal papillary mucinous neoplasms (IPMN). Only serous cystadenomas carry no significant risk for progression to pancreatic cancer. Because pancreatic cancer is associated with such poor clinical outcomes, determining the risk a cyst poses to a patient is important for deciding whether to proceed with surgical removal. A variety of clinical criteria for determining the potential risk of a pancreatic cyst have been developed, but these approaches are imperfect, because >20% of surgically resected cysts are subsequently found to be benign, and 75% of IPMNs exhibit only low- or intermediate-grade dysplasia that also could have been observed.In this issue of Gastroenterology, Springer et al report on their efforts to stratify pancreatic cysts according to molecular and clinical criteria. This retrospective study was enabled by new technologies that include massively parallel sequencing that can be performed using 0.25 mL of cyst fluid. A total of 130 cyst fluid samples were collected at the time of surgical removal, 96 of which were IPMNs and the remaining 34 evenly distributed between the 3 remaining classifications. For 24 of the samples, cyst fluid was obtained by both endoscopic ultrasound and surgical resection. The results between the 2 sample sets were consistent.The analysis focused on 3 molecular features: mutations of 6 oncogenes (BRAF, CTNNB1, GNAS, KRAS, NRAS, and PIK3CA) and 5 tumor suppressors (CDK2NA, RNF43, SMAD4, TP53, and VHL), loss of heterozygosity of the same tumor suppressors, and an assessment for aneuploidy. The final dataset was combined with identified clinical features and analyzed with multivariate organization of combinatorial alterations, an algorithm that is able to produce a combination of molecular and clinical features that best categorize the cysts. In doing so, the authors established criteria that would potentially be able to reduce the number of unnecessary surgeries by 91%. The study provides impetus for future validation studies that utilize molecular biomarkers.See page 1501.Similarity of T-cell Responses in Children and Adults with Celiac DiseaseCeliac disease is an autoimmune disorder characterized by intestinal damage that is precipitated by CD4+ T lymphocytes that are reactive against wheat-derived gluten peptides presented by HLA-DQ2.5, HLA-DQ2.2, or HLA-DQ8. C disease is first manifested between the ages of 1 and 6. The prevalent belief was that the spectrum of gluten reactive CD4+ T lymphocytes was heterogenous and differed between children and adults with celiac disease. If true, different strategies for the diagnosis and treatment of celiac disease may be necessary for children and adults.In this issue of Gastroenterology, Hardy et al report on their characterization of gluten-reactive T cells from children and adults with celiac disease. They enrolled a total of 41 children and 4 adults. The subjects, who had been on gluten-free diets, were given a wheat challenge for 3 days before blood was collected. Symptoms consistent with celiac diseases were induced in a majority of the subjects. T cells derived from the subjects were exposed to gluten-derived peptides that included amino acid sequences representing different epitopes and peptides that were deamidated. T-cell activation after exposure to a variety of different peptides was assessed using an interferon (IFN)-γ enzyme-linked immunospot assay. The assay measures the IFN-γ secreted by activated T cells with an enzyme-linked immunosorbent assay. The most dominant peptides in eliciting a T-cell response were ranked within each test subject. The 4 most potent peptides were consistent in all age groups, including comparisons between adults and children. Consistent with previous work, deamidated peptides were significantly more potent than their amidated versions. The experiments were performed on patients from England, Italy, Norway, and Australia; and all demonstrated similar results. The T-cell response to specific gluten peptides, therefore, develops early in the course of the disease and remains consistent throughout its natural history. The authors established that there is no difference in T-cell reactivity to peptides between children and adults with celiac disease.See page 1541. Low FODMAPs Versus Traditional Dietary Advice for Treatment of Irritable Bowel SyndromeVisceral hypersensitivity, abnormal gastrointestinal motility, altered brain–gut communication, and altered gut microbiota, among other mechanisms, are thought to be factors in the pathophysiology