Post-infectious Functional Dyspepsia Research Articles

Post-COVID-19 Gastro-Intestinal Disturbances.

Since the end of 2019, SARS-CoV-2 has been responsible for the multisystemic hyper-inflammatory disease, namely, COVID-19, as a majorly impactful pandemic. Gastrointestinal (GI) symptoms occurring during and after disease are gaining increasing attention among experts. We briefly review and comment on preliminary and recent evidences on prevalence, pathophysiology, and perspective treatment options for GI disturbances during and after COVID-19. Several reports from the literature show a significant portion of COVID-19 patients suffering from GI symptoms both at the early stages of the disease and after the end of it, sometimes for several months, namely "long-COVID-19" patients, irrespective of vaccination. An unsolved issue regarding COVID-19 is the association between GI symptoms and the outcome of COVID-19 patients. Several studies and metanalyses suggest a worse evolution of COVID-19 in patients presenting with GI symptoms. However, these data have not been agreed. Indeed, only one uniform observation can be found in the literature: patients with chronic liver disease have a worse outcome from COVID-19 infection. Upper and lower GI symptoms have similarities with postinfectious functional dyspepsia (FD) and irritable bowel syndrome (IBS). FD and IBS following infection are recognize as pathophysiological factor the gut microbial, which is a gut microbial quali- and quantitative unbalance, namely dysbiosis. Furthermore, several preliminary reports and ongoing clinical trials have shown gut microbiota modulation by pre-, pro- and postbiotics to be effective in changing and preventing COVID-19 natural course. GI symptoms characterize both long- and non-long-COVID-19 with a potentially significant impact on its natural course. Gut microbiota modulation seems to be a sensible target for disease treatment and/or prevention.

Functional Disorders of the Gastrointestinal Tract During the Pandemic of a New Coronavirus Infection

Aim. To analyze the literature data devoted to the study of the features of functional gastrointestinal diseases (FGID) during the pandemic of a new coronavirus infection.Key findings. Measures taken in connection with the pandemic of COVID-19 infection (introduction of lockdown, social isolation) leads to an increase in the level of depression and anxiety and, as a consequence, to an increase in the frequency and prevalence of functional dyspepsia (FD) and irritable bowel syndrome (IBS), as well as an increase in the severity of clinical symptoms of these diseases. In turn, the overcoming of COVID-19 infection contributes to an increase in the permeability of the mucous membrane of the gastrointestinal tract and the occurrence of its inflammatory changes, which lead to the development of postinfectious (postcovid) FD and postinfectious (postcovid) IBS.Conclusion. The problem of functional gastrointestinal diseases during the pandemic of a new coronavirus infection is very important and requires further research.

Postinfectious onset in functional dyspepsia is a risk factor for weight loss

Functional dyspepsia (FD) is differentiated into two subgroups: the postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). Acute gastroenteritis and Helicobacter pylori (HP) infection have been identified as risk factors for FD. It is unclear how these risk factors relate to Rome IV subgroups and their clinical impact. We aimed to study the association of postinfectious FD (PI-FD) and HP status with clinical profiles and weight loss. Consecutive FD patients were assessed for symptom frequency and severity. Patients were identified as PDS, EPS or the overlap group according to severity scores. Additionally, PI history and HP status were determined. In a cohort of 459 FD-patients, 36% were characterized as having PDS, 9% as having EPS and 55% showed overlap. PI onset and positive HP status were reported by, respectively, 20% and 14% of patients, not significantly differing between subgroups (respectively, p = 0.31 and p = 0.40). Weight loss was reported by 63% in PDS, 36% in EPS and 56% in overlap patients (p = 0.011). Only early satiety severity correlated with more severe weight loss in the PDS (r 0.31, p < 0.0001) and overlap group (r 0.38, p < 0.0001). PI-FD patients were more likely to experience weight loss (OR 2.27, p = 0.0013). HP status was not significantly associated with weight loss (p = 0.90). In this cohort, PI onset of FD symptoms emerged as a risk factor for weight loss, but was not associated with the symptom patterns of PDS, EPS or overlap subgroups. Patients with HP infection were not more likely to experience important weight loss.

