Gastroduodenal Motility Research Articles

Efficacy and Safety of Liraglutide in Patients With an Ileal Pouch-Anal Anastomosis and Chronic High Bowel Frequency: A Placebo-Controlled, Crossover, Proof-of-Concept Study.

After colectomy with ileoanal pouch anastomosis (IPAA), many patients develop high bowel frequency (BF) refractory to antimotility agents, despite normal IPAA morphology. Low circulating levels of glucagon-like protein-1 (GLP-1), a modulator of gastroduodenal motility, have been reported after colectomy. Double-blind crossover study of 8 IPAA patients with refractory high BF treated with daily administration of the GLP-1 receptor agonist liraglutide or placebo. Liraglutide, but not placebo, reduced daily BF by more than 35% ( P < 0.03). Larger randomized controlled studies are warranted to delineate the treatment potential of GLP-1 receptor agonists in IPAA patients suffering from noninflammatory high BF.

In silico study of luminal transport of bile salts from the duodenum to the gastric mucosa: Role of small intestinal peristalsis

Biliary reflux plays a key role in the progression of gastric carcinoma over the long term. The reflux of alkaline duodenal contents (Duodenogastric Reflux) is presumed to be mediated by changes in the gastroduodenal motility, with no clear insights into the mechanisms. Considering mechanism comes under the perspective of fluid transport, a mathematical model is formulated for investigating the transport of the bile as a non-reactive species, assuming non-Newtonian nature as the power law fluids in the antropyloroduodenal segment using lubrication approximation. An analytical approach is employed to derive the exact solutions, and further computational results are simulated using MATLAB coding. To assess the pathophysiology of reflux, transport of the bile salt was quantified for various duodenal motility patterns by considering the following peristalsis parameters, such as elementary contraction (Antegrade Propagating Wave, Retrograde Propagating Wave, and Stationary Wave), wavelength, velocity and occlusion of the wave, and frequency of the contraction. Results of the bile transport are presented for the duodenal peristalsis and analyzed for the relative displacement from its initial position across various motility patterns. The particle transport is driven by wave traversal in the vicinity at the duodenum, whereas at the pylorus and proximal pylorus, transport of the imaginary particles, such as bile salts, is accelerated by increased occlusion of the wave (particles travel longer distances owing to higher occlusion, with 90% occlusion showing more transit than 70% occlusion) and wave speed, with pylorus contributing to hydrodynamic hindrance (owing to pyloric channel width, where the resistance scales to 1/R4) with oscillatory excursion.

Pathogenetic role of cholecystokinin in functional dyspepsia

Introduction. The high prevalence of functional dyspepsia in the population requires detailing the mechanisms of its development with the definition of the role of hormones of the gastrointestinal tract in the development of clinical symptoms.Purpose of the study: to clarify the pathogenetic role of cholecystokinin in functional dyspepsia.Materials and methods. A prospective examination of 90 people aged 22.3 ± 0.17 years, divided into 3 groups, was carried out: patients with postprandial distress syndrome (PDS), patients with epigastric pain syndrome (EPS), practically healthy. The participants of the study were questioned according to the GSRS questionnaire, their anthropometric data, the concentration of cholecystokinin in the blood before and after the drinking test were determined. Statistical processing included calculation of means, their errors, Mann-Whitney U-test for independent samples and Wilcoxon W-test for related samples, Spearman’s rank correlation test.Results. Patients with EPS are characterized by a statistically significantly greater severity of abdominal pain syndrome (4.33 ± 0.51 points) than those suffering from PDS (2.47 ± 0.38 points) and healthy people (2.19 ± 0.22 points). Dyspeptic syndrome is more typical for patients with PDS (2.07 ± 0.12 points) than those with EPS (1.10 ± 0.04 points). Patients with PDS are characterized by higher values of height, hip volume, lean mass, waist to hip ratio than patients with EPS. The concentration of cholecystokinin in the blood on an empty stomach in patients with EPS (213.37 ± 14.35 pg/ml) is statistically significantly higher than in those examined with PDS (129.45 ± 10.44 pg/ml) and healthy people (146.99 ± 5.17 pg/ml). The level of cholecystokinin in the blood after water exercise in patients with PDS increased statistically significantly to 176.14 ± 8.16 pg/ml, with EPS – decreased to 187.98 ± 7.26 pg/ml. Correlations between the magnitude of cholecystokininemia and the main anthropometric data in EPS and PDS are multidirectional.Conclusion. Cholecystokinin plays an important role in the pathogenesis of gastroduodenal motility disorders in patients with functional dyspepsia.

