Real-time evaluation of dyspeptic symptoms and gastric motility induced by duodenal acidification using noninvasive transnasal endoscopy

Background  Although different pathophysiological mechanisms have been suggested to be involved in functional dyspepsia, a practical method to clarify them has not been established. The aim of this study was to evaluate dyspeptic symptoms and gastric motility induced by duodenal acidification using transnasal endoscopy. Methods  Fourteen healthy volunteers (mean age, 32 years) were enrolled. Transnasal endoscopy was performed on all fasting volunteers. Dyspeptic symptoms and antral contractions were evaluated before and after duodenal infusions of pure water (20 ml/min for 5 min) and acid (0.1 N HCl, 20 ml/min for 5 min). The severity of various symptoms was assessed by each subject using a 10-cm visual analog scale every 2 min. The maximum severity scale was calculated as the mean of the individual maximum values. The motility number was defined as the mean number of antral contractions in 1 min. Results  The maximum severity score for a heavy feeling in the stomach and other symptoms significantly increased after the acid infusion compared with after the pure water infusion. During pure water infusion, there were no changes in the motility number. On the other hand, the motility number significantly decreased after duodenal acidification (before vs. after, 2.93 ± 0.12 times vs. 1.11 ± 0.23 times, P < 0.0001). Conclusions  Duodenal acid exposure induces dyspeptic symptoms and inhibits antral motility. Transnasal endoscopy enabled us to evaluate both dyspeptic symptoms and gastric motility simultaneously.     

Dyspeptic patients with visceral hypersensitivity: sensitisation of pain specific or multimodal pathways?

BACKGROUND AND AIMS: Patients with functional dyspepsia who have hypersensitivity to gastric distension have more prevalent pain, suggesting the presence of hyperalgesia. It is unclear whether this reflects activation of pain specific afferent pathways or multimodal afferent pathways that also mediate non-painful sensations. In the former case, hyperalgesia should occur when intensity of non-painful sensations is still low. The aim of the study was to analyse whether the symptom profile during gastric dissentions in functional dyspepsia patients with hyperalgesia reflects sensitisation of pain specific or multimodal pathways. METHODS: Forty eight consecutive dyspeptic patients (35 female) underwent gastric sensitivity testing with a barostat balloon using a double random staircase protocol. At the end of every distending step, patients scored perception of upper abdominal sensations on a graphic 0-6 rating scale and completed visual analogue scales (VAS 0-100 mm) for pain, nausea, satiety, and fullness. The end point was a rating scale of 5 or more. RESULTS: Hypersensitivity was present in 20 patients (40%); gastric compliance did not differ between normo- and hypersensitive patients. At maximal distension (score 5 or more), hypersensitive patients had significantly lower distending pressures and intra-balloon volumes, but similar VAS scores for pain, nausea, satiety, and fullness compared with normosensitive patients. In both normosensitive and hypersensitive patients, elevation of pain VAS scores with increasing distending pressures paralleled the elevation in VAS scores for nausea, satiety, and fullness. CONCLUSIONS: Hypersensitive dyspeptic patients reach the same intensity of painful and non-painful sensations as normosensitive patients but at lower distending pressures. Hyperalgesia occurs in hypersensitive dyspeptic patients at distending pressures that also induce intense non-painful sensations. These findings argue against isolated upregulation of pain specific afferents in functional dyspepsia patients with visceral hypersensitivity.     

Nutrient-specific modulation of gastric mechanosensitivity in patients with functional dyspepsia

Intraduodenal lipid infusion induces symptoms and increases sensitivity to gastric distension in patients with functional dyspepsia. To test whether these effects are specific for lipid, we compared the effects of intraduodenal infusions of either lipid or glucose on symptoms and gastric sensory and motor responses to gastric distension. Eighteen dyspeptic patients and nine controls were studied. The stomach was distended with a flaccid bag during isocaloric infusions (1 kcal/ml) of saline and either 10% Intralipid (nine patients) or 26.7% glucose (nine patients) into the duodenum. Dyspeptic symptoms and sensory thresholds for epigastric fullness and discomfort were assessed. Gastric pressure profiles during distensions were similar during lipid and glucose infusions in patients and controls, but both were significantly lower than during saline infusion. Lower volumes were required to induce fullness and discomfort in the patients compared with the controls. In the controls, the threshold volumes required to induce fullness and discomfort were greater during infusion of lipid and glucose than during saline infusion, but in the patients, the threshold volumes were increased during glucose infusion but further reduced during lipid infusion. Moreover, in the patients, nausea was more common during lipid than glucose infusion and did not occur during saline. The controls did not experience any symptoms during any infusion. In conclusion, intraduodenal lipid but not glucose sensitizes the stomach to distension in patients with functional dyspepsia but not in controls.     

