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V Stanghellini

Publications and source records attributed to V Stanghellini.

At least 37 records · Page 2Linked to original sources
PubMed2003

Development and validation of a patient-assessed gastroparesis symptom severity measure: the Gastroparesis Cardinal Symptom Index.

BACKGROUND: Patient-based symptom assessments are necessary to evaluate the effectiveness of medical treatments for gastroparesis. AIM: To summarize the development and measurement qualities of the Gastroparesis Cardinal Symptom Index (GCSI), a new measure of gastroparesis-related symptoms. METHODS: The GCSI was based on reviews of the medical literature, clinician interviews and patient focus groups. The measurement qualities (i.e. reliability, validity) of the GCSI were examined in 169 gastroparesis patients. Patients were recruited from seven clinical centres in the USA to participate in this observational study. Patients completed the GCSI, SF-36 Health Survey and disability day questions at a baseline visit and again after 8 weeks. Clinicians independently rated the severity of the patients' symptoms, and both clinicians and patients rated the change in gastroparesis-related symptoms over the 8-week study. RESULTS: The GCSI consists of three sub-scales: post-prandial fullness/early satiety, nausea/vomiting and bloating. The internal consistency reliability was 0.84 and the test-re-test reliability was 0.76 for the GCSI total score. Significant relationships were observed between the clinician-assessed symptom severity and the GCSI total score, and significant associations were found between the GCSI scores and SF-36 physical and mental component summary scores and restricted activity and bed disability days. Patients with greater symptom severity, as rated by clinicians, reported greater symptom severity on the GCSI. The GCSI total scores were responsive to changes in overall gastroparesis symptoms as assessed by clinicians (P = 0.0002) and patients (P = 0.002). CONCLUSION: The findings of this study indicate that the GCSI is a reliable and valid instrument for measuring the symptom severity in patients with gastroparesis.

Adolescent↗
PubMed2003

Unsolved problems in the management of patients with gastro-oesophageal reflux disease.

Gastro-oesophageal reflux disease is a common problem that brings large numbers of patients to physicians every day. It lowers the quality of life of affected individuals and exposes them to potentially dangerous complications. An increasing awareness exists among patients, doctors and authorities about the relevance of this pathological condition. Despite an improved understanding of many aspects of gastro-oesophageal reflux disease, clinical management of several cases is still unsatisfactory. Atypical cases with extra-oesophageal manifestations often defy diagnosis. Even typical symptoms are often misunderstood and considered to be part of the poorly defined area of dyspepsia by both patients and doctors. As a consequence, management remains uncertain for too many cases. If correctly diagnosed, gastro-oesophageal reflux disease can be efficaciously treated with proton pump inhibitors (PPIs). Although standard doses of PPIs can heal mucosal lesions and provide symptom relief in the vast majority of oesophagitis patients, non-oesophagitis symptomatic individuals and those with extra-oesophageal manifestations may fail to respond to similar regimens. Antireflux surgery is a possible alternative to PPI therapy, but it is hampered by complications in a substantial percentage of cases and by sporadic casualties even when performed by experienced surgeons. The high prevalence of gastro-oesophageal reflux disease in the general population and the relatively high management costs should prompt any doctor to seek the best possible therapeutic approach.

Disease Management↗
PubMed2003

Predictors of gastroparesis in out-patients with secondary and idiopathic upper gastrointestinal symptoms.

BACKGROUND: Delayed gastric emptying occurs frequently in patients with upper gastrointestinal symptoms associated with functional or organic diseases. AIMS: To evaluate whether: (i) the prevalence of delayed gastric emptying is influenced by the presence of organic disease; (ii) demographic or clinical factors predict modestly or markedly (gastroparesis) delayed emptying. PATIENTS: A total of 327 consecutive out-patients with upper gastrointestinal symptoms. METHODS: Routine diagnostic work-up and evaluation of demographic factors, gastrointestinal symptom evaluation and scintigraphic gastric emptying of solids were performed. RESULTS: Organic diseases were detected in 227/327 (65%) patients: 33% had delayed emptying and 20% gastroparesis. Female gender (OR: 2.1; 95% C.I.: 1.3-3.4). overweight (0.5; 0.3-0.9), relevant postprandial fullness (1.8; 1.1-3.2) and relevant epigastric bloating (1.8; 1.1-2.9), but not the presence of organic diseases, were associated with delayed emptying. Female gender (3.9; 1.3-11.9) and relevant postprandial fullness (4.1; 1.7-10.2) were associated with gastroparesis. CONCLUSIONS: (i) There is a high prevalence of delayed gastric emptying and gastroparesis in out-patients with upper gastrointestinal symptoms, which is not influenced by the presence of organic disease; (ii) female gender, low body weight, relevant fullness and bloating are associated with delayed emptying; female gender and relevant postprandial fullness predict gastroparesis.