Dispepsia funcional y gastroparesia: ¿dos entidades superpuestas? De la fisiopatología a la terapéutica

Functional dyspepsia and gastroparesis represent the most common sensory-motor disorders of the upper gastrointestinal tract. Scientific advances in the last decade have shown that there is significant overlap between them. This review aims to address current knowledge about their pathophysiology, diagnosis and treatment. Functional dyspepsia is a medical condition that is characterized by one or more of the following symptoms: early satiety, postprandial fullness, and epigastric pain or burning. The pathophysiological mechanisms involved are: the gastroduodenal motility and sensory abnormalities, the immune dysfunction, the duodenal inflammation, the gastrointestinal infections, the alterations in the gastrointestinal microbiota and the dysfunction of the gut-brain axis. The Rome IV criteria make possible to establish a presumptive diagnosis of functional dyspepsia in most patients, although it continues to be a diagnosis of exclusion that requires the performance of an upper digestive video endoscopy to confirm it. The recommended therapeutic options are: the eradication of Helicobacter pylori, the proton pump inhibitors, the tricyclic antidepressants and prokinetics. Gastroparesis is a chronic disorder characterized by delayed gastric emptying in the absence of a mechanical obstruction. The pathophysiology is caused by neuromuscular abnormalities of gastric motor function. Gastric emptying scan is the current gold standard for diagnosis. The mainstays of treatment are restoration of hydration and nutrition, and pharmacological treatment with prokinetics and antiemetics.

Changes in ghrelin, substance P and vasoactive intestinal peptide levels in the gastroduodenal mucosa of patients with morbid obesity

AimsThe aim of the study was to assess changes in levels of substance P (SP), vasoactive intestinal peptide (VIP) and ghrelin in the gastroduodenal mucosa of obese individuals, which has not been studied before. MethodsForty-six patients with a body mass index (BMI) of >40 kg/m2 and 20 patients with a BMI of 18–25 kg/m2 were included in the study. VIP and SP levels in the fundus, antrum and duodenal mucosa were measured in freshly frozen tissues using enzyme-linked immunosorbent assay (ELISA). Fasting levels of ghrelin in blood were also measured with ELISA. Tissue levels of ghrelin were assessed by immunohistochemical staining, and immunoreactivity scores were used for ghrelin evaluation in tissues. ResultsAntrum SP levels were higher in the obese group than in the control group. A significant number of obese patients had low VIP levels in the fundus and antrum. Intense ghrelin staining was observed in a limited number of cells in the mucosal area of the gastric fundus that was similar in the control and patient groups. In the antrum and duodenum, ghrelin staining was low in all the samples examined. ConclusionHere, we found that SP levels are increased, while VIP levels are decreased in the antrum of morbidly obese individuals. Previous studies show that SP increases gastroduodenal motility, that VIP slows it down, and that the gastric emptying rate is higher in obese individuals, preventing negative feedback mechanisms upon food intake. Therefore, increases in SP and decreases in VIP levels in the antrum may contribute to obesity by accelerating gastric emptying.

Bile in excess

The article presents consideration for the pathogenetic mechanisms of the occurrence of duodenogastric reflux (DGR), duodenogastroesophageal reflux (DGER), their role in the occurrence of biliary reflux gastritis and reflux esophagitis. The fundamental bases for the formation of bile reflux are the failure of the sphincter apparatus, antroduodenal dysmotility, elimination of the natural antireflux barrier. Gallbladder dysfunction and duodenal dysmotility are considered the risk factors for primary DGR. The leading mechanism for the development of DGR, DGER after cholecystectomy is a violation of gastroduodenal motility and gastroduodenal hypertension. These syndromes are formed also at gallstone disease and other organic and functional pathological conditions, including pancreatic insufficiency. The syndrome of chronic duodenal hypertension or «duodenal demon» is manifested by heaviness in the epigastrium, belching, heartburn, nausea, vomiting, flatulence, and stool disorders. It is supplemented by the phenomena of psychosomatic asthenization, decreased mental and physical performance, apathy, and a negative assessment of life prospects. The clinical features of hologenous diarrhea are considered, differential diagnostic signs of diarrhea in chronic duodenal hypertension and irritable bowel syndrome are demonstrated.The clinical and pathogenetic substantiation of the treatment of chronic duodenal hypertension accompanied by hologenous diarrhea with colloidal bismuth preparations is presented. The summary of the comparative analysis has been presented of the physicochemical and structural properties of tablet formulations, containing bismuth tripotassium subcitrate, the original drug De‑Nol (Astellas) and the generic Ulcavis (KRKA). It has been concluded that it is advisable to include Ulcavis in the treatment regimen for patients with hologenous diarrhea.