of irritable bowel syndrome (IBS), yet there are few effective treatment options for patients suffering from this common functional gastrointestinal disorder. The majority of patients with IBS identify certain foods as triggers of their symptoms and, consequently, many dietary interventions have been proposed in the management of IBS, despite the absence of a large number of controlled clinical trials and concerns about the long-term safety of overly restricted diets. For example, a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs), has been advocated recently based on clinical trials demonstrating benefit in patients with IBS. However, there have been no randomized controlled trials comparing a low FODMAP diet with traditional dietary recommendations, such as maintaining regular meal patterns, avoiding large meals, reducing fat intake, avoiding excessive insoluble fiber intake, reducing caffeine, and avoiding foods that produce intestinal gas. In this issue of Gastroenterology, Böhn et al describe a single-blind randomized controlled study, involving 3 centers in Sweden, of 67 outpatients meeting Rome III criteria for IBS, comparing the effect of 4 weeks of a low FODMAP diet with traditional dietary advice on symptoms of IBS. Female patients predominated (n = 56) and all patients had medium to severe symptoms based on an IBS Symptom Severity Score (IBS-SSS) of ≥175. Symptom severity was reduced in both groups compared with baseline, with significant improvement in abdominal pain frequency, severity of abdominal distention, and life interference in both groups and reduction in the number of bowel movements per day in the low FODMAP diet group (Figure 1). A similar number of patients were defined as responders (IBS-SSS reduction of >50) in both treatment groups (19 in the FODMAP diet group and 17 in the traditional IBS diet group). Responders in the low FODMAP diet group had lower intake of FODMAPs at baseline, were older, and were almost exclusively female. Although IBS subtype did not affect the likelihood of response in the low FODMAP diet group, responders in the traditional IBS diet group were less likely to be patients with constipation-predominant IBS. These findings, using an active comparator with a low FODMAP diet, suggest that providing dietary advice to patients with IBS in the outpatient setting improves symptoms, regardless of whether that dietary advice is a low FODMAP or a traditional IBS diet.See page 1399. Visceral hypersensitivity, abnormal gastrointestinal motility, altered brain–gut communication, and altered gut microbiota, among other mechanisms, are thought to be factors in the pathophysiology of irritable bowel syndrome (IBS), yet there are few effective treatment options for patients suffering from this common functional gastrointestinal disorder. The majority of patients with IBS identify certain foods as triggers of their symptoms and, consequently, many dietary interventions have been proposed in the management of IBS, despite the absence of a large number of controlled clinical trials and concerns about the long-term safety of overly restricted diets. For example, a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs), has been advocated recently based on clinical trials demonstrating benefit in patients with IBS. However, there have been no randomized controlled trials comparing a low FODMAP diet with traditional dietary recommendations, such as maintaining regular meal patterns, avoiding large meals, reducing fat intake, avoiding excessive insoluble fiber intake, reducing caffeine, and avoiding foods that produce intestinal gas. In this issue of Gastroenterology, Böhn et al describe a single-blind randomized controlled study, involving 3 centers in Sweden, of 67 outpatients meeting Rome III criteria for IBS, comparing the effect of 4 weeks of a low FODMAP diet with traditional dietary advice on symptoms of IBS. Female patients predominated (n = 56) and all patients had medium to severe symptoms based on an IBS Symptom Severity Score (IBS-SSS) of ≥175. Symptom severity was reduced in both groups compared with baseline, with significant improvement in abdominal pain frequency, severity of abdominal distention, and life interference in both groups and reduction in the number of bowel movements per day in the low FODMAP diet group (Figure 1). A similar number of patients were defined as responders (IBS-SSS reduction of >50) in both treatment groups (19 in the FODMAP diet group and 17 in the traditional IBS diet group). Responders