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 impaired 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.
Aluminum Hydroxide ; Carbonates ; Deglutition ; Gastric Acid ; Gastroesophageal Reflux ; Quality of Life ; Salivation ; Sleep Wake Disorders

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.
Burns ; Diagnosis ; Duodenum ; Dyspepsia* ; Endoscopy ; Eosinophilia ; Eosinophils ; Helicobacter pylori ; Pathology ; Peptic Ulcer ; Proton Pumps ; Serotonin

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 pre-test 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.
Anxiety ; Cytokines ; Diagnosis* ; Dyspepsia* ; Eosinophilia ; Epidemiology ; Gastroenteritis ; Gastroesophageal Reflux ; Heartburn ; Humans ; Inflammation ; Natural History ; Necrosis ; Risk Factors ; T-Lymphocytes

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.
Adult* ; Australia ; Body Mass Index ; Constipation ; Diarrhea ; Feeding Behavior ; Gastrointestinal Diseases ; Humans ; Meals ; Prevalence ; Weight Gain ; Weight Loss

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.
Abdominal Pain ; Appetite ; Surveys and Questionnaires ; Gastric Emptying ; Gastroparesis ; Humans ; Linear Models ; Postal Service ; Prevalence ; Surveys and Questionnaires ; Reference Values ; Weight Loss