Functional Dyspepsia: Diagnostic and Therapeutic Approaches.

Functional dyspepsia is a common functional gastrointestinal (GI) disorder of gastroduodenal origin, diagnosed clinically in the presence of prototypical symptoms of epigastric pain and meal-related symptoms, and without structural explanation. The most recent diagnostic criteria provide for two functional dyspepsia subtypes, epigastric pain syndrome (EPS) and post-prandial distress syndrome (PDS) based on the predominant symptom pattern. The evaluation of dyspepsia should keep laboratory, imaging, and invasive testing to a minimum, as extensive or repetitive investigations are of rather low diagnostic yield in the absence of localizing symptoms or alarm features. Factors with etiopathologic relationships to functional dyspepsia include micro-inflammation, GI infections, abnormalities of gastroduodenal motility, visceral hypersensitivity, disturbances along the brain-gut axis, and psychological factors; all of these causative mechanisms have potential to partially explain symptoms in some functional dyspepsia patients, thus providing a rationale for the efficacy of a diversity of therapeutic approaches to functional dyspepsia. Management of dyspepsia symptoms relies upon both pharmacologic treatments and non-pharmacologic approaches, including psychological and complementary interventions. The evidence in support of established functional dyspepsia therapies is reviewed, and forms the basis for an effective functional dyspepsia treatment strategy emphasizing the patient's current symptom severity, pattern, and impact on the function and quality of life of the individual.

ATG16L1 Single Nucleotide Polymorphism Confers High Cardiac Artery Disease Risk in H. Pylori Chronic Gastritis Patients

AbstractBackground: Chronic Helicobacter pylori (HP) gastritis affects two-thirds of the world's population and is one of the most common chronic inflammatory disorders of humans, the infection clearly results in chronic mucosal inflammation in the stomach and duodenum which in turn might lead to abnormalities in gastroduodenal motility and sensitivity and is the most frequent cause of dyspepsia and peptic disease. The increased inflammatory response related to HP gastroin-testinal disease may also lead to damage in non-gastrointestinal tissues. The damage caused by HP is believed to be associated with increased inflammatory markers resulting from immune response and blood cells activation. Autophagy related gene 16 like 1 single nucleotide polymorphism (ATG16L1 SNP) may be associated with impaired autophagy which predisposes to HP persistence and chronicity. Chronic infection is a suspected risk factor for cardiac artery disease.Aim of Study: The aim of this study is to assess the association between (ATG16L1) SNP and coronary artery disease, pro-inflammatory and atherogenic risk factors in HP patients.Patients and Methods: This study was carried out on 80 patients suffering from dyspepsia and reflux symptoms. According to the urea breath test results, patients were divided into two groups: group I (45 positive H. pylori) patients and group II (35 negative H. pylori) patients as control group. All patients were subjected to full medical history taking, clinical examination and laboratory investigations included urea breath testing for H. pylori infection, complete blood count (CBC), (ATG16L1) SNP, pro-inflammatory HDL assay and high sensitivity CRP (hs-CRP) assay.Results: H. pylori gastritis patients with AG+GG genotypes had statistically higher levels of hs-CRP, N/L, P/L, pro-oxidant HDL-c index when compared to H. pylori gastritis patients with AA genotype and both patient groups had higher levels of these parameters when compared to healthy control subjectsConclusion: The ATG16L1 SNP impairs autophagy and has a role in persistence of H. pylori intracellular infection leading to chronic gastritis and increases the CAD pro-inflammatory pro-atherogenic risk factors; the mutant G allele is accused allele.

Opioid-Induced Foregut Dysfunction.