A pilot study on duodenal acid exposure and its relationship to symptoms in functional dyspepsia with prominent nausea

BACKGROUND: Duodenal hypersensitivity to acid and decreased duodenal clearance of exogenous acid have been reported in functional dyspepsia (FD). However, the relevance of these abnormalities to spontaneous duodenal acid exposure and dyspeptic symptoms in FD is unknown. AIMS: To determine spontaneous duodenal acid exposure and its relationship with symptoms, duodenal sensitivity to acid, and the effects of a 5-HT(3) receptor antagonist on duodenal responses to acid in FD. METHODS: Eleven FD patients with prominent nausea and 11 healthy controls underwent 24-h ambulatory duodenal pH monitoring with assessment of dyspeptic symptoms. On the next day, duodenal bolus infusions of 5 ml of acid and normal saline were given in a randomized double-blind manner and repeated after ondansetron or a placebo. RESULTS: Nighttime duodenal acid exposure was similar, but FD patients had lower duodenal pH and higher duodenal % time (pH < 4) than controls during the daytime and in the second postprandial 2 h (p < 0.05). Seven patients (64%) with duodenal acid exposure above the normal range had higher severity scores for several dyspeptic symptoms including nausea. However, the symptom severity was poorly or weakly correlated to duodenal pH, and brief duodenal acid infusion did not affect any symptoms. Duodenal responses to exogenous acid were unaffected by 5-HT(3) receptor antagonism. CONCLUSIONS: Spontaneous duodenal acid exposure is increased in a subset of FD patients with prominent nausea, and this is associated with more severe dyspeptic symptoms. However, a direct relationship between duodenal acid exposure and symptom severity is lacking.     

Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia

BACKGROUND/AIMS: We aimed to evaluate the role of fat and cholecystokinin (CCK) in the pathophysiology of functional dyspepsia (FD) by investigating symptoms and plasma CCK levels following increasing doses of duodenal lipid during gastric distension, and the effect of CCK-A receptor blockade. SUBJECTS/METHODS: In study A, six FD patients were studied on three occasions during duodenal infusion of saline or lipid (1.1 (L-1) or 2 kcal/min (L-2)) and proximal gastric distensions. Six healthy subjects were also studied as controls during L-2 only. In study B, the effect of the CCK-A antagonist dexloxiglumide (5 mg/kg/h) on L-2 induced symptoms was studied in 12 FD patients. Changes in gastric volume at minimal distending pressure and plasma CCK (study A) were assessed, gastric distensions were performed using a barostat, and dyspeptic symptoms were monitored. RESULTS: Lipid increased gastric volume compared with saline (DeltaV (ml): saline 15 (20), L-1 122 (42), L-2 114 (28)) in patients and even more so in controls (221 (37); p<0.05). During distensions, symptoms were greater during L-2 than during saline or L-1, and greater in patients than in controls, while gastric compliance was smaller in patients than in controls (p<0.05). Lipid increased plasma CCK levels in patients and controls (p>0.05). Dexloxiglumide abolished the increase in gastric volume (DeltaV (ml): dexloxiglumide 17 (9), placebo 186 (49)) and dyspeptic symptoms (sum of scores: dexloxiglumide 24 (7), placebo 44 (19)) during duodenal lipid infusion. Dexloxiglumide also reduced gastric compliance (ml/mm Hg: dexloxiglumide 51 (7), placebo 72 (11)) and symptoms (sum of scores: dexloxiglumide 101 (17), placebo 154 (21)) during gastric distension. CONCLUSION: CCK-A receptors are involved in the generation of dyspeptic symptoms by duodenal lipid during gastric distension.     

