Dyspepsia and Functional Dyspepsia

Talley, Nicholas J. 대한소화관운동학회 1994 Journal of Neurogastroenterology and Motility (JNM Vol.1 No.-

REVIEWS : Functional dyspepsia: new insights into pathogenesis and therapy

( Nicholas J. Talley ) 대한내과학회 2016 The Korean Journal of Internal Medicine Vol.31 No.3

One in 10 people suffer from functional dyspepsia (FD), a clinical syndrome comprising chronic bothersome early satiety, or postprandial fullness, or epigastric pain or burning. Postprandial distress syndrome (PDS, comprising early satiety and/or postprandial fullness) and epigastric pain syndrome (EPS) are increasingly accepted as valid clinical entities, based on new insights into the pathophysiology and the results of clinical trials. Diagnosis is based on the clinical history, and exclusion of peptic ulcer and cancer by endoscopy. Evidence is accumulating FD and gastroesophageal ref lux disease are part of the same disease spectrum in a major subset. The causes of FD remain to be established, but accumulating data suggest infections and possibly food may play an important role in subsets. FD does not equate with no pathology; duodenal eosinophilia is now an accepted association, and Helicobacter pylori infection is considered to be causally linked to dyspepsia although only a minority will respond to eradication. In those with EPS, acid suppression therapy is a first line therapy; consider a H2 blocker even if proton pump inhibitor fails. In PDS, a prokinetic is preferred. Second line therapy includes administration of a tricyclic antidepressant in low doses, or mirtazapine, but not a selective serotonin reuptake inhibitor.

Functional Dyspepsia: Advances in Diagnosis and Therapy

( Nicholas J. Talley ) 대한간학회 2017 Gut and Liver Vol.11 No.3

Functional dyspepsia (FD) is a common but under-recognized syndrome comprising bothersome recurrent postprandial fullness, early satiety, or epigastric pain/burning. Epidemiologically, there are two clinically distinct FD syndromes (although these often overlap clinically): postprandial distress syndrome (PDS; comprising early satiety or meal-related fullness) and epigastric pain syndrome. Symptoms of gastroesophageal reflux disease overlap with FD more than expected by chance; a subset has pathological acid reflux. The pretest probability of FD in a patient who presents with classical FD symptoms and no alarm features is high, approximately 0.7. Coexistent heartburn should not lead to the exclusion of FD as a diagnosis. One of the most exciting observations in FD has been the consistent finding of increased duodenal eosinophilia, notably in PDS. Small bowel homing T cells, signaling intestinal inflammation, and increased cytokines have been detected in the circulation, and elevated tumor necrosis factor-α levels have been significantly correlated with increased anxiety. Postinfectious gastroenteritis is a risk factor for FD. Therapeutic options remain limited and provide only symptomatic benefit in most cases. Only one therapy is known to change the natural history of FD-Helicobacter pylori eradication. Treatment of duodenal eosinophilia is under investigation. (Gut Liver 2017;11:349-357)

Non-ulcer Dyspepsia : What Measures Help?

Talley, Nicholas, J. Medical Publications Korea 1987 Medical Progress Vol.9 No.4

Role of the Duodenum in the Pathogenesis of Functional Dyspepsia: A Paradigm Shift

( Hye-kyung Jung ),( Nicholas J Talley ) 대한소화기기능성질환·운동학회(구 대한소화관운동학회) 2018 Journal of Neurogastroenterology and Motility (JNM Vol.24 No.3

Functional dyspepsia (FD) is a common disorder characterized by chronic epigastric pain or burning, or bothersome postprandial fullness or early satiation, without a definitive organic cause. The pathogenesis of FD is likely heterogeneous. Classically, motor disorders, visceral hypersensitivity, and brain-gut interactions have been implicated in the pathophysiology of FD, but recently an important role for chronic low-grade inflammation and infection in FD has been reported and confirmed. Duodenal low-grade inflammation is frequently observed in FD in those with and without documented previous gastroenteritis. Duodenal eosinophils and in some cases mast cells may together or separately play a key role, and immune activation (eg, circulating homing small intestinal T cells) has been observed in FD. Low-grade intestinal inflammation in patients with FD may provoke impairment in motor-sensory abnormalities along the gastrointestinal neural axis. Among FD patients, the risk of developing dyspeptic symptoms after a bout of gastroenteritis is 2.54 (95% CI, 1.76-3.65) at more than 6 months after acute gastroenteritis. Gut host and microbial interactions are likely important, and emerging data demonstrate both quantitative and qualitative changes of duodenal mucosal and fecal microbiota in FD. Food antigens (eg, wheat proteins) may also play a role in inducing duodenal inflammation and dyspepsia. While causation is not established, the hypothesis that FD is a disorder of microscopic small intestinal inflammation in a major subset is gaining acceptance, opening the possibility of novel treatment approaches that may be able to alter the natural history of the disorder. (J Neurogastroenterol Motil 2018;24:345-354)

Dysmotility Symptoms Are Independently Associated With Weight Change: A Population-based Study of Australian Adults

