Pseudo-obstruction Research Articles

Comorbid functional dyspepsia reflects IL-33–mediated airway neuronal dysfunction in asthma

BackgroundNeuronal dysfunction is implicated in the pathophysiology of asthma and functional dyspepsia (FD). However, the relationship between these diseases remains unclear. ObjectiveThis study aimed to clarify the clinical implications of comorbid FD in asthma and to explore the unified pathway between asthma and FD by focusing on airway neuronal dysfunction. MethodsClinical indices and biomarkers, including capsaicin cough sensitivity (C-CS), were compared between patients with asthma with and without FD. C-CS was determined based on the capsaicin concentration that induced at least two (C2) or five coughs (C5). Additionally, the associations of airway inflammation with airway innervation and gastrointestinal motility were evaluated in mouse models of type 2 airway inflammation. ResultsPatients with asthma with FD had worse asthma control and cough severity and lower C2 and C5 thresholds than those without FD. The severity of FD symptoms was negatively correlated with C2 and C5 thresholds. FD and poor asthma control were predictors of heightened C-CS (defined as C5 of ≤ 2.44 μM) in asthma. A mouse model of papain-induced airway inflammation developed airway hyperinnervation and gastrointestinal dysmotility, and both pathologies were ameliorated by an anti-interleukin (IL)-33 antibody. Moreover, papain-induced gastrointestinal dysmotility was mitigated by silencing the airway sensory neurons using QX-314, a sodium channel blocker. Furthermore, sputum IL-33 levels were significantly elevated in patients with asthma with FD or heightened C-CS compared with those in their counterparts. ConclusionFD is significantly associated with airway neuronal dysfunction in asthma. IL-33-mediated airway neuronal dysfunction may contribute to the interaction between asthma and FD.

Acute colonic pseudo-obstruction in polytrauma patients.

Acute colonic pseudo-obstruction (ACPO) is characterized by severe colonic distension without mechanical obstruction. It has an uncertain pathogenesis and poses diagnostic challenges. This study aimed to explore risk factors and clinical outcomes of ACPO in polytrauma patients and contribute information to the limited literature on this condition. This retrospective study, conducted at a Level 1 trauma center, analyzed data from trauma patients with ACPO admitted between July 2009 and June 2018. A control cohort of major trauma patients was used. Data review encompassed patient demographics, abdominal imaging, injury characteristics, analgesic usage, interventions, complications, and mortality. Statistical analyses, including logistic regression and correlation coefficients, were employed to identify risk factors. There were 57 cases of ACPO, with an incidence of 1.7 per 1,000 patients, rising to 4.86 in major trauma. Predominantly affecting those older than 50 years (75%) and males (75%), with motor vehicle accidents (50.8%) and falls from height (36.8%) being the commonest mechanisms. Noteworthy associated injuries included retroperitoneal bleeds (RPBs) (37%), spinal fractures (37%), and pelvic fractures (37%). Analysis revealed significant associations between ACPO and shock index >0.9, Injury Severity Score >18, opioid use, RPBs, and pelvic fractures. A cecal diameter of ≥12 cm had a significant association with cecal ischemia or perforation. This study underscores the significance of ACPO in polytrauma patients, demonstrating associations with risk factors and clinical outcomes. Clinicians should maintain a high index of suspicion, particularly in older patients with RPBs, pelvic fractures, and opioid use. Early supportive therapy, vigilant monitoring, and timely interventions are crucial for a favorable outcome. Further research and prospective trials are warranted to validate these findings and enhance understanding of ACPO in trauma patients. Prognostic and Epidemiological; Level IV.