The impact of opioid use on the lower gastrointestinal tract is well described, but recent opioid crisis has caused increased awareness of the detrimental effects of these drugs on esophageal and gastroduodenal motility. Opioid use has been associated with increased incidence of spastic esophageal motility disorders and gastroduodenal dysfunction. Opioid receptors are present with high abundance in the myenteric and submucosal plexus of the enteric nervous system. Activation of these receptors leads to suppressed excitability of the inhibitory musculomotor neurons and unchecked tonic contraction of the autogenic musculature (such as the lower esophageal sphincter and the pylorus).

Gastroduodenal motility disorders.

This review summarizes recent progress in the epidemiology, pathophysiology and treatment of gastroduodenal motility disorders with an emphasis on functional dyspepsia and gastroparesis. Pathophysiological research has focused on the association of delayed emptying and impaired accommodation with symptom pattern. Studies also confirmed the presence of altered mucosal integrity and low-grade immune activation in the duodenum in functional dyspepsia, while changes in numbers of interstitial cells of Cajal and myenteric neurons were confirmed in gastroparesis. Treatment advances in gastroparesis include new prokinetics such as the ghrelin receptor agonist relamorelin and the antiemetic agent aprepitant. The efficacy and use of neuromodulators were reviewed and new management guidelines for functional dyspepsia were published. Pathophysiological research has focused on cellular changes in gastroparesis and gastroduodenal motility disorders. New treatments include relamorelin and aprepitant for gastroparesis.

Peripheral apelin mediates stress-induced alterations in gastrointestinal motor functions depending on the nutritional status.

Exposure to stress induces gastrointestinal (GI) dysmotility. In rodents, acute restraint stress (ARS) inhibits gastric emptying (GE) and intestinal transit (IT) via central and peripheral corticotropin-releasing factor (CRF)-mediated pathways. Peripherally administered apelin-13 was shown to inhibit GI motor functions; moreover, stress-induced upregulation of gastric apelin content was demonstrated in rats suggesting that peripheral apelin may mediate stress-induced alterations in GI motility. We investigated the role of endogenous peripheral apelin in stress-induced GI dysfunction. GE, IT and gastro-duodenal fasting motility were measured in non-stressed (NS), CRF-injected and ARS-loaded rats. CRF and apelin receptor antagonists astressin or F13A was administered before ARS or peripheral CRF injection. Apelin and APJ receptor expressions were determined using immunohistochemistry and quantified by qRT-PCR. Double immunofluorescence was performed for enteric neuronal apelin. GE and IT were delayed by CRF and ARS. ARS-induced changes were attenuated by F13A, whereas astressin was ineffective. CRF-induced alterations in GE and IT were restored completely by astressin, while they were diminished by F13A. Antral phase III-like contractions were disturbed following ARS which were preserved by preadministration of astressin, but not F13A. CRF impaired gastric and duodenal fasting contractions, while these changes were not altered by F13A. ARS increased apelin expression in stomach and duodenum. Apelin immunoreactivity was detected in mucosa, smooth muscles and myenteric plexi, whereas dense APJ receptor expression was observed within tunica muscularis. APJ receptor was downregulated in rats fasted overnight. These results suggest that enteric apelin acts as an inhibitor stress mediator in the postprandial state.

When a White Horse is a Horse: Embracing the (Obvious?) Overlap Between Acupuncture and Neuromodulation.

When a White Horse is a Horse: Embracing the (Obvious?) Overlap Between Acupuncture and Neuromodulation.

Peripheral Corticotropin Releasing Factor Signaling Inhibits Gastric Emptying: Mechanisms of Action and Role in Stress-related Gastric Alterations of Motor Function.