Role of autonomic dysfunction in patients with functional dyspepsia

BACKGROUND: The role of autonomic dysfunction in patients with functional dyspepsia is not completely understood. AIMS: 1. to prospectively assess abnormalities of autonomic function in patients with functional dyspepsia, 2. to assess whether autonomic dysfunction in these patients is associated with a. visceral hypersensitivity or b. delayed gastric emptying or c. severity of dyspeptic symptoms. PATIENTS: A series of 28 patients with functional dyspepsia and 14 healthy volunteers without gastrointestinal symptoms were studied. METHODS: All patients and controls were submitted to a battery of five standard cardiovascular autonomic reflex tests, dyspeptic questionnaire, gastric barostat tests and gastric emptying tests. RESULTS: 1. Autonomic function tests showed that both sympathetic and parasympathetic scores of dyspeptic patients were significantly higher than in controls; 2. visceral hypersensitivity was confirmed in dyspeptics in response to proximal gastric distension, demonstrating lower pain threshold; 3. delayed gastric emptying occurred more frequently in patients with functional dyspepsia than in controls; 4. epigastric pain and epigastric burning were significantly more prevalent in patients with definite evidence of autonomic dysfunction; 5. No significant association was found between presence of autonomic dysfunction and presence of visceral hypersensitivity or presence of delayed gastric emptying in patients with functional dyspepsia. CONCLUSIONS: We concluded that a possible role of autonomic dysfunction in eliciting dyspeptic symptoms could not be determined from alterations in visceral hypersensitivity or delayed gastric emptying. Autonomic dysfunction might not be the major explanation for symptoms associated with functional dyspepsia.     

Neurotensin-like immunoreactivity released into the portal vein by duodenal acidification in the dog

The present study in the dog evaluates neurotensin as a potential hormone, mediating the inhibition of gastric acid secretion by duodenal acidification. Histamine-stimulated acid output was determined before and during duodenal acidification. Portal vein blood was obtained and assayed for carboxy-terminal neurotensin-like immunoreactivity (NTLI). Duodenal perfusion with 15 mmol HCL for 30 min significantly inhibited histamine-stimulated acid output to 67% of control output. This inhibition was not associated with any change in the peripheral plasma NTLI, but the portal plasma NTLI was significantly elevated from 27 to 78 pM. The effect of duodenal acidification on liver extract meal-stimulated acid secretion was determined in a second group of dogs without portal vein catheter. Duodenal perfusion with 15 mmol HCl for 30 min significantly inhibited meal-stimulated acid secretion to 37% of control output. Intravenous infusion of synthetic neurotensin to a plasma level of 130 pM was required to inhibit meal-stimulated acid output significantly. In summary, NTLI is elevated in portal, but not peripheral, plasma after duodenal acidification. The associated inhibition of acid secretion is not due to hormonal action of neurotensin.     

Luminal Stimuli Acutely Sensitize Visceromotor Responses to Distension of the Rat Stomach

Inflammation can enhance responses to different stimuli consistent with the development of hypersensitivity. To determine whether sequentially applied stimuli interact, we determined visceromotor responses (VMR) to gastric distension, measured at baseline and 60 min after instillation of saline, glycocholic acid (GCA) or ethanol through a gastrostomy in controls and rats with gastric ulcers. In another series of experiments, chemicals were administered before and 60 min after repeated distension of the stomach. Ethanol, but not saline or GCA, increased VMR in controls with a more significant rise in rats with gastric ulcerations. GCA increased responses to gastric distension in controls, whereas GCA and ethanol enhanced responses to gastric distensions in rats with gastric ulcers. Responses to saline, GCA, or ethanol were not affected by repeated noxious distension of the stomach. Luminal stimuli can trigger visceromotor responses and sensitize gastric afferents to mechanical stimulation, thus potentially contributing to dyspeptic symptoms. Supported by a grant from the National Institutes of Health (NS 35790).     

Pathophysiology of functional dyspepsia

Functional dyspepsia is a highly prevalent symptom complex and a heterogeneous disorder. Recent studies showed potential associations between specific pathophysiologic disturbances and dyspeptic symptoms. Delayed gastric emptying reported in about 30% of patients with functional dyspepsia is associated with the symptoms of postprandial fullness, nausea, and vomiting. Impaired gastric accommodation present in 40% of functional dyspepsia patients is found to be associated with early satiety. Hypersensitivity to gastric distension is observed in 37% of functional dyspepsia patients and associated with the symptoms of postprandial pain, belching, and weight loss. Psychosocial factors and altered response to duodenal lipids or acid have also been identified as pathophysiologic mechanisms.     