Intestinal pseudo-obstruction as systemic lupus erythematosus complication: is it time to reconsider the role of surgery?: A case report of a tailored multidisciplinary managed 44-year-old male patient

Rationale: Intestinal pseudo-obstruction (IPO) represents an unclarified dysmotility disorder characterized by clinic-radiological signs of intestinal obstruction not associated with organic conditions. IPO may occur as a rare complication of autoimmune connective tissue diseases, including Systemic Lupus Erythematosus (SLE). Surgery is recognized as having a marginal management position for IPO patients: this case investigates its role, in the context of a multidisciplinary approach, in the diagnosis and treatment of acute complications of IPO. Patient concerns: An SLE-affected 44-year-old man with a history of recurring nonspecific abdominal sub-obstructive episodes was admitted to our department for constipation, vomiting, and unintentional weight loss. Clinical examination revealed a family history of eosinophilic gastroenteritis (EG). Laboratory tests, including Systemic Sclerosis screening, presented no significant alterations. Abdominal X-ray highlighted multiple air-fluid levels; contrast-enhanced CT showed fluid surrounding dilated loops, and fluid-filled ileal loops, without evidence of organic intrinsic/ab-extrinsic obstruction, perforation, or extraluminal gas. Considering these findings, stenosing-pattern Crohn disease and strictures-complicated EG were mainly suspected. However, ileum-colonoscopy with the histological analysis resulted in inconclusive for Crohn disease and EG. Diagnosis: The histological examination, by showing an SLE fibro-inflammatory pattern, not sparing the enteric plexus, infiltrating the intestinal wall of the surgical samples collected during the right hemicolectomy intervention, allowed the diagnosis of IPO. Interventions and outcomes: The patient, indeed, was initially managed conservatively with nasogastric decompression, immunosuppressive therapy, and parenteral nutrition by a multidisciplinary team including gastroenterologists, rheumatologists, and nutritionists. Unfortunately, 2 weeks later, the worsening symptoms required a lifesaving right hemicolectomy followed by ileostomy. Lessons: IPO should be suspected in SLE patients presenting treated-unresponsive GI symptoms. Its early recognition finalized to start a tailored multidisciplinary approach appears prognostically crucial. Surgery could represent a paramount diagnostic moment and therapeutic life-saving approach.

Case report: acute intestinal pseudo-obstruction as a rare complication of pheochromocytoma

Case report: acute intestinal pseudo-obstruction as a rare complication of pheochromocytoma

COQ7 defect causes prenatal onset of mitochondrial CoQ10 deficiency with cardiomyopathy and gastrointestinal obstruction

COQ7 pathogenetic variants cause primary CoQ10 deficiency and a clinical phenotype of encephalopathy, peripheral neuropathy, or multisystemic disorder. Early diagnosis is essential for promptly starting CoQ10 supplementation. Here, we report novel compound heterozygous variants in the COQ7 gene responsible for a prenatal onset (20 weeks of gestation) of hypertrophic cardiomyopathy and intestinal dysmotility in a Bangladesh consanguineous family with two affected siblings. The main clinical findings were dysmorphisms, recurrent intestinal occlusions that required ileostomy, left ventricular non-compaction cardiomyopathy, ascending aorta dilation, arterial hypertension, renal dysfunction, diffuse skin desquamation, axial hypotonia, neurodevelopmental delay, and growth retardation. Exome sequencing revealed compound heterozygous rare variants in the COQ7 gene, c.613_617delGCCGGinsCAT (p.Ala205HisfsTer48) and c.403A>G (p.Met135Val). In silico analysis and functional in vitro studies confirmed the pathogenicity of the variants responsible for abolished activities of complexes I + III and II + III in muscle homogenate, severe decrease of CoQ10 levels, and reduced basal and maximal respiration in patients’ fibroblasts. The first proband deceased at 14 months of age, whereas supplementation with a high dose of CoQ10 (30 mg/kg/day) since the first days of life modified the clinical course in the second child, showing a recovery of milestones acquirement at the last follow-up (18 months of age). Our study expands the clinical spectrum of primary CoQ10 deficiency due to COQ7 gene defects and highlights the essential role of multidisciplinary and combined approaches for a timely diagnosis.

Thyroid disorders and gastrointestinal dysmotility: an old association.