The activation of Corticotrophin Releasing-Factor (CRF) receptors in the brain is well established to coordinate the endocrine, behavioral, autonomic and visceral responses to stress. In addition, CRF receptors are also expressed within the gut where they exert biological actions and play a role in modulating stress-related gastrointestinal function. In particular, peripheral injection of CRF and related peptides, urocortin 1, 2 or 3 inhibit Gastric Emptying (GE) and alters fasted and fed pattern of gastroduodenal motility in several experimental species. Urocortin 1 interacts synergistically with cholecystokin-8 to inhibit gastric emptying in lean mice which is no longer observed in diet-induced obese rats. In in vitro circular or longitudinal muscle preparation of rat antrum, CRF and urocortin 1 and 2 suppressed spontaneous contractile activity. CRF and urocortins interact with the CRF receptor 2 (CRF-R2) to inhibit gastric motor function monitored both in vivo and in vitro. The CRF-R2 mediated inhibition of antral and corpus contractility involves a direct action on gastric myenteric neurons where CRF-R2 is expressed and may also involve the activation of serotonin acting on 5-HT3 receptor. The involvement of peripheral CRF receptors in gastric motor alterations occurring under stress conditions are stressors specific with CRF-R2 mediating the early phase of gastric ileus induced by abdominal surgery and the delayed emptying elicited by acute restraint stress. However gastric stasis elicited by endotoxin is not mediated by CRF-R2 and CRF receptors are not involved in the basal regulation of fed or fasted pattern of gastric motility.

Acute physiological and electrical accentuation of vagal tone has no effect on pain or gastrointestinal motility in chronic pancreatitis

BackgroundThe effective management of pain in chronic pancreatitis (CP) remains a therapeutic challenge. Analgesic drugs, such as opioids, and the underlying pathology can impair gut function. The autonomic nervous system influences hormone secretion and gut motility. In healthy volunteers, electrical (using noninvasive transcutaneous vagal nerve stimulation [t-VNS]) and physiological (using deep slow breathing [DSB]) modulation of parasympathetic tone results in pain attenuation and enhanced gut motility. Thus, the aims were to investigate whether t-VNS and DSB could enhance the parasympathetic tone, decrease pain sensitivity and improve gut motility in CP.Patients and methodsA total of 20 patients (12 males, mean age=61 years, range: 50–78 years) with CP were randomized to short-term (60 minutes) t-VNS and DSB, or their placebo equivalent, in a crossover design. Cardiometrically derived parameters of autonomic tone, quantitative sensory testing of bone and muscle pain pressure, conditioned pain modulation (CPM) and assessments of gastroduodenal motility with ultrasound were performed.ResultsIn comparison to sham, t-VNS and DSB increased cardiac vagal tone (CVT) (P<0.001). However, no changes in pain pressure thresholds for bone (P=0.95) or muscle (P=0.45) were seen. There was diminished CPM (P=0.04), and no changes in gastroduodenal motility were observed (P=0.3).ConclusionThis explorative study demonstrated that t-VNS and DSB increased CVT in patients with CP. However, this short-lasting increase did not affect pain sensitivity to musculoskeletal pain or gastroduodenal motility. The chronic pain in CP patients is complex, and future trials optimizing neuromodulation for pain relief and improved motility are needed.

A link between platelet to lymphocyte ratio and Helicobacter pylori infection

Chronic Helicobacter pylori gastritis affects two-thirds of the world's population and is one of the most common chronic inflammatory disorders of humans, the infection clearly results in chronic mucosal inflammation in the stomach and duodenum, which, in turn, might lead to abnormalities in gastroduodenal motility and sensitivity and is the most frequent cause of dyspepsia and peptic disease. Some studies showed that there was a correlation between low-grade inflammation as CRP and HP infection. The purpose of this study was to investigate the relationship between the presence of HP infection and platelet/lymphocyte ratio (PLR). A total of 200 patients who met the HP criteria and 180 age- and gender-matched control subjects were included in this randomized controlled trial. Patients were diagnosed to have HP according stomach biopsy and urea breath test, PLR was calculated from complete blood count at time of diagnosis and before initiating the treatment. Patients with HP infection had significantly higher PLR compared to those without HP. Moreover, the patients with symptomatic HP had higher PLR than those with asymptomatic HP. While PLR increased as the severity of HP symptoms increased (r=.452, P<.001). Our study indicated, for the first time, a significant association between HP infection and symptoms based on PLR, a simple and reliable indicator of inflammation. Furthermore, there an increase in PLR as the severity of HP increases.