Adult↗
PubMed2003

Best cut-off values for [14C]-urea breath tests for Helicobacter pylori detection.

BACKGROUND: The 'test and treat' strategy for Helicobacter pylori is recommended in dyspeptic patients under 55 years of age with no alarm symptoms. Reliable non-invasive tests are therefore needed. The aim of this study was to assess the pre- and post-treatment accuracy of a low dose (1 microCi [37kBq]), short collecting time [14C]-UBT (urea breath test) in diagnosing H pylori infection, examining different methods to analyse the best cut-off points. METHODS: The study included 119 patients. Endoscopy and [14C]-UBT were performed in the pre- and post-treatment setting. [14C]-UBT results were expressed in three different ways: 1) the measured disintegrations per minute (dpm) at sample time, 2) the difference (D) in dpm between sample time and the dpm at T0, 3) the ratio of dpm at sample time to dpm at T0. RESULTS: Seventy-six out of the 119 patients (63.9%; 95% CI: 54.9 to 71.9) were infected. Seventy-three (96%) patients completed the follow-up. The most accurate results in both pre- (sensitivity 95.9%; specificity 97.7%) and post-treatment (sensitivity 90.9%; specificity 100%) were obtained using the difference (D) in dpm between sample time at T0 and at T12.5. CONCLUSION: A low dose [14C]-UBT, with a short collecting time, is a reliable method to evaluate H. pylori infection in both the pre- and post-treatment setting.

Adult↗
PubMed2003

Neutral endopeptidase (EC 3.4.24.11) downregulates the onset of intestinal inflammation in the nematode infected mouse.

BACKGROUND AND AIMS: Substance P (SP) release from sensory nerves induces neurogenic inflammation. Neutral endopeptidase (NEP) degrades SP, thereby limiting its proinflammatory effects. Intestinal inflammation following Trichinella spiralis infection markedly downregulates NEP, resulting in diminished SP degradation, with unknown functional consequences. We hypothesised that diminished expression of NEP would exacerbate T spiralis induced enteritis. METHODS: NEP knockout (NEP-/-) and wild-type (NEP+/+) mice were infected with T spiralis and studied at 6, 12, 24, and 48 hours post infection (PI). Tissue inflammation was quantified by computerised cell counting and myeloperoxidase activity (MPO). The leucocyte adhesion molecule, intercellular adhesion molecule 1 (ICAM-1), and SP were assessed by immunohistochemistry. RESULTS: Before infection, the lack of NEP was not associated with changes in mucosal cellularity or MPO activity. Twelve hours PI, NEP-/- mice showed a 2.5-fold increase in MPO activity at a time when values in NEP+/+ mice were still within normal limits. MPO activity and cellularity peaked at 24 hours PI. This was accompanied by increased staining for both ICAM-1 and SP in NEP-/- mice. Infusion of rhNEP to NEP-/- mice significantly reduced MPO activity 24 hours PI. CONCLUSIONS: These findings demonstrate that NEP downregulates the early onset of nematode intestinal inflammation and that increased bioavailability of SP and overexpression of ICAM-1 in NEP-/- mice likely play a role in the earlier onset of intestinal inflammation.

Animals↗
PubMed2003

Management of gastroesophageal reflux disease.

Gastroesophageal reflux disease (GERD) is a frequent clinical condition which leads to reduced quality of life. Atypical manifestations of the disease can confound diagnosis, and even the typical symptoms of heartburn and regurgitation can lead to misinterpretation. Proton pump inhibitors (PPIs) are the standard treatment for GERD and the different formulations show equivalence on a milligram to milligram basis in terms of efficacy and tolerability. With standard dosing, 8 weeks of treatment has been shown to heal most patients. However, as GERD is a chronically relapsing disease, maintenance treatment with lower dose PPIs is frequently required. Pantoprazole is the only PPI found not to interact with the metabolism of other drugs and is therefore the treatment of choice especially for patients with co-morbidities and co-medication.

Anti-Ulcer Agents↗
PubMed2002

A role for inflammation in irritable bowel syndrome?

Attention has been directed to the putative role of low grade mucosal inflammation in irritable bowel syndrome (IBS) on the basis of evidence showing that some patients with IBS have an increased number of inflammatory cells in the colonic and ileal mucosa. Previous episodes of infectious enteritis, genetic factors, undiagnosed food allergies, and changes in bacterial microflora may all play a role in promoting and perpetuating this low grade inflammatory process. Human and animal studies support the concept that inflammation may perturb gastrointestinal reflexes and activate the visceral sensory system even when the inflammatory response is minimal and confined to the mucosa. Thus abnormal neuroimmune interactions may contribute to the altered gastrointestinal physiology and hypersensitivity that underlies IBS. A brief review of the human and animal studies that have focused on the putative role of intestinal inflammation and infections in the pathogenesis of IBS is given.