Gastrointestinal motility symptoms may be closely related to thyroid diseases. Sometimes, such symptoms are the only thyroid disease-related clue although the degree of the symptoms may vary. The exact mechanism of action of thyroid hormones on gastrointestinal motility is not completely understood, however, a clue lies in the fact that muscle cell receptors can be directly acted upon by thyroxines. Both hypo- and hyperthyroidism can cause impairment of gastrointestinal motility, modifying structure and function of pharynx and esophagus, and regulating esophageal peristalsis through neuro-humoral interaction. In hyperthyroid patients, alterations of postprandial and basic electric rhythms have been observed at gastro-duodenal level, often resulting in slower gastric emptying. Gastric emptying may also be delayed in hypothyroidism, but an unrelated gastric mucosa-affecting chronic modification may also cause such pattern. Hyperthyroidism commonly show malabsorption and diarrhoea, while hypothyroidism frequently show constipation. In summary, it can be stated that symptoms of gastrointestinal motility dysfunction can be related to thyroid diseases, affecting any of the gastrointestinal segment. Clinically, the typical thyroid disease manifestations may be missing, borderline, or concealed because of intercurrent sicknesses. Motility-linked gastrointestinal problems may easily conceal a misdetected, underlying dysthyroidism that should be carefully analyzed. Here, we aim to elaborate on the associations between thyroid disorders and GI dysmotility and the common clinical manifestations associated with GI dysmotility.

AB021. SOH24AB_125. Outcomes of children with intestinal failure secondary to gastrointestinal dysmotility

AB021. SOH24AB_125. Outcomes of children with intestinal failure secondary to gastrointestinal dysmotility

The Presence of Ganglionic Acetylcholine Receptor Antibodies in Sera from Patients with Functional Gastrointestinal Disorders: A Preliminary Study.

Functional gastrointestinal disorders (FGIDs), including functional dyspepsia (FD) and irritable bowel syndrome (IBS), are characterized by chronic and recurrent gastrointestinal symptoms. Clinically, FD and IBS often resemble gastrointestinal dysmotility caused by autoimmune autonomic neuropathy. We examined the seropositive frequency of autoantibodies against ganglionic nicotinic acetylcholine receptors (gnAChRs) in patients presenting with FGIDs. To elucidate the seropositivity of gnAChR antibodies and the clinical features of seropositive FD and IBS. We measured autoantibodies against the gnAChR α3 and β4subunits using luciferase immunoprecipitation systems. Serum samples from patients with any autonomic symptoms were obtained from hospitals in Japan between January 2012 and August 2018 (1787 serum samples of 1381 patients). We selected FD and IBS patients and compared the clinical characteristics and prevalence of autonomic symptoms between those with seropositive and seronegative IBS and FD. Nine IBS and two FD cases (one comorbid case with IBS) were found. We found four patients (36.4%) in whom gnAChR antibodies were positive in these eleven patients. Sicca symptoms were observed in three of four cases (75%) of seropositive FGID compared with zero of seven cases (0%) of seronegative FGID. We found patients with gnAChR antibodies in FD and IBS patients. These data will be valuable for elucidating the pathophysiology of these FGIDs and developing new treatment strategies.

Visible Peristalsis in a Patient Referred for Chronic Intestinal Pseudo-Obstruction

Visible Peristalsis in a Patient Referred for Chronic Intestinal Pseudo-Obstruction

Updates in Treatment of Refractory Inflammatory Myositis

Idiopathic immune myopathies (IIM), also known as myositis, are a heterogeneous group of autoimmune diseases with varying phenotypes, prognoses, and treatment responses. They are primarily characterized by muscle inflammation, however, many patients have extramuscular involvement including skin rash, arthritis, interstitial lung disease (ILD), cardiomyopathy, and gastrointestinal dysmotility. The discovery of myositis-specific autoantibodies (MSAs) has been a major advancement in the field of IIMs, shaping the new landscape of the clinical, phenotypical, histological, and serological correlations. Based on this discovery, IIM can be more specifically classified into dermatomyositis (DM) (including amyopathic DM), antisynthetase syndrome (ASyS), immune-mediated necrotizing myopathy (IMNM), inclusion body myositis (IBM), polymyositis (PM), and overlap myositis (OM). An increasing number of histological studies have revealed a misdiagnosis of PM because many patients who were previously diagnosed with PM were later reclassified to other forms of IIM, including IBM, IMNM, ASyS, or DM without a rash.