( Guy D Eslick ),( Stuart C Howell ),( Nicholas J Talley ) 대한소화기기능성질환·운동학회 2015 Journal of Neurogastroenterology and Motility (JNM Vol.21 No.4

Background/Aims Weight loss is a recognized alarm symptom for organic gastrointestinal (GI) disease, yet the association between weight change (loss or gain) and specific GI symptoms remains poorly described. We assess the associations between GI symptoms and weight change in a population-based sample of Australian adults. Methods The prevalence of 26 GI symptoms was determined by a postal survey to 5000 residents in western Sydney, Australia (60% response rate). These were classified a priori into 5 symptom groups.abdominal pain, esophageal symptoms, dysmotility symptoms, diarrhea and constipation. Weight change was measured by two items which assessed weight loss and weight gain. Clinically relevant weight change was defined as a loss or gain of 3 or more kilograms in the past 3 months. Results Prevalence estimates for clinically relevant weight loss and gain in the past 3 months were 10.3% and 8.1%, respectively. When the 5 symptom groups were evaluated simultaneously, the dysmotility symptoms of fullness after meals emerged as a predictor of both weight loss (OR, 1.57; 95% CI, 1.32-1.88; P < 0.001) and weight gain (OR, 0.85; 95% CI, 0.72-0.99; P = 0.040), which also included bloating (OR, 1.64; 95% CI 1.46-1.84; P < 0.001). The associations remained significant following adjustment for socio-economic status, body mass index, and eating behaviors. Conclusions Specific dysmotility symptoms are independently predictive of both weight loss and weight gain. Different pathogenic mechanisms may be involved. (J Neurogastroenterol Motil 2015;21:603-611)

Functional Dyspepsia

Holtmann, Gerald,Hu, Wayne H.C.,Talley, Nicholas J. Medical Publications Korea 1996 Medical Progress Vol.18 No.8

Review : Gastroesophageal Reflux Disease and Sleep Disorders: Evidence for a Causal Link and Therapeutic Implications

( Hye Kyung Jung ),( Rok Seon Choung ),( Nicholas J. Talley ) 대한소화관운동학회 2010 Journal of Neurogastroenterology and Motility (JNM Vol.16 No.1

Gastroesophageal reflux disease (GERD) and sleep disturbances are both common health problems. There is a significant association between disturbed sleep and GERD, and this may be bidirectional. Sleep disorders may induce gastrointestinal (GI) disturbances, while GI symptoms also may provoke or worsen sleep derangements. Reflux of gastric acid is a Less frequent event during sleep, however, acid clearance mechanisms (including swallowing, salivation and primary esophageal motility) are im -paired during sleep resulting in prolongation of acid contact time. Nighttime reflux can Lead to sleep disturbance and sleep disturbance may further aggravate GERD by prolonged acid contact time and heightened sensory perception. This may facilitate the occurrence of complicated GERD and decreased quality of Life. However, the interplay between sleep problems and GERD is complex, and there are still relatively Limited data on this issue. Further investigation of sleep-related GERD may identify common pathophysiological themes and new therapeutic targets.(J Neurogastroenterol Motil 2010;16:22-29)

Prevalence of Hidden Gastroparesis in the Community: The Gastroparesis "Iceberg"

( Enrique Rey ),( Rok Seon Choung ),( Cathy D Schleck ),( Alan R Zinsmeister ),( Nicholas J Talley ),( G Richard Locke ) 대한소화기기능성질환·운동학회 (구 대한소화관운동학회) 2012 Journal of Neurogastroenterology and Motility (JNM Vol.18 No.1

Background/Aims The prevalence of diagnosed gastroparesis is 24.2/100,000 inhabitants, but a large group of people with gastroparesis-like symptoms have never had a gastric emptying (GE) test. Some of them may have undiagnosed gastroparesis. Our aim was to estimate the prevalence of hidden gastroparesis in the community. Methods The study was conducted in 2 parts: (1) Patients referred for a scintigraphic GE test completed a validated questionnaire (Bowel Disease Questionnaire). Multiple linear regression models to predict 2 hours and 4 hours GE rates were developed. (2) A revised Bowel Disease Questionnaire was mailed to a random sample of 4,194 Olmsted County residents. GE rates were estimated with the models for each subject and delayed GE was considered when they were lower than normal values. Hidden gastroparesis was defined in community subjects with predicted delayed GE that had not been diagnosed with gastroparesis prior to the survey. Results The regression models for GE rates were constructed using data from 450 patients. In addition to age and gender, the symptoms found significant were nausea/vomiting, early satiety, upper abdominal pain, bloating, loss of appetite and weight loss more than 7 pounds. 2,298 (55%) community subjects returned a questionnaire. Five subjects were excluded due to a prior diagnosis of gastroparesis. When models were applied to the community survey data, 42 (1.8%) subjects were estimated to have delayed GE. Conclusions Delayed GE was estimated to occur in 1.8% of community subjects. Since the prevalence of diagnosed gastroparesis is low (0.02%), many subjects with gastroparesis may remain undiagnosed. (J Neurogastroenterol Motil 2012;18:34-42)