in the low FODMAP diet group had lower intake of FODMAPs at baseline, were older, and were almost exclusively female. Although IBS subtype did not affect the likelihood of response in the low FODMAP diet group, responders in the traditional IBS diet group were less likely to be patients with constipation-predominant IBS. These findings, using an active comparator with a low FODMAP diet, suggest that providing dietary advice to patients with IBS in the outpatient setting improves symptoms, regardless of whether that dietary advice is a low FODMAP or a traditional IBS diet. See page 1399. Genetics of Lynch Syndrome and IBD in African AmericansAlthough the prevalence of inflammatory bowel disease (IBD) is less in African Americans (AA) compared with Caucasian Americans, AAs have the highest incidence of and mortality from colorectal cancer (CRC) in the United States. However, little is known about the molecular genetic susceptibility of AAs, an admixed population with recent introduction of European genetic lineages into a West African–derived population, to these 2 major gastrointestinal disorders. In this issue of Gastroenterology, 2 studies begin to address this deficiency by examining the genetic susceptibility of AAs to Lynch syndrome, or hereditary nonpolyposis CRC, the most common inherited CRC syndrome, known to be caused by mutations in the DNA mismatch repair (MMR) genes, MLH1, MSH2, MSH6, PMS2 and EPCAM, and to IBD.Guindalini et al performed a retrospective study of MMR gene mutations in 920 members of 51 AA families from 13 US referral centers. Thirty-one families had MLH1 mutations, 11 had MSH2 mutations, 3 had MSH6 mutations, and 6 had PMS2 mutations. Of 39 distinctive mutations, 11 had not been described previously, including 6 in MLH1 and 2 in PMS2. The predominance of mutations in MLH1 was distinct from the mutation spectrum previously reported in individuals of European descent, where MSH2 mutations predominate. For all MMR gene mutation carriers combined, the cumulative risk of CRC to 80 years was estimated to be 36.2% for male carriers and 29.7% for female carriers. For MLH1 and MSH2 mutation carriers, the cumulative risk of CRC was even higher; 53.9% for male carriers and 45.6% for female carriers (Figure 2).Huang et al, using the Immunochip genotyping array, which has identified 163 susceptibility loci for IBD in Caucasians, performed a genetic mapping study, of 1088 AA patients with Crohn’s disease, 361 with ulcerative colitis, 62 with unknown IBD-type, and 1797 controls. Although established Caucasian associations were replicated in AAs, loci and variants were observed that had not previously been associated with IBD. The high frequency of genes associated with infectious diseases in both AAs and Caucasians with IBD supports the hypothesis that genetic susceptibility to IBD across populations may be the result of evolutionary adaptation to geographically distinct human pathogens.See pages 1446 and 1575; editorial on page 1323. Although the prevalence of inflammatory bowel disease (IBD) is less in African Americans (AA) compared with Caucasian Americans, AAs have the highest incidence of and mortality from colorectal cancer (CRC) in the United States. However, little is known about the molecular genetic susceptibility of AAs, an admixed population with recent introduction of European genetic lineages into a West African–derived population, to these 2 major gastrointestinal disorders. In this issue of Gastroenterology, 2 studies begin to address this deficiency by examining the genetic susceptibility of AAs to Lynch syndrome, or hereditary nonpolyposis CRC, the most common inherited CRC syndrome, known to be caused by mutations in the DNA mismatch repair (MMR) genes, MLH1, MSH2, MSH6, PMS2 and EPCAM, and to IBD. Guindalini et al performed a retrospective study of MMR gene mutations in 920 members of 51 AA families from 13 US referral centers. Thirty-one families had MLH1 mutations, 11 had MSH2 mutations, 3 had MSH6 mutations, and 6 had PMS2 mutations. Of 39 distinctive mutations, 11 had not been described previously, including 6 in MLH1 and 2 in PMS2. The predominance of mutations in MLH1 was distinct from the mutation spectrum previously reported in individuals of European descent, where MSH2 mutations predominate. For all MMR gene mutation carriers combined, the cumulative risk of CRC to 80 years was estimated to be 36.2% for male carriers and 29.7% for female carriers. For MLH1 and MSH2 mutation carriers, the cumulative risk of