The gut microbiota in adults with chronic intestinal failure

Fecal microbiota was investigated in adult patients with chronic intestinal failure (CIF) due to short bowel syndrome (SBS) with jejunocolonic anastomosis (SBS-2). Few or no data are available on SBS with jejunostomy (SBS-1) and CIF due to intestinal dysmotility (DYS) or mucosal disease (MD). We profiled the fecal microbiota of various pathophysiological mechanisms of CIF. Cross-sectional study on 61 adults with CIF (SBS-1 30, SBS-2 17, DYS 8, MD 6). Fecal samples were collected and profiled by 16S rRNA amplicon sequencing. Healthy controls (HC) were selected from pre-existing cohorts, matched with patients by sex and age. Compared to HC, SBS-1, SBS-2 and MD patients showed lower alpha diversity; no difference was found for DYS. In beta diversity analysis, SBS-1, SBS-2 and DYS groups segregated from HC and from each other. Taxonomically, the CIF groups differed from HC even at the phylum level. In particular, CIF patients' microbiota was dominated by Lactobacillaceae and Enterobacteriaceae, while depleted in typical health-associated taxa belonging to Lachnospiraceae and Ruminococcaceae. Notably, compositional peculiarities of the CIF groups emerged. Furthermore, in the SBS groups, the microbiota profile differed according to the amount of parenteral nutrition required and the duration of CIF. CIF patients showed marked intestinal dysbiosis with microbial signatures specific to the pathophysiological mechanism of CIF as well as to the severity and duration of SBS.

Protective effect of oxytocin on vincristine-induced gastrointestinal dysmotility in mice.

Aims: Vincristine (VCR), an antineoplastic drug, induces peripheral neuropathy characterized by nerve damage, limiting its use and reducing the quality of life of patients. VCR causes myenteric neuron damage, inhibits gastrointestinal motility, and results in constipation or paralytic ileus in patients. Oxytocin (OT) is an endogenous neuropeptide produced by the enteric nerve system, which regulates gastrointestinal motility and exerts neuroprotective effects. This study aimed to investigate whether OT can improve VCR-induced gastrointestinal dysmotility and evaluate the underlying mechanism. Methods: Mice were injected either with saline or VCR (0.1mg/kg/d, i. p.) for 14 days, and OT (0.1mg/kg/d, i.p.) was applied 1h before each VCR injection. Gastrointestinal transit and the contractile activity of the isolated colonic segments were assessed. The concentration of OT in plasma was measured using ELISA. Immunofluorescence staining was performed to analyze myenteric neurons and reactive oxygen species (ROS) levels. Furthermore, the indicators of oxidative stress were detected. The protein expressions of Nrf2, ERK1/2, P-ERK1/2, p38, and P-p38 in the colon were tested using Western blot. Results: VCR reduced gastrointestinal transit and the responses of isolated colonic segments to electrical field stimulation and decreased the amount of neurons. Furthermore, VCR reduced neuronal nitric oxide synthase and choline acetyltransferase immunopositive neurons in the colonic myenteric nerve plexus. VCR increased the concentration of OT in plasma. Exogenous OT pretreatment ameliorated the inhibition of gastrointestinal motility and the injury of myenteric neurons caused by VCR. OT pretreatment also prevented the decrease of superoxide dismutase activity, glutathione content, total antioxidative capacity, and Nrf2 expression, the increase of ROS levels, and the phosphorylation of ERK1/2 and p38 MAPK following VCR treatment. Conclusion: Our results suggest that OT pretreatment can protect enteric neurons from VCR-induced injury by inhibiting oxidative stress and MAPK pathways (ERK1/2, p38). This may be the underlying mechanism by which it alleviates gastrointestinal dysmotility.