Eradication of intestinal bacterial overgrowth as a treatment method for functional dyspepsia

Functional dyspepsia (FD) is one of the most common gastrointestinal functional diseases, occurring in an average of 10 % of the adult population. Recently, much attention is being paid to the infectious factor in FD pathophysiology. In addition to H. pylori infection and acute gastrointestinal infections, consideration is given to the syndrome of intestinal bacterial overgrowth (SIBO), in which the number of bacteria in the small intestine increases significantly.&#x0D; Objective — to establish the SIBO prevalence in patients with different FD subtypes and to establish the clinical and microbiological efficacy of rifaximin‑a (Alpha Normix®) at this pathology.&#x0D; Materials and methods. To refine the SIBO prevalence, 118 patients with FD were examined in three gastroenterological centers, including 45 men, 73 women aged 22 to 45 years (mean age — 35 ± 10 years). The control group consisted of 30 clinically healthy people with the mean age 33 ± 12 years. The diagnosis of FD and establishment of its subtype was performed according to Rome IV criteria. All patients underwent upper endoscopy with biopsy and H. pylori testing, which did not show any structural abnormalities. To diagnose SIBO, all patients underwent H2‑breath test with lactulose (H2‑LBT). All patients, depending on the FD subtype, received basic therapy with either a proton pump inhibitor (Omeprazole 20 mg once a day) at FD with epigastric pain syndrome (EPS) (group 1, n = 37), or prokinetic (Itopride in a dose of 50 mg three times a day) at FD with postprandial distress syndrome (PDS) (group 2, n = 36) for two weeks. Patients with positive H2‑LBT result, which predicted SIBO presence, were administered monotherapy with rifaximin‑a (Alpha Normix®) in a dose of 1200 mg/day for 10 days. The effectiveness of the treatment was assessed after 2 and 4 weeks based on the dynamics of the scores of SAGIS (Structured Assessment of Gastrointestinal Symptom) scale.&#x0D; Results. According to the positive H2‑LBT results, SIBO presence was recorded in 45 of 118 patients with FD (38.1 %) and 2 (6.6 %) subjects from the control group. Positive H2‑LBT result was significantly more often recorded in patients with FD‑PDS (45.4 %) compared with patients with FD‑EPS (28.8 %, p &lt; 0.01) and all patients with FD (38.1 %). Moreover, SIBO was significantly more common in patients with postinfectious FD (50 % of patients, p &lt; 0.01). The use of rifaximin in a dose of 1200 mg/day for 10 days was accompanied by the clinical improvement in 28 of 45 patients (62.2 %) after 4 weeks of treatment. The clinical efficacy of rifaximin in FD patients on the SAGIS scale did not differ significantly from the efficacy of PPIs and prokinetics used in FD‑EPS and FD‑PDS, respectively. After 4 weeks, in 36 of 45 patients, repeated H2‑LBT was negative, which indirectly indicated the SIBO eradication and high antibacterial efficacy of rifaximin. Rifaximin treatment was safe, and minor side effects were observed in only 3 patients (6.6 %).&#x0D; Conclusions. SIBO is quite often associated with FD and is observed in more than every third patient. In patients with FD‑PDS, SIBO was found significantly more often than in patients with FD‑EPS, which emphasizes the important role of slowing gastric emptying in the development of SIBO. Also, SIBO is significantly more common in patients with postinfectious FD, which emphasizes the important role of the intestinal microbiome in maintaining the stability of the structural and functional state of the gastrointestinal tract. The obtained data allow to consider SIBO as a possible pathogenetic factor of FD, at least in some patients. This requires timely diagnosis and correction of SIBO in patients with FD, in particular with the use of rifaximin‑a.

Functional dyspepsia in children: A study of pathophysiological factors.

Functional dyspepsia (FD) is common in children, and treatment targeted towards the altered pathophysiology can improve outcome. We evaluated FD children for abnormality of gastric accommodation and emptying, psychological stressors (PS), Helicobacter pylori (HP) infection, and post-infectious FD. Diagnosis of FD was based on ROME III criteria. Clinical evaluation including dyspeptic symptom scoring and assessment for PS was performed. Satiety drink test for gastric accommodation, gastroscopy with biopsy for HP infection, and solid meal gastric emptying were performed. Sixty-seven healthy children were enrolled for assessing PS and satiety drink test. Fifty-five FD children (33 boys, age 12 [6-18] years) with symptoms for 4 (2-48) months and dyspeptic score of 5 (1-13) were enrolled. PS were more common in FD than in controls (46/55 vs 9/67; P<0.001). Median satiety drink volume was 360mL (180-1320mL); no patients had satiety drink volume of <5th centile of healthy children. The frequency (98% vs 85%; P=0.01) and severity (65 [10-175] vs 50 [5-130]; P<0.001) of postprandial symptoms were higher in FD than in controls. Of the postprandial symptoms, pain (20.3% vs 0%; P=0.000) was present only in FD. Delayed gastric emptying was present in 6.5%, HP infection in 11%, and post-infectious FD in 13% cases. Etiological factor was identified in 87% children, with 20% having multiple factors. Abnormality of gastric sensorimotor function is seen in one-fourth of FD cases. HP infection and post-infectious FD are present in 11% and 13% cases, respectively.