Functional dyspepsia through chronic gastritis in patients with marfan syndrome and marfan-like states

The article presents the results of clinical and endoscopic examination of patients (n = 89; 33 ± 9,3 years; F : M/23 : 66) with confirmed chronic gastritis associated with hereditary disorders of connective tissue (Marfan syndrome phenotype and Marfan-like states) in order to examine the relationship associated HDCT as monogenic diseases - Marfan syndrome, as well as related pathology in the form of Marfan-like states with the clinical manifestations of functional dyspepsia and endoscopic picture of H. pylori infection in chronic gastritis. Diagnosis of Marfan syndrome was based on the revised criteria of Ghent. For the differential diagnosis with other “related” diseases of the connective tissue used syndrome diagnostic criteria of hypermobility of joints, Ehlers - Danlos syndrome. Evaluation of complaints and diagnosis of functional dyspepsia was based on the criteria of Rome III (2006) and the Florence Agreement. Evaluation of the symptoms of functional dyspepsia showed different from control (p &lt; 0,05) lower frequency of epigastric pain syndromes and postprandial distress syndrome in a group with Marfan syndrome not associated with H. pylori infection and, at the same time, does not correlate with available in this group of patients a high frequency of precancerous lesions in the gastric mucosa. Frequent endoscopic manifestations associated with the HDCT served esophagitis gastroduodenal motility disorders and the development of GERD with catarrhal esophagitis (p &lt; 0,05) and the absence of erosive and ulcerative lesions of gastroduodenal mucosa (p &lt; 0,05). The findings strongly indicate the absolute necessity of endoscopic and morphological screening regardless of the presence of gastrointestinal complaints in patients with associated HDCT.

Modulation of vagal tone enhances gastroduodenal motility and reduces somatic pain sensitivity

The parasympathetic nervous system, whose main neural substrate is the vagus nerve, exerts a fundamental antinociceptive role and influences gastrointestinal sensori-motor function. Our research question was to whether combined electrical and physiological modulation of vagal tone, using transcutaneous electrical vagal nerve stimulation (t-VNS) and deep slow breathing (DSB) respectively, could increase musculoskeletal pain thresholds and enhance gastroduodenal motility in healthy subjects. Eighteen healthy subjects were randomized to a subject-blinded, sham-controlled, cross-over study with an active protocol including stimulation of auricular branch of the vagus nerve, and breathing at full inspiratory capacity and forced full expiration. Recording of cardiac derived parameters including cardiac vagal tone, moderate pain thresholds to muscle, and bone pressure algometry, conditioned pain modulation using a cold pressor test and a liquid meal ultrasonographic gastroduodenal motility test were performed. Cardiac vagal tone increased during active treatment with t-VNS and DSB compared to sham (p=0.009). In comparison to sham, thresholds to bone pain increased (p=0.001), frequency of antral contractions increased (p=0.004) and gastroduodenal motility index increased (p=0.016) with active treatment. However, no effect on muscle pain thresholds and conditioned pain modulation was seen. This experimental study suggests that this noninvasive approach with combined electrical and physiological modulation of vagal tone enhances gastroduodenal motility and reduces somatic pain sensitivity. These findings warrant further investigation in patients with disorders characterized with chronic pain and gastrointestinal dysmotility such as functional dyspepsia and irritable bowel syndrome.

Association of Neutrophil to Lymphocyte Ratio With Presence and Severity of Gastritis Due toHelicobacter pyloriInfection

Infection with the bacterial pathogen Helicobacter pylori (HP) clearly results in chronic mucosal inflammation in the stomach and duodenum, which, in turn, might lead to abnormalities in gastroduodenal motility and sensitivity and is the most frequent cause of dyspepsia and peptic disease. Some studies have shown that there was a correlation between low-grade inflammation as C-reactive protein (CRP) and HP infection. The aim of this study was to investigate the relationship between the presence of gastritis due to HP infection and neutrophil/lymphocyte ratio (NLR), a simple and reliable indicator of inflammation. Fifty patients met the HP criteria and half of them have had severe symptoms and upper endoscopy showed atrophic gastritis, and fifty age- and sex-matched control subjects with gastritis without HP infection were included in this randomized controlled trial. Patients were diagnosed to have HP according to the use of urea breath testing (UBT) and multiple biopsies. NLR was calculated from complete blood count at the time of diagnosis and before initiating the treatment to all groups. Patients with HP infection had significantly higher NLR compared to those without HP. Moreover, the patients with symptomatic HP and grade 4 gastritis had higher NLR than those asymptomatic with past history of peptic disease (P 0.007 and P 0.068, respectively). Although NLR increased as the severity of gastritis and HP symptoms increased (r = 0.564, P < 0.001), Receiver operating characteristic (ROC) Curve analysis was performed. The cut-off level for NLR with optimal sensitivity and specificity was calculated as 1.82 (area under curve [AUC] = 0.825 [0.753-0.884], P < 0.001). The present study indicated, for the first time, a significant correlation between HP infection and inflammation on the basis of NLR, a simple and reliable indicator of inflammation. Furthermore, there is an increase in NLR as the severity of gastritis with HP increases. This elevated ratio gets normalized with treatment.