Inhibition of calcium-sensing receptor by its antagonist promotes gastrointestinal motility in a Parkinson’s disease mouse model

BackgroundThe Calcium-sensing receptor (CaSR) participates in the regulation of gastrointestinal (GI) motility under normal conditions and might be involved in the regulation of GI dysmotility in patients with Parkinson's disease (PD). MethodsCaSR antagonist-NPS-2143 was applied in in vivo and ex vivo experiments to study the effect and underlying mechanisms of CaSR inhibition on GI dysmotility in the MPTP-induced PD mouse model. FindingsOral intake of NPS-2143 promoted GI motility in PD mice as shown by the increased gastric emptying rate and shortened whole gut transit time together with improved weight and water content in the feces of PD mice, and the lack of influence on normal mice. Meanwhile, the number of cholinergic neurons, the proportion of serotonergic neurons, as well as the levels of acetylcholine and serotonin increased, but the numbers of nitrergic and tyrosine hydroxylase immunoreactive neurons, and the levels of nitric oxide synthase and dopamine decreased in the myenteric plexus in the gastric antrum and colon of PD mice in response to NPS-2143 treatment. Furthermore, the numbers of c-fos positive neurons in the nucleus tractus solitarius (NTS) and cholinergic neurons in the dorsal motor nucleus of the vagus (DMV) increased in NPS-2143 treated PD mice, suggesting the involvement of both the enteric (ENS) and central (CNS) nervous systems. However, ex vivo results showed that NPS-2143 directly inhibited the contractility of antral and colonic strips in PD mice via a non-ENS mediated mechanism. Further studies revealed that NPS-2143 directly inhibited the voltage gated Ca2+ channels, which might, at least in part, explain its direct inhibitory effects on the GI muscle strips. InterpretationCaSR inhibition by its antagonist ameliorated GI dysmotility in PD mice via coordinated neuronal regulation by both ENS and CNS in vivo, although the direct effects of CaSR inhibition on GI muscle strips were suppressive.

Neurological, cardiac, musculoskeletal, and renal manifestations of scleroderma along with insights into its genetics, pathophysiology, diagnostic, and therapeutic updates.

Scleroderma, also referred to as systemic sclerosis, is a multifaceted autoimmune condition characterized by abnormal fibrosis and impaired vascular function. Pathologically, it encompasses the persistent presence of inflammation, abnormal collagen buildup, and restructuring of blood vessels in various organs, resulting in a wide range of clinical symptoms. This review incorporates the most recent scientific literature on scleroderma, with a particular emphasis on its pathophysiology, clinical manifestations, diagnostic approaches, and treatment options. A comprehensive investigation was carried out on numerous databases, such as PubMed, MEDLINE, Scopus, Web of Science, and Google Scholar, to collect pertinent studies covering diverse facets of scleroderma research. Scleroderma presents with a range of systemic manifestations, such as interstitial lung disease, gastrointestinal dysmotility, Raynaud's phenomenon, pulmonary arterial hypertension, renal complications, neurological symptoms, and cardiac abnormalities. Serological markers, such as antinuclear antibodies,anti-centromere antibodies,and anti-topoisomerase antibodies,are important for classifying diseases and predicting their outcomes. The precise identification of scleroderma is crucial for promptly and correctly implementing effective treatment plans. Treatment approaches aim to improve symptoms, reduce complications, and slow down the progression of the disease. An integrated approach that combines pharmacological agents, including immunosuppressants, endothelin receptor antagonists, and prostanoids, with nonpharmacological interventions such as physical and occupational therapy is essential for maximizing patient care. Through the clarification of existing gaps in knowledge and identification of emerging trends, our goal is to improve the accuracy of diagnosis, enhance the effectiveness of therapeutic interventions, and ultimately enhance the overall quality of life for individuals suffering from scleroderma. Ongoing cooperation and creative research are necessary to advance the field and achieve improved patient outcomes and new therapeutic discoveries.