CRC was even higher; 53.9% for male carriers and 45.6% for female carriers (Figure 2). Huang et al, using the Immunochip genotyping array, which has identified 163 susceptibility loci for IBD in Caucasians, performed a genetic mapping study, of 1088 AA patients with Crohn’s disease, 361 with ulcerative colitis, 62 with unknown IBD-type, and 1797 controls. Although established Caucasian associations were replicated in AAs, loci and variants were observed that had not previously been associated with IBD. The high frequency of genes associated with infectious diseases in both AAs and Caucasians with IBD supports the hypothesis that genetic susceptibility to IBD across populations may be the result of evolutionary adaptation to geographically distinct human pathogens. See pages 1446 and 1575; editorial on page 1323. Use of Clinical and Molecular Features to Classify Pancreatic CystsLargely owing to their improved resolving power and increased utility, the incidence of pancreatic cysts continues to increase. Pancreatic cysts are classified according to pathological criteria as either serous cystadenomas, solid pseudopapillary neoplasms, mucinous cystic neoplasms, or intraductal papillary mucinous neoplasms (IPMN). Only serous cystadenomas carry no significant risk for progression to pancreatic cancer. Because pancreatic cancer is associated with such poor clinical outcomes, determining the risk a cyst poses to a patient is important for deciding whether to proceed with surgical removal. A variety of clinical criteria for determining the potential risk of a pancreatic cyst have been developed, but these approaches are imperfect, because >20% of surgically resected cysts are subsequently found to be benign, and 75% of IPMNs exhibit only low- or intermediate-grade dysplasia that also could have been observed.In this issue of Gastroenterology, Springer et al report on their efforts to stratify pancreatic cysts according to molecular and clinical criteria. This retrospective study was enabled by new technologies that include massively parallel sequencing that can be performed using 0.25 mL of cyst fluid. A total of 130 cyst fluid samples were collected at the time of surgical removal, 96 of which were IPMNs and the remaining 34 evenly distributed between the 3 remaining classifications. For 24 of the samples, cyst fluid was obtained by both endoscopic ultrasound and surgical resection. The results between the 2 sample sets were consistent.The analysis focused on 3 molecular features: mutations of 6 oncogenes (BRAF, CTNNB1, GNAS, KRAS, NRAS, and PIK3CA) and 5 tumor suppressors (CDK2NA, RNF43, SMAD4, TP53, and VHL), loss of heterozygosity of the same tumor suppressors, and an assessment for aneuploidy. The final dataset was combined with identified clinical features and analyzed with multivariate organization of combinatorial alterations, an algorithm that is able to produce a combination of molecular and clinical features that best categorize the cysts. In doing so, the authors established criteria that would potentially be able to reduce the number of unnecessary surgeries by 91%. The study provides impetus for future validation studies that utilize molecular biomarkers.See page 1501. Largely owing to their improved resolving power and increased utility, the incidence of pancreatic cysts continues to increase. Pancreatic cysts are classified according to pathological criteria as either serous cystadenomas, solid pseudopapillary neoplasms, mucinous cystic neoplasms, or intraductal papillary mucinous neoplasms (IPMN). Only serous cystadenomas carry no significant risk for progression to pancreatic cancer. Because pancreatic cancer is associated with such poor clinical outcomes, determining the risk a cyst poses to a patient is important for deciding whether to proceed with surgical removal. A variety of clinical criteria for determining the potential risk of a pancreatic cyst have been developed, but these approaches are imperfect, because >20% of surgically resected cysts are subsequently found to be benign, and 75% of IPMNs exhibit only low- or intermediate-grade dysplasia that also could have been observed. In this issue of Gastroenterology, Springer et al report on their efforts to stratify pancreatic cysts according to molecular and clinical criteria. This retrospective study was enabled by new technologies that include massively parallel sequencing that can be performed using 0.25 mL of cyst fluid. A total of 130 cyst fluid samples were collected at the time of