CLINICAL FEATURES AND SEVERITY OF GASTRIC EMPTYING DELAY IN BRAZILIAN PATIENTS WITH GASTROPARESIS

Gastroparesis is defined by delayed gastric emptying without mechanical obstruction of the gastroduodenal junction, which has been increasingly investigated. Nevertheless, knowledge on the relationships between etiology, symptoms and degree of delayed gastric emptying is limited. The demographic, clinical and etiological features of Brazilian patients with gastroparesis were studied and the relationships between these findings and the severity of gastric emptying were determined. This is a retrospective study of medical records of 41 patients with symptoms suggestive of gastroparesis admitted between 1998 and 2011, who had evidence of abnormally delayed gastric emptying on abdominal scintigraphy. Cases with idiopathic gastroparesis were compared with those of patients with neurologic disorders or diabetes mellitus, in whom autonomic neuropathy is likely to occur. The majority of the patients were women (75.6%) with a median age of 41 years and a long-term condition (median: 15 years). Twelve patients (29.3%) had a body mass index of less than 20 kg/m2. The most common presenting symptoms were dyspepsia (53.6%), nausea and vomiting (46.3%), weight loss (41.4%) and abdominal pain (24.3%). Regarding etiology, 16 patients had digestive disorders including idiopathic gastroparesis (n = 12), 12 had postoperative conditions, 11 had diseases of the nervous system, five had diabetes mellitus and in three cases gastroparesis was associated to a variety of conditions. In the majority of patients (65.8%) gastric emptying was severely delayed. There was no association between etiology of gastroparesis, type of presenting symptoms and the degree of delay in gastric emptying. Gastroparesis patients with proven (neurological conditions) or presumed (diabetes) nervous system involvements were significantly younger (P = 0.001), had more recent symptom onset (P = 0:03) and a trend towards more severe gastric empty (P = 0:06). There were no significant differences between this subgroup of patients and that comprising cases of idiopathic gastroparesis regarding any of the variables studied. The demographic, clinical and etiological characteristics of Brazilian patients with gastroparesis are quite varied, but there is a predominance of women with long-standing symptoms and marked delay in gastric emptying. The type of presenting symptoms and the degree of delay in gastric emptying do not predict the etiology of gastroparesis. However, severely delayed gastric emptying in younger patients with recent symptom onset should raise the suspicion of impaired neural control of gastro-duodenal motility.

Gastric distension activates NUCB2/nesfatin-1-expressing neurons in the nucleus of the solitary tract

Brainstem structures such as the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus nerve (DMNX) are essential for the digestive function of the stomach. A large number of neurotransmitters including glutamate and gamma-aminobutyric acid (GABA) are involved in the central control of gastric functions. However, the neuropeptidergic systems implicated in this process remain undetermined. Nesfatin-1 was recently identified as a neuropeptide cleaved from the N-terminal part of NEFA/nucleobindin 2 precursor (NUCB2). Central administration of this neuropeptide inhibits food consumption and gastroduodenal motility in rodents. Interestingly, the NTS and the DMNX contain a dense population of NUCB2/nesfatin-1 cell bodies. These observations led us to investigate the possible involvement of NUCB2/nesfatin-1 neurons in the brainstem neuronal pathways that modulate gastric functions. We observed an activation of NTS NUCB2/nesfatinergic neurons after gastric distention in rats. In addition, we found that several NTS NUCB2/nesfatinergic neurons were GABAergic. Finally, when fluorogold was injected at the stomach level, many retrogradely labeled neurons were observed in the DMNX which were also positive for NUCB2/nesfatin-1. Taken together, these observations suggest for the first time that NUCB2/nesfatin-1 neurons of the NTS are sensitive to gastric distension and then may contribute to the satiety signal.