Circulating Anti-cytolethal Distending Toxin B and Anti-vinculin Antibodies as Biomarkers in Community and Healthcare Populations With Functional Dyspepsia and Irritable Bowel Syndrome.

OBJECTIVES:Anti-cytolethal distending toxin B (CdtB) and anti-vinculin antibodies have been proposed as biomarkers that discriminate irritable bowel syndrome (IBS) diarrhea from inflammatory bowel disease; however, it is unknown whether they can also discriminate patients with IBS and IBS subtypes and functional dyspepsia (FD) from healthy individuals in the general population. We aimed to determine whether anti-CdtB and anti-vinculin can discriminate IBS and FD from health and from organic gastrointestinal (GI) disease.METHODS:Adults were enrolled from 2 Australian studies: (i) a random, population-based study (n = 331) with subjects diagnosed with IBS (n = 63) or FD (n = 61) by modified Rome III criteria or healthy control subjects (n = 246) who did not meet criteria for IBS and/or FD and (ii) an outpatient-based study with subjects diagnosed with IBS (n = 256) and/or FD (n = 55) or organic GI disease (n = 182) by an independent clinician. Serum levels of anti-CdtB/anti-vinculin antibodies were determined by enzyme-linked immunosorbent assay.RESULTS:There was a significantly higher mean value of anti-CdtB in FD vs healthy controls (mean = 2.46 [SD = 0.72] vs mean = 2.14 [SD = 0.77]; P = 0.005) and IBS/FD overlap vs healthy controls (mean = 2.47 [SD = 0.78] vs mean = 2.14 [SD = 0.77]; P = 0.02). There were no significant differences in anti-CdtB in IBS and FD outpatients or IBS/FD subgroups compared with patients with organic GI disease. In terms of anti-vinculin, there were no significant differences between IBS and FD and healthy controls or between IBS and FD and organic GI disease controls.DISCUSSION:We did not confirm that anti-CdtB/anti-vinculin discriminated IBS diarrhea from organic GI disease in Australian subjects. However, we did find higher anti-CdtB in FD and IBS/FD overlap vs healthy controls. Postinfectious FD may be more common than currently recognized.

E‐Poster Presentations – A2) Gastric and Duodenal

E‐Poster Presentations – A2) Gastric and Duodenal

The long-term functional consequences of acute infectious diarrhea.

The study reviews recent publications that build on previous studies showing that acute enteric infection can produce persistent dysfunction in the lower gut (postinfectious irritable bowel syndrome) and proximal gut (postinfectious functional dyspepsia). The review addresses risk factors, the pathophysiological basis of persistent gut dysfunction, and the factors that initiate and maintain it. Recent work has identified several loci of host genetic predisposition to these syndromes that focus attention on host immune responses that may lead to gut dysfunction, including changes in intestinal barrier function and cytokine responses to the initial infection. Human and animal studies identify changes in the serotonergic and cannabinoid pathways regulating visceral pain responses and gut motility. Recent work has also focused attention on the putative role of the intestinal microbiota or dysbiosis in maintaining gut dysfunction and this is reviewed in depth. The development of long-term consequences following an acute episode of gastroenteritis reflects a convergence of host factors that include genetic predisposition and psychological factors, as well as the development of intestinal dysbiosis. It is anticipated that future research will generate biomarkers of susceptibility as well as novel microbiota-directed preventive and therapeutic strategies.

Systematic review with meta-analysis: post-infectious functional dyspepsia.