surgical removal, 96 of which were IPMNs and the remaining 34 evenly distributed between the 3 remaining classifications. For 24 of the samples, cyst fluid was obtained by both endoscopic ultrasound and surgical resection. The results between the 2 sample sets were consistent. The analysis focused on 3 molecular features: mutations of 6 oncogenes (BRAF, CTNNB1, GNAS, KRAS, NRAS, and PIK3CA) and 5 tumor suppressors (CDK2NA, RNF43, SMAD4, TP53, and VHL), loss of heterozygosity of the same tumor suppressors, and an assessment for aneuploidy. The final dataset was combined with identified clinical features and analyzed with multivariate organization of combinatorial alterations, an algorithm that is able to produce a combination of molecular and clinical features that best categorize the cysts. In doing so, the authors established criteria that would potentially be able to reduce the number of unnecessary surgeries by 91%. The study provides impetus for future validation studies that utilize molecular biomarkers. See page 1501. Similarity of T-cell Responses in Children and Adults with Celiac DiseaseCeliac disease is an autoimmune disorder characterized by intestinal damage that is precipitated by CD4+ T lymphocytes that are reactive against wheat-derived gluten peptides presented by HLA-DQ2.5, HLA-DQ2.2, or HLA-DQ8. C disease is first manifested between the ages of 1 and 6. The prevalent belief was that the spectrum of gluten reactive CD4+ T lymphocytes was heterogenous and differed between children and adults with celiac disease. If true, different strategies for the diagnosis and treatment of celiac disease may be necessary for children and adults.In this issue of Gastroenterology, Hardy et al report on their characterization of gluten-reactive T cells from children and adults with celiac disease. They enrolled a total of 41 children and 4 adults. The subjects, who had been on gluten-free diets, were given a wheat challenge for 3 days before blood was collected. Symptoms consistent with celiac diseases were induced in a majority of the subjects. T cells derived from the subjects were exposed to gluten-derived peptides that included amino acid sequences representing different epitopes and peptides that were deamidated. T-cell activation after exposure to a variety of different peptides was assessed using an interferon (IFN)-γ enzyme-linked immunospot assay. The assay measures the IFN-γ secreted by activated T cells with an enzyme-linked immunosorbent assay. The most dominant peptides in eliciting a T-cell response were ranked within each test subject. The 4 most potent peptides were consistent in all age groups, including comparisons between adults and children. Consistent with previous work, deamidated peptides were significantly more potent than their amidated versions. The experiments were performed on patients from England, Italy, Norway, and Australia; and all demonstrated similar results. The T-cell response to specific gluten peptides, therefore, develops early in the course of the disease and remains consistent throughout its natural history. The authors established that there is no difference in T-cell reactivity to peptides between children and adults with celiac disease.See page 1541. Celiac disease is an autoimmune disorder characterized by intestinal damage that is precipitated by CD4+ T lymphocytes that are reactive against wheat-derived gluten peptides presented by HLA-DQ2.5, HLA-DQ2.2, or HLA-DQ8. C disease is first manifested between the ages of 1 and 6. The prevalent belief was that the spectrum of gluten reactive CD4+ T lymphocytes was heterogenous and differed between children and adults with celiac disease. If true, different strategies for the diagnosis and treatment of celiac disease may be necessary for children and adults. In this issue of Gastroenterology, Hardy et al report on their characterization of gluten-reactive T cells from children and adults with celiac disease. They enrolled a total of 41 children and 4 adults. The subjects, who had been on gluten-free diets, were given a wheat challenge for 3 days before blood was collected. Symptoms consistent with celiac diseases were induced in a majority of the subjects. T cells derived from the subjects were exposed to gluten-derived peptides that included amino acid sequences representing different epitopes and peptides that were deamidated. T-cell activation after exposure to a variety of different peptides was assessed using an interferon (IFN)-γ enzyme-linked immunospot assay. The