Animals↗
PubMed2001

Helicobacter pylori infection and gastric function in patients with fundic atrophic gastritis.

In the present study we evaluated the relation among histology, H. pylori, IgG to H. pylori, gastric emptying, and acid secretion in 43 patients with fundic atrophic gastritis. On the basis of gastric acid secretion, patients were divided into three subgroups: patients with preserved acid secretion (Group 1), patients with hypochlorhydria (Group 2), and patients with achlorhydria (Group 3). Fundic glandular atrophy was more severe in hypoachlorhydric patients than in those with preserved acid secretion (P < 0.05 vs Group 2, P < 0.005 vs Group 3). H. pylori colonization was found in 94% of patients in Group 1, in 61% of patients in Group 2, and in only 8% of patients in Group 3 (P < 0.001 vs Group 1, P < 0.05 vs Group 2). Conversely, serological positivity to H. pylori was high in all three subgroups of patients (100% in Group 1, 77% in Group 2, 92% in Group 3). Gastric emptying was delayed in atrophic patients, particularly in those with hypoachlorhydria. Our data suggest that fundic atrophic gastritis represents a possible end stage of H. pylori infection, characterized by a progressive disappearance of the bacterium and a progressive deterioration of gastric functions.

Achlorhydria↗
PubMed2001

Review article: Helicobacter pylori, mucosal inflammation and symptom perception--new insights into an old hypothesis.

The role of Helicobacter pylori and the accompanying mucosal inflammatory response in functional dyspepsia is still undefined. Human and animal studies have clearly demonstrated a link between intestinal mucosal inflammation and changes in sensory-motor function. Growing clinical and basic evidence supports the concept that a similar paradigm may occur in H. pylori-related dyspepsia. The infection may both induce gastric dysmotility and trigger neuroplastic changes in the afferent neural pathways leading to visceral hyperalgesia. A reduction of central antinociceptive control systems may also play a pathophysiological role. H. pylori eradication has provided disappointing results in terms of improvement of symptoms. This may reflect the long-term recovery of neuroplastic changes occurring in the afferent nervous system or, alternatively, the incomplete resolution of gastritis and the persistent production of inflammatory mediators by resident cells in the muscularis externa. The identification of these mechanisms may provide a better understanding of the pathophysiology of H. pylori-related dyspepsia and prompt innovative therapeutic approaches.

Animals↗
PubMed2001

Review article: managing the dyspeptic patient--an interactive discussion.

Dyspepsia, a common disorder, can present some difficult clinical dilemmas. Physicians should explore some of the more challenging cases of dyspepsia in a setting that fosters interactive dialogue among colleagues, as was the case at the interactive discussion reported below. A panel of experts presented and discussed three case histories. The audience was able to choose from among several options for diagnosis or treatment and recorded their votes by means of an electronic handset. The first case concerned the relationship between continued non-steroidal anti-inflammatory drug (NSAID) use and recurrent upper gastrointestinal (GI) symptoms without ulcer or Helicobacter pylori infection. The second was a woman with complex upper GI symptoms including heartburn. The last featured a young man with dyspepsia and no alarm symptoms. The first case showed that a standard dose of proton pump inhibitor (PPI) is the best treatment for patients with gastritis who continue to use NSAIDs. The second case revealed that 24-h pH monitoring can be used to establish a relationship between symptoms and reflux episodes. The third case demonstrated that it can be difficult to make a definitive diagnosis based on clinical symptoms, and that patients with endoscopy-negative reflux disease usually respond well to PPI therapy.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Review Article: pain versus discomfort--is differentiation clinically useful?

Functional dyspepsia is highly variable in its clinical presentation and multifactorial in its underlying causes. Since many of the symptoms included in the definition of dyspepsia are intuitively suggestive of different pathogenic mechanisms, it has been proposed that patients with functional dyspepsia be divided into distinct dyspepsia sub-groups according to symptom clusters. The goal was to classify patients more homogeneously for research purposes as well as to target treatment. However, recent epidemiological, pathophysiological, and clinical studies indicate that a priori definitions based on the presence/absence of symptoms or clusters of symptoms have no clinical utility due to the considerable overlap between symptoms, as well as the poor correlation between pathogenic factors and responses to treatment. Attention is now focused on identifying predominant symptoms. Recent studies suggest that the analysis of predominant symptoms, demographic features, and overlapping digestive syndromes can help to identify dyspepsia sub-groups with different underlying pathophysiological features and aid in selecting appropriate treatment. The utility of this approach has been demonstrated in gastro-oesophageal reflux disease, which can be reliably diagnosed and managed on the basis of the presence and severity of the predominant symptom, heartburn. It is likely that precise symptom definitions and history-taking will be of pivotal importance in management strategies for functional dyspepsia.