The prevalence of functional dyspepsia (FD) following infectious gastroenteritis has not been systematically reviewed. To conduct a systematic review and calculate the summary odds ratio (OR) for the development of FD following infectious gastroenteritis, as compared to a control population. Published studies in PubMed, EmBASE, and Cochrane Database and abstracts from standard sources were screened for eligible studies. Data from studies meeting inclusion criteria were pooled for meta-analysis. Nineteen studies were eligible for inclusion. The mean prevalence of FD following acute gastroenteritis (AGE) was 9.55% (FD, n=909; AGE, n=9517) in adult populations. The summary OR for the development of post-infectious FD was 2.54 (95% CI=1.76-3.65) at more than 6months after AGE, as compared to the prevalence in controls within the same population. This is compared with the summary OR (3.51; 95% CI=2.05-6.00) for the development of post-infectious irritable bowel syndrome (IBS) in the same population at more than 6months after AGE. There was significant statistical heterogeneity with an I(2) of 72.8% for the summary OR of post-infectious FD. Several pathogens, including Salmonella spp., Escherichia coli O157, Campylobacter jejuni, Giardia lamblia and Norovirus have been shown to be associated with post-infectious FD symptoms. Infectious gastroenteritis is associated with an increased risk for subsequent dyspepsia as well as for irritable bowel syndrome. Post-infectious FD and post-infectious irritable bowel syndrome may represent different aspects of the same pathophysiology. Further studies will be needed to determine this.

Tu1845 In Functional Dyspepsia, Are Meal-Related Symptoms Linked to Less Drinking Capacity?

Background: Serotonin (5-HT) signaling in the small intestine is involved in motor, sensory and secretory pathways. Studies of neuroendocrine cell mapping in functional dyspepsia (FD), characterized by upper gastrointestinal motor and sensory disturbances, are scarce although it has been previously noted that there is no significant difference in numbers of 5HT cells in duodenum in post infectious FD vs. controls1. In patients with irritable bowel syndrome, another functional bowel disorder, a low density of duodenal neuroendocrine cells is also described2. Aim: To examine the content of neuroendocrine cells in the duodenum of subjects with FD, specifically the relative content of serotonin (5-HT) containing cells and to investigate a possible relationship between neuroendocrine cell numbers and FD subtypes. Methods: A random sample of an adult Swedish population (n = 1000) (the Kalixanda study) underwent upper endoscopy and biopsies taken from the duodenal bulb (D1) and the second part of duodenum (D2). From this study 23 subjects with FD were identified, 13 with postprandial distress syndrome (PDS), 10 with epigastric pain syndrome (EPS) and 12 healthy controls. Immunocytochemistry was performed for Chromogranin A (CGA) and 5-HT. Positive cells were quantified per mm2. Results: Cases and controls showed similar demographics. The number of CGA stained cells was significantly lower in FD patients both in D1 (p = 0.01) and D2 (p = 0.04) whereas there was no significant difference in 5-HT content. See figure. When EPS and PDS were studied separately, the number of CGA stained cells was significantly decreased in D1 in patients with EPS (p = 0.03). Conclusions: The number of duodenal neuroendocrine cells is decreased in FD compared with control subjects, but this is not due to a reduction in the number of 5-HT containing cells. It is possible that this reduction reflects reduced cellular densities of other hormones (e.g. somatostatin) which could result in a high secretion of gastric acid, with a change in motility or visceral sensitivity leading to dyspeptic symptoms in these cases. 1. Futagami S et al. Am J Gastroenterol. 2010 ;105:1835-42. 2. El-Salhy M et al. Scand J Gastroenterol. 2010 ;45:1435-9.

Tu1842 Neuroendocrine Cells in the Duodenum in Functional Dyspepsia

Background: Serotonin (5-HT) signaling in the small intestine is involved in motor, sensory and secretory pathways. Studies of neuroendocrine cell mapping in functional dyspepsia (FD), characterized by upper gastrointestinal motor and sensory disturbances, are scarce although it has been previously noted that there is no significant difference in numbers of 5HT cells in duodenum in post infectious FD vs. controls1. In patients with irritable bowel syndrome, another functional bowel disorder, a low density of duodenal neuroendocrine cells is also described2.Aim: To examine the content of neuroendocrine cells in the duodenum of subjects with FD, specifically the relative content of serotonin (5-HT) containing cells and to investigate a possible relationship between neuroendocrine cell numbers and FD subtypes. Methods: A random sample of an adult Swedish population (n = 1000) (the Kalixanda study) underwent upper endoscopy and biopsies taken from the duodenal bulb (D1) and the second part of duodenum (D2). From this study 23 subjects with FD were identified, 13 with postprandial distress syndrome (PDS), 10 with epigastric pain syndrome (EPS) and 12 healthy controls. Immunocytochemistry was performed for Chromogranin A (CGA) and 5-HT. Positive cells were quantified per mm2. Results: Cases and controls showed similar demographics. The number of CGA stained cells was significantly lower in FD patients both in D1 (p = 0.01) and D2 (p = 0.04) whereas there was no significant difference in 5-HT content. See figure. When EPS and PDS were studied separately, the number of CGA stained cells was significantly decreased in D1 in patients with EPS (p = 0.03). Conclusions: The number of duodenal neuroendocrine cells is decreased in FD compared with control subjects, but this is not due to a reduction in the number of 5-HT containing cells. It is possible that this reduction reflects reduced cellular densities of other hormones (e.g. somatostatin) which could result in a high secretion of gastric acid, with a change in motility or visceral sensitivity leading to dyspeptic symptoms in these cases. 1. Futagami S et al. Am J Gastroenterol. 2010 ;105:1835-42. 2. El-Salhy M et al. Scand J Gastroenterol. 2010 ;45:1435-9.