Effect of the 5-HT3 receptor antagonist, ondansetron, on gastric size in dyspeptic patients with impaired gastric accommodation

BACKGROUND: A reduction of gastric accommodation after a meal has been documented in patients with idiopathic dyspepsia. In these patients the administration of a 5-HT3 receptor antagonist may reduce some of the dyspeptic symptoms; it is not clear however, whether these drugs influence gastric adaptation to distension as well. AIM: To evaluate the effects of the 5-HT3 receptor antagonist, ondansetron, on gastric distension after a liquid meal in dyspeptic patients with reduced gastric accommodation. METHODS: Before and after a 500 ml water load, gastric accommodation (area of the proximal and distal stomach) was evaluated using real-time ultrasonography in 21 idiopathic dyspepsia patients and 26 healthy controls. In dyspeptic patients, the test was repeated twice: after the administration of placebo and after ondansetron 8 mg i.v. (in both cases, 15 min prior to the water load). Secondary outcomes were epigastric pain, fullness and nausea as assessed by a visual analogue scale at basal and after ondansetron. RESULTS: Fasting gastric size was similar in dyspeptic and controls. Compared with controls, dyspeptic patients showed a statistically significant smaller area of the proximal stomach (14.7+/-1.2 cm(2) vs. 18.6+/-1.4 cm(2), respectively; p=0.0247). In dyspeptic patients, gastric proximal and distal size did not change significantly following placebo, whereas after the administration of ondansetron the mean area of the proximal and distal stomach significantly increased (proximal stomach: 14.6+/-1.6 cm(2) placebo, 20.4+/-1.9 cm(2) ondansetron, p=0.0095; distal stomach: 8.9+/-0.9 placebo, 11.4+/-1.2cm(2) ondansetron, p=0.0409). Of the symptoms, only nausea was significantly reduced after ondansetron. CONCLUSION: In dyspeptic patients with impaired gastric accommodation, ondansetron reverts gastric accommodation to within the range of controls.     

Abnormal clearance of exogenous acid and increased acid sensitivity of the proximal duodenum in dyspeptic patients

BACKGROUND & AIMS: Although acid is likely to play a role in the genesis of symptoms in dyspeptic patients, most studies have failed to show an increase in gastric acid secretion. The aim of this study was to investigate clearance of acid from the duodenum and its relationship with symptoms in patients with functional dyspepsia. METHODS: Twelve patients and 10 healthy volunteers were studied using an assembly allowing recording of pressures and pH. Acid and saline were infused intraduodenally during phase II and postprandially. Sensations were scored before and 1 and 5 minutes after each infusion. RESULTS: After acid infusion in the fasting period, a greater increase in acidity in the duodenal bulb (P = 0.007) and fewer duodenal pressure waves (P = 0.002) were observed in dyspeptic patients. No significant differences in the time with pH < 4 and duodenal motor activity were observed in the postprandial period. Acid infusion reproducibly increased the sensation of nausea in patients (P < 0.001) but not in the controls. Saline infusion had no effect on upper gastrointestinal sensations. CONCLUSIONS: In fasting dyspeptic patients, clearance of exogenous acid from the duodenal bulb and duodenal motor activity are decreased. The duodenal bulb in dyspeptic patients is hypersensitive to acid infusion, which induces the nausea.     

Water load test before and after PPI therapy in patients with gastro-oesophageal reflux disease