Diagnostic Techniques and Procedures↗
PubMed2001

Review article: the pharmacological treatment of acute colonic pseudo-obstruction.

Acute colonic pseudo-obstruction (Ogilvie's syndrome) can be defined as a clinical condition with symptoms, signs and radiological appearance of acute large bowel obstruction unrelated to any mechanical cause. Recent reports of the efficacy of cholinesterase inhibitors in relieving acute colonic pseudo-obstruction have fuelled interest in the pharmacological treatment of this condition. The aim of the present review is to outline current perspectives in the pharmacological treatment of patients with acute colonic pseudo-obstruction. The best documented pharmacological treatment of Ogilvie's syndrome is intravenous neostigmine (2-2.5 mg), which leads to quick decompression in a significant proportion of patients after a single infusion. However, the search for new colokinetic agents for the treatment of lower gut motor disorders has made available a number of drugs that may also be therapeutic options for Ogilvie's syndrome. Among these agents, the potential of 5-hydroxytryptamine-4 receptor agonists and motilin receptor agonists is discussed.

Acute Disease↗
PubMed2001

Tachykinin-dependent and -independent components of peristalsis in the guinea pig isolated distal colon.

BACKGROUND & AIMS: In the intestine, tachykinins regulate motility by participating in neuromuscular and neuro-neuronal transmission. The aim of this study was to test the hypothesis that colonic propulsion is regulated by an interplay between tachykinergic and cholinergic transmission. METHODS: Propulsion was elicited by intraluminal distention of a thin rubber balloon, which traveled from the oral to the anal end of guinea pig isolated distal colon segments. The overall contribution of endogenous tachykinins to colonic propulsion was examined by blocking NK1, NK2, and NK3 receptors simultaneously. RESULTS: NK2-receptor blockade by MEN 11420 inhibited propulsion, whereas blockade of NK(1) by SR 140333 or of NK3 receptors by SR 142801 had minor effects on motility. Blockade of muscarinic or nicotinic receptors by hyoscine or hexamethonium decelerated peristalsis up to propulsion arrest. In the presence of partial muscarinic receptor blockade, the NK1-receptor antagonist SR 140333 and the NK2-receptor antagonist MEN 11420 markedly inhibited propulsion. Propulsion was also inhibited by the NK3-receptor antagonist SR 142801 in the presence of partial nicotinic receptor blockade. The simultaneous administration of the 3 tachykinin antagonists inhibited propulsion by 50%. CONCLUSIONS: This study demonstrates the existence of an interplay between tachykinergic and cholinergic pathways during peristalsis and the importance of endogenous tachykinins acting at multiple receptor sites in the control of colonic propulsion.

Animals↗
PubMed2001

Intestinal inflammation and activation of sensory nerve pathways: a functional and morphological study in the nematode infected rat.

BACKGROUND: In the rat, gastric distension elicits an intensity dependent pseudoaffective bradycardia mediated via capsaicin sensitive afferent and cholinergic efferent vagal pathways. Inflammation alters visceral perception although the mediators responsible have not been identified. In the nematode infected rat, there is a substantial increase in neuronal substance P (SP) content of the gut. AIMS: To examine the effects of inflammation on perception of a noxious visceral stimulus and on SP and neurokinin 1 (NK-1) receptor immunoreactivity (IR) in visceral afferent pathways. METHODS: Immunohistochemistry was performed on sections from the jejunum, dorsal root ganglia (DRG), and spinal cord (T1-L1) using SP and NK-1 rabbit polyclonal antibodies. In the DRG, the number of SP-IR or NK-1-IR neurones per section was visually quantified. The pseudoaffective cardiac reflex response to gastric stimulation was compared in control and Trichinella spiralis infected rats. RESULTS: Intestinal inflammation induced a rightward shift in the intensity dependent bradycardic response to gastric distension. This was associated with a marked increase in SP-IR not only in the gut wall but also in the DRG and dorsal horn of the spine. In contrast, NK-1-IR was not increased in the gut wall. Moreover, inflammation evoked a decrease in NK-1-IR in the dorsal horn. No NK-1-IR was identified in the DRG of either control or infected animals. CONCLUSIONS: Intestinal inflammation modulates the capsaicin sensitive pseudoaffective autonomic response to gastric distension, increases SP-IR in afferent pathways, and downregulates dorsal horn NK-1-IR. As the pseudoaffective response is capsaicin sensitive, the rightward shift of the response is likely the consequence of the decrease in NK-1 receptors in the sensory pathways.

Animals↗