Tu1844 Symptom Stability and Economic Burden in Patients With Functional Dyspepsia: Observational 12 Month Follow-Up After a Short-Term Clinical Trial

Background: Serotonin (5-HT) signaling in the small intestine is involved in motor, sensory and secretory pathways. Studies of neuroendocrine cell mapping in functional dyspepsia (FD), characterized by upper gastrointestinal motor and sensory disturbances, are scarce although it has been previously noted that there is no significant difference in numbers of 5HT cells in duodenum in post infectious FD vs. controls1. In patients with irritable bowel syndrome, another functional bowel disorder, a low density of duodenal neuroendocrine cells is also described2.Aim: To examine the content of neuroendocrine cells in the duodenum of subjects with FD, specifically the relative content of serotonin (5-HT) containing cells and to investigate a possible relationship between neuroendocrine cell numbers and FD subtypes. Methods: A random sample of an adult Swedish population (n = 1000) (the Kalixanda study) underwent upper endoscopy and biopsies taken from the duodenal bulb (D1) and the second part of duodenum (D2). From this study 23 subjects with FD were identified, 13 with postprandial distress syndrome (PDS), 10 with epigastric pain syndrome (EPS) and 12 healthy controls. Immunocytochemistry was performed for Chromogranin A (CGA) and 5-HT. Positive cells were quantified per mm2. Results: Cases and controls showed similar demographics. The number of CGA stained cells was significantly lower in FD patients both in D1 (p = 0.01) and D2 (p = 0.04) whereas there was no significant difference in 5-HT content. See figure. When EPS and PDS were studied separately, the number of CGA stained cells was significantly decreased in D1 in patients with EPS (p = 0.03). Conclusions: The number of duodenal neuroendocrine cells is decreased in FD compared with control subjects, but this is not due to a reduction in the number of 5-HT containing cells. It is possible that this reduction reflects reduced cellular densities of other hormones (e.g. somatostatin) which could result in a high secretion of gastric acid, with a change in motility or visceral sensitivity leading to dyspeptic symptoms in these cases. 1. Futagami S et al. Am J Gastroenterol. 2010 ;105:1835-42. 2. El-Salhy M et al. Scand J Gastroenterol. 2010 ;45:1435-9.

Su2031 Postinfectious Irritable Bowel Syndrome and Functional Dyspepsia Following an Outbreak of Tap Water Contamination

Su2031 Postinfectious Irritable Bowel Syndrome and Functional Dyspepsia Following an Outbreak of Tap Water Contamination

Postinfectious Chronic Gut Dysfunction: From Bench to Bedside

The relationship between acute infectious gastroenteritis and the subsequent development of chronic gastrointestinal dysfunction has been established on the basis of clinical observations, prospective and epidemiological clinical studies, and from animal models. Clinically, two specific syndromes have been identified: postinfectious irritable bowel syndrome and postinfectious functional dyspepsia. These syndromes may develop in up to 30% of patients with gastroenteritis and both host and microbial risk factors have been identified. Initially, these conditions were considered to be short lived but recent epidemiological data indicate that they can persist for at least 8 years or more. Studies on animal models as well as in patients have identified changes in intestinal barrier and motor functions, as well as evidence of immune activation and low-grade inflammation. These findings prompt ongoing research into the role of anti-inflammatory medication treatment for these conditions. In addition, current research examines possible changes in the intestinal microbiota as a basis for the low-grade inflammation and symptom generation. The long-term consequences of these syndromes remain to be determined.

PWE-175 Duodenal eosinophilia and early satiety in functional dyspepsia (FD): confirmation of a positive biomarker association for FD in an Australian Cohort

IntroductionFunctional dyspepsia (FD), defined by unexplained pain or discomfort centred in the upper abdomen, affects 15% of the population. Diagnosis and treatment of FD based on the symptom-based Rome III...