BACKGROUND: Patients with gastro-oesophageal reflux disease may complain of epigastric pain, bloating, early satiety, epigastric fullness, epigastric burning, nausea and vomiting. AIMS: To evaluate the symptoms in response to gastric distension and its relationship to a therapeutic course in patients with gastro-oesophageal reflux disease using the water load test, compared to healthy controls. METHODS: Thirty gastro-oesophageal reflux disease patients with grade A oesophagitis (studied before and after 4 weeks of therapy with esomeprazole, 40 mg per day) and 15 patients with reflux-related symptoms demonstrated at wireless pH monitoring (non-erosive reflux disease) were compared to 30 healthy volunteers. RESULTS: Patients with grade A oesophagitis and with reflux-related symptoms ingested significantly lower water volumes than did controls, before onset of fullness, without statistically significant difference between erosive or non-erosive gastro-oesophageal reflux disease; this variable improved in patients after treatment. Nausea scores were higher basally in patients, pre- and post-therapy, and improved after therapy. Thirty-minute fullness and bloating scores improved after therapy in all gastro-oesophageal reflux disease patients compared to controls and pre-therapy. In all pre-treatment patients, a significant correlation was found only with epigastric fullness; after treatment, there was no significant relationship between the water load and the symptom scores. CONCLUSIONS: In patients with reflux-related symptoms, with or without grade A oesophagitis, the water load test is frequently abnormal, suggesting an altered gastric function. This could explain the incomplete resolution of symptoms after treatment in some patients, and should lead to additional studies aimed at exploring gastric function in gastro-oesophageal reflux disease patients.     

Function of the proximal stomach after partial versus complete laparoscopic fundoplication

OBJECTIVES: After antireflux surgery, more than 30% of patients develop dyspeptic symptoms such as fullness and early satiety. We have previously shown that these symptoms are related to fundoplication-induced changes in proximal gastric motor and sensory function, especially impaired postprandial relaxation. We hypothesize that impaired fundus relaxation may be more pronounced after complete versus partial fundoplication. METHODS: Fasting and postprandial proximal gastric motor and sensory function were measured with an electronic barostat in patients after laparoscopic partial (n = 14) and complete (n = 14) fundoplication, in gastroesophageal reflux disease (GERD) patients (n = 12), and in healthy control subjects (n = 15). Gastric emptying and vagus nerve function tests were performed in all patients. RESULTS: Minimal distending pressure (MDP) and proximal gastric compliance were not significantly different among patients after antireflux surgery, GERD patients, and healthy controls. Maximal postprandial fundus relaxation was significantly (p < 0.01) reduced in patients after partial (267 +/- 32 ml) and complete (294 +/- 34 ml) fundoplication compared with GERD patients (448 +/- 30 ml) and healthy controls (409 +/- 25 ml). Sensations of fullness were not significantly different between patients with partial and complete fundoplication. There was a significant positive correlation between the postoperative duration and the degree of postprandial fundus relaxation (r = 0.67; p < 0.001). CONCLUSIONS: Both after complete and after partial fundoplication, proximal gastric motor function is affected, with impaired postprandial relaxation and increased sensation of fullness. These alterations are not related to the type of fundoplication but correlate significantly with the duration of the postoperative period.     

功能性消化不良患者胃排空与症状的相关性及影响因素分析

目的了解胃排空异常与消化不良症状的相关性,分析影响功能性消化不良（FD）患者胃排空的因素。方法纳入32例FD患者。量化记录餐后上腹饱胀、上腹痛、上腹烧灼感、早饱、嗳气、恶心、呕吐7组症状及静息心率。以心率的中位数将其转化为二分类变量进行非条件Logistic回归分析统计。运用核素闪烁法检测空腹固体试餐,试餐参考美国胃肠动力学会、神经胃肠学会及核医学联合推荐的标准低脂试餐以及诊断标准。结果 32例FD患者,8例（25%）T1/2延迟,7例（21.88%）Retention%2 h增加,Retention%1 h均在正常范围内。Retention%2 h正常组与Retention%2 h增加组以及T1/2正常组与T1/2延长组之间,心率均存在显著差异（P=0.031,P=0.022）,心率与Retention%2 h、T1/2存在正相关（r=0.448,P=0.01;r=0.423,P=0.016）。在控制了性别、年龄及其他症状因素的影响下,心率〉70 bpm是Retention%2 h增加、T1/2延长的独立因素（OR=12.378,P=0.042;OR=8.180,P=0.072）。在Retention%2 h正常组与Retention%2 h增加组之间恶心症状指数有显著差异（P=0.003）,恶心与Retention%2 h、T1/2存在正相关（r=0.527,P=0.002;r=0.381,P=0.032）。结论心率、恶心症状与功能性消化不良患者的胃排空存在一定相关性,在控制了性别、年龄、BMI及其他症状的因素影响下,静息心率增加、出现恶心症状可能是胃排空延缓的独立因素。     

Effect of cisapride on gastric sensitivity to distension, gastric compliance and duodeno-gastric reflexes in healthy humans