assay measures the IFN-γ secreted by activated T cells with an enzyme-linked immunosorbent assay. The most dominant peptides in eliciting a T-cell response were ranked within each test subject. The 4 most potent peptides were consistent in all age groups, including comparisons between adults and children. Consistent with previous work, deamidated peptides were significantly more potent than their amidated versions. The experiments were performed on patients from England, Italy, Norway, and Australia; and all demonstrated similar results. The T-cell response to specific gluten peptides, therefore, develops early in the course of the disease and remains consistent throughout its natural history. The authors established that there is no difference in T-cell reactivity to peptides between children and adults with celiac disease. See page 1541. Consistency in Polyclonal T-cell Responses to Gluten Between Children and Adults With Celiac DiseaseGastroenterologyVol. 149Issue 6PreviewDeveloping antigen-specific approaches for diagnosis and treatment of celiac disease requires a detailed understanding of the specificity of T cells for gluten. The existing paradigm is that T-cell lines and clones from children differ from those of adults in the hierarchy and diversity of peptide recognition. We aimed to characterize the T-cell response to gluten in children vs adults with celiac disease. Full-Text PDF Diet Low in FODMAPs Reduces Symptoms of Irritable Bowel Syndrome as Well as Traditional Dietary Advice: A Randomized Controlled TrialGastroenterologyVol. 149Issue 6PreviewA diet with reduced content of fermentable short-chain carbohydrates (fermentable oligo-, di-, monosaccharides, and polyols [FODMAPs]) has been reported to be effective in the treatment of patients with irritable bowel syndrome (IBS). However, there is no evidence of its superiority to traditional dietary advice for these patients. We compared the effects of a diet low in FODMAPs with traditional dietary advice in a randomized controlled trial of patients with IBS. Full-Text PDF A Combination of Molecular Markers and Clinical Features Improve the Classification of Pancreatic CystsGastroenterologyVol. 149Issue 6PreviewThe management of pancreatic cysts poses challenges to both patients and their physicians. We investigated whether a combination of molecular markers and clinical information could improve the classification of pancreatic cysts and management of patients. Full-Text PDF Deciphering the Genetic Code of Gastrointestinal Diseases Among African AmericansGastroenterologyVol. 149Issue 6PreviewThe susceptibility of individuals to diseases is influenced by a complex interplay of their genetic makeup and interaction with the environment. Although we cannot change our genes, lifestyle modification and appropriate disease-specific medical interventions including screening may significantly minimize its risk or alter the course of disease. To prevent disease or treat it optimally, a thorough understanding of its pathogenesis is required. For many common diseases, ancestral events such as exposure to specific pathogens have shaped genetic susceptibility. Full-Text PDF Mutation Spectrum and Risk of Colorectal Cancer in African American Families with Lynch SyndromeGastroenterologyVol. 149Issue 6PreviewAfrican Americans (AAs) have the highest incidence of and mortality resulting from colorectal cancer (CRC) in the United States. Few data are available on genetic and nongenetic risk factors for CRC among AAs. Little is known about cancer risks and mutations in mismatch repair (MMR) genes in AAs with the most common inherited CRC condition, Lynch syndrome. We aimed to characterize phenotype, mutation spectrum, and risk of CRC in AAs with Lynch syndrome. Full-Text PDF Characterization of Genetic Loci That Affect Susceptibility to Inflammatory Bowel Diseases in African AmericansGastroenterologyVol. 149Issue 6PreviewInflammatory bowel disease (IBD) has familial aggregation in African Americans (AAs), but little is known about the molecular genetic susceptibility. Mapping studies using the Immunochip genotyping array expand the number of susceptibility loci for IBD in Caucasians to 163, but the contribution of the 163 loci and European admixture to IBD risk in AAs is unclear. We performed a genetic mapping study using the Immunochip to determine whether IBD susceptibility loci in Caucasians also affect risk in AAs and identify new associated loci. Full-Text PDF
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