975 Duodenal Eosinophilia and Early Satiety in Functional Dyspepsia (FD): Confirmation of a Positive Biomarker Association for FD in an Australian Cohort

Introduction Functional dyspepsia (FD), defined by unexplained pain or discomfort centred in the upper abdomen, affects 15% of the population. Diagnosis and treatment of FD based on the symptom-based Rome III criteria remains challenging. Recently, subtle eosinophilic inflammation in the duodenum has been implicated in the pathophysiology of FD in adults based on a Swedish case-control study. 1 Specifically, increased eosinophils in early satiety and postprandial distress have been replicated in the UK, 2 in paediatric dyspepsia in the USA 3 and in post-infectious FD in Japan, 4 but the association remains controversial. The aim of this study was to characterise upper gastrointestinal tract pathology in an Australian cohort and correlate this with available clinical data in FD cases and controls. Methods Patients prospectively referred for an upper gastrointestinal endoscopy (n=55; mean age, 49.6 years; 61.8% female) were entered to the study (with informed consent), stratified to FD cases (n=33) and controls (n=22) by Rome II criteria and completed a validated Bowel Symptom Questionnaire. Two blinded independent observers assessed the eosinophil count in five high power fields, in the duodenal bulb (D1) and second part (D2). H pylori status was assessed by gastric histology. Associations with clinical symptoms were assessed by Mann–Whitney U test. Results Cases and controls were demographically similar. There was a significant increase in eosinophils in D1 vs D2 for both cases (p=0.0003) and controls (p=0.008). Abdominal pain was associated with eosinophilia in both D1 (p=0.03) and D2 (p=0.007). Duodenal eosinophilia was significantly increased in subjects experiencing early satiety, (p=0.015). This association remained after exclusion of coeliac disease (n=2) and H pylori (n=9, 16%) (p=0.04) in D2 but not in D1. Subjects who “felt food staying in their stomach” similarly had increased D2 eosinophilia (p=0.002); this remained significant on exclusion of coeliac disease and H pylori (p=0.004). Smoking was also associated with eosinophilia in D2 (p=0.008). Conclusion Data supporting subtle duodenal eosinophilia in subsets of FD has become credible. The potential role of duodenal eosinophils as biomarkers has implications for diagnosis and therapeutic trials. Competing interests None declared.

Current understanding of pathogenesis of functional dyspepsia

Functional dyspepsia (FD) is a disorder in which upper abdominal symptoms occur in the absence of organic disease that explains them. Many pathogenic factors have been proposed for FD, including motility abnormalities, visceral hypersensitivity, psychosocial factors, excessive gastric acid secretion, Helicobacter pylori, genetics, environment, diet, lifestyle, and post-infectious FD. Many of those pathogenic factors are also common to irritable bowel syndrome and other functional gastrointestinal disorders, so understanding FD offers a glimpse into the nature of functional gastrointestinal disorders in general. Motility abnormalities and visceral hypersensitivity are thought to be important in the manifestation of FD symptoms, but the other factors are also thought to contribute by interacting and modifying motility and visceral hypersensitivity.

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Functional Dyspepsia: Eosinophils, Macrophages, and the Postinfectious State

Futagami S, Shindo T, Kawagoe T, et al. (Division of Gastroenterology, Department of Internal Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan). Migration of eosinophils and CCR2-/CD68-double positive cells into the duodenal mucosa of patients with postinfectious functional dyspepsia. Am J Gastroenterol 2010;105:1835–1842.

Duodenal Implications in the Pathophysiology of Functional Dyspepsia

Functional dyspepsia (FD) is a heterogeneous disorder associated with diverse pathophysiologic mechanisms. Studies have shown duodenal implications in the pathophysiology of FD. Duodenal hypersensitivity to acid, increased duodenal acid exposure, and abnormal responses to duodenal lipids or released cholecystokinin have been observed in patients with FD. Moreover, there is evidence indicating duodenal immune activation in FD. Alterations in the number of duodenal eosinophils or intraepithelial lymphocytes have been reported in a subset of FD patients, particularly in patients with post-infectious FD. Whether these abnormalities in the duodenum play a crucial role in the generation of dyspeptic symptoms needs to be elucidated. Further investigations on the relationship between duodenal abnormalities and well-known pathophysiologic mechanisms of FD are required. Furthermore, the causative factors related to the development of duodenal abnormalities in FD warrant further study.