BACKGROUND AND AIMS: Visceral hypersensitivity and impaired gastric relaxation after the ingestion of a meal are frequent features in patients with functional dyspepsia. Cisapride improves dyspeptic symptoms. The study aims to evaluate whether cisapride influences gastric sensitivity to distension as well as gastric compliance and duodenogastric reflexes. PATIENTS AND METHODS: Eight healthy males were studied on two different days, each after 7 days' treatment either with placebo or cisapride 10 mg qid in randomized order. A spherical bag connected to a barostat was placed in the gastric fundus and an 8-lumen manometric catheter was positioned with 4 side holes in antrum and 4 in duodenum. During a phase II of the migrating motor complex, the intragastric bag was inflated at a constant pressure 1 mm Hg above the intra-abdominal pressure and the gastric volume was measured during intraduodenal infusion of lipids and citric acid at different rates. Once the stomach returned to the basal volume, the bag was distended according to two different protocols until subjects reported discomfort. Antroduodenal motility was measured throughout the study. RESULTS: Intraduodenal infusion of lipids and citric acid caused relaxation of gastric fundus. Relaxation was similar for lipids and acid (203 +/- 30 vs 199 +/- 43 ml), and was not influenced by cisapride and infusion rate. Cisapride did not influence gastric sensitivity to distension (10 +/- 1.5 vs 9.7 +/- 1.3 mm Hg) and gastric compliance (52.7 +/- 1.2 vs 49.8 +/- 1.8 ml/mm Hg). The antral motor index significantly decreased following infusion of acid and lipids with placebo but not with cisapride. CONCLUSIONS: Cisapride inhibits the physiological duodenoantral reflexes but does not influence either the mechanical properties of the gastric fundus nor the gastric sensitivity to distension.     

Evaluation of duodenal hypersensitivity induced by duodenal acidification using transnasal endoscopy

Background and Aim: Although duodenal hypersensitivity has been suggested as one of the causes of functional dyspepsia (FD), a practical method to clarify this has not yet been established. The aim of this study was to evaluate whether patients with FD have duodenal hypersensitivity to acid, using transnasal endoscopy. Methods: In all, 44 patients with FD and 16 healthy volunteers were enrolled, and all the subjects received transnasal endoscopy in the morning after overnight fasting. After ordinary transnasal endoscopy, an infusion tube was introduced into the duodenal bulb by transnasal endoscopy and acid (20 mL, 0.1 N HCl, 20 mL/min, 36.5°C) was injected via the infusion tube. The severity of 12 symptoms was assessed by each subject using a 100‐mm visual analogue scale. The maximum severity scale was defined as the maximum score of the symptom severity scale. The total score was defined as the aggregate score of the maximum severity scale of the 12 symptoms. The maximum severity scales and the total scores between patients with FD and healthy volunteers were evaluated. Results: The maximum severity scales of nine symptoms increased significantly more after acid infusion in patients with FD than in healthy volunteers (P < 0.05). There were significant differences in the total scores (patients with FD vs healthy volunteers 233.8 ± 37.8 vs 63.9 ± 14.6, mean ± standard error of the mean, P < 0.001). Conclusions: Duodenal acidification using transnasal endoscopy enabled the evaluation of duodenal hypersensitivity to acid in healthy volunteers and patients with FD.     

Rapid initial gastric emptying and hypersensitivity to gastric filling in functional dyspepsia: effects of duodenal lipids

OBJECTIVE: Impaired distension-induced gastric accommodation and hypersensitivity to distension have been demonstrated by gastric barostat in patients with functional dyspepsia (FD). In this study we investigated distension-induced responses to gastric filling with water in healthy volunteers and FD patients, using non-invasive ultrasonography. MATERIAL AND METHODS: Eighteen healthy volunteers and 18 FD patients were given infusions of 10 ml saline or lipid (3 kcal/ml) through a nasoduodenal tube. After tube retraction, the stomach was filled with 1000 ml water during 10 min. Intragastric volume was monitored by 3D ultrasonography, and fullness, pain and nausea were assessed. RESULTS: Compared with healthy volunteers, patients with FD had faster gastric emptying at 5 min (p = 0.0008) and reported more fullness (p = 0.006) during gastric filling with water. Prior duodenal lipid exposure reduced initial gastric emptying rate in FD patients to the level seen in healthy volunteers. However, despite similar gastric volumes, the patients still reported greater fullness (p = 0.002) and nausea (p = 0.01). CONCLUSIONS: Patients with FD had abnormally rapid initial gastric emptying of water and hypersensitivity to gastric filling. Though normalizing gastric emptying rate and volumes, duodenal lipid exposure did not improve hypersensitivity. Rapid initial gastric emptying of water might be a sign of impaired distension-induced gastric accommodation.     

Gastric hypochlorhydria is associated with an exacerbation of dyspeptic symptoms in female patients

Background

Gender and gastric acid have been suggested to be independently involved in the pathophysiology of functional dyspepsia, but the interrelationship among gender, dyspeptic symptoms, and gastric acid secretion remains to be evaluated. We sought to explore this issue in dyspeptic patients.

Methods

A total of 89 outpatients (male, 36; mean age, 55.6 years) with dyspeptic symptoms were analyzed. The degree of dyspeptic symptoms was evaluated and scored using a symptom questionnaire consisting of 3 subcategories: dysmotility-related symptoms, reflux-related symptoms, and epigastric pain-related symptoms. Stimulated gastric acid secretion was directly measured using an endoscopic gastrin test.

Results

The total symptom scores and the epigastric pain-related symptom scores were significantly higher in female patients than in male patients. The dysmotility-related and reflux-related symptom scores were also higher, but not significantly, in the female patients. Multiple regression analysis of age, gender, habitual drinking, smoking, Helicobacter pylori infection, and gastric acid secretion revealed that gender and gastric hypochlorhydria, defined as less than 2.1 mEq/10 min in the endoscopic gastrin test, were significantly associated with higher dyspeptic symptom scores. The total scores and the dysmotility-related scores were significantly higher in the patients with gastric hypochlorhydria than in those with gastric non-hypochlorhydria, and this difference was found to be present only in females.

Conclusions

Gastric hypochlorhydria in female dyspeptic patients may be involved in the exacerbation of dyspeptic symptoms. Differences in the responsiveness to gastric hypochlorhydria between males and females may be partly responsible for the gender differences in the prevalence and severity of dyspeptic symptoms.     

功能性消化不良患者胃机械感觉过敏

背景：功能性消化不良（FD）是临床上常见的症候群，其发病机制目前尚未完全阐明，现逐步认识到胃感觉过敏可能在FD的发病中起着重要作用。目的：探讨FD患者是否存在胃机械感觉过敏，同时了解胃顺应性变化。方法：应用电子恒压器对52例FD患者和15名健康对照者进行检查，采用恒压梯度扩张法扩张近端胃，获得胃机械扩张感知、不适、疼痛的压力和容积闽值，计算近端胃顺应性。结果：FD患者与健康对照者相比最小扩张压（MDP）无显著性差异：FD患者对胃机械扩张刺激的感知阈值、不适闽值、疼痛压力阈值均较健康对照者显著下降，40．4％的患者胃感知感觉过敏，46．2％的患者胃不适感觉过敏，51．9％的患者胃疼痛感觉过敏；FD患者胃感知和疼痛容积闽值较健康对照者显著降低。FD患者近端胃顺应性与健康对照组相比无显著性差异（P〉0．05）。胄机械感觉压力闽值与近端胃顺应性无关。结论：部分FD患者中存在着胃机械感觉过敏，近端胃顺应性正常。     

Causes and treatment of functional dyspepsia

Functional dyspepsia is a clinical syndrome defined by upper abdominal symptoms without identifiable cause by conventional diagnostic means. Recent studies have established that functional dyspepsia is a heterogeneous disorder in which different pathophysiologic disturbances underlie different symptom profiles. Delayed gastric emptying is associated with postprandial fullness, nausea, and vomiting; impaired accommodation is associated with early satiety and weight loss; and hypersensitivity to gastric distention is associated with epigastric pain, belching, and weight loss. The pathogenesis of functional dyspepsia is unknown but may be postinfectious in a subgroup of patients. The role of psychological disturbances and of duodenal hypersensitivity requires further study. Treatment of the underlying pathophysiologic abnormality seems logical, but options for pharmacotherapy are limited to acid suppression, prokinetic drugs, and antidepressants. Psychotherapy can be considered for refractory patients. Several novel drug therapies are under evaluation.