Хронічна інтестинальна псевдообструкція в дітей (огляд літератури)

Hirschsprung disease and chronic intestinal pseudo-obstruction (CIPO) in children are the most common and severe disorders of gastro-intestinal tract motility. While the problems connected with the Hirschsprung disease widely coverage in native literature, the publications that devoted the CIPO absent. Aim of the study was to analyze the literature data that devoted to the diagnosis and treatment of children with CIPO. Intestinal pseudo-obstruction refers to heterogeneous groups of disorders with a similar phenotypic presentation characterized by obstructive intestinal symptoms in the absence of true anatomical obstruction. CIPO classification based on the primary dysfunction: affected enteral nervous system (neuropathy), affected smooth muscle (myopathy) or interstitial cells Cajal (mesenchymopathy). Besides that, the intestinal pseudo-obstruction is divided into primary and secondary, congenital and acquired, total and segmentary. The main clinical features, methods of investigation in suspected CIPO such as radiological (roentgenography and roentgenoscopy, computed tomography, cine magnetic resonance), endoscopic, manometry, pathohistological, etc. were listed. The main principles of nutrition support, conventional therapy, and surgical management were presented. Conclusions. CIPO is a severe disorder of gastrointestinal motility that caused by various factors, which can be congenital and/or acquired. Diagnosis of CIPO based on the results of clinical, instrumental, and pathohistological investigation. The management of children with CIPO should include nutritional support, conventional therapy, and, for the clear indices, surgical correction. No conflict of interests was declared by the authors.

Meningoencephalitis in a novel mutation in MNGIE (mitochondrial neurogastrointestinal encephalomyopathy) ending a familial diagnostic odyssey: A case series report.

MNGIE (Mitochondrial Neurogastrointestinal Encephalomyopathy) is an ultra-rare autosomal recessive disorder that leads to mutations in the nuclear genes encoding thymidine phosphorylase. Symptoms include gastrointestinal dysmotility, cachexia, ptosis, external ophthalmoplegia, sensorimotor neuropathy and asymptomatic leukoencephalopathy. We describe the first case of MNGIE with meningoencephalitis that ultimately led to a familial diagnosis ending a diagnostic odyssey. We retrospectively reviewed the electronic medical records and sent whole exome sequencing for the index case and his family members. We report the variant c.877T>C p.(Cys293Arg) found in TYMP gene in all affected siblings showed typical clinical manifestations related to MNGIE. To the best of our knowledge, this is not described in the literature nor in the population databases dbSNP (Single Nucleotide Polymorphism Database) and gnomAD (Genome Aggregation Database). Additionally, it is located in a highly conserved residue and the bioinformatic analysis suggests it is most probably deleterious. Moreover, we estimated 550 number of cases of MNGIE (including 5 cases in this study) after performing an extensive search in the literature across 3 databases from 1983-2023. In addition, we identified 44 patients with MNGIE-like phenotype in genes other than TYMP. MNGIE-like phenotype affects POLG1, RRM2B, LIG3, RRM1, MTTV1, and MT-RNR1 genes.

Idiopathic chronic intestinal pseudo-obstruction syndrome is strongly associated with low serum levels of vitamin D.

Idiopathic chronic intestinal pseudo-obstruction (CIPO) is associated with intestinal inflammation and malabsorption and may cause serum vitamin D deficiency. We aimed to assess whether there is an association between idiopathic CIPO and serum levels of 25-hydroxy-vitamin D. Consecutive patients with confirmed diagnosis of idiopathic CIPO were prospectively enrolled and matched with healthy controls by gender, age, and BMI. Median serum level of 25-hydroxy-vitamin D of patients with CIPO was compared with that of healthy subjects using the Wilcoxon signed-rank test for matched samples. A total of 35 patients with CIPO and 35 matched healthy subjects were enrolled. All patients with CIPO had a 25-hydroxy-vitamin D deficiency with serum levels <12 ng/ml. The median serum level of vitamin D was significantly lower in patients with CIPO than in healthy controls (5.7 vs. 29.7 ng/ml, P < 0.0001). Serum level of vitamin D was not associated with gender ( P = 0.27), age ( P = 0.22), BMI ( P = 0.95), high (>10 000 × ml) WBC count ( P = 0.08), or high (>5 mg/l) C-reactive protein ( P = 0.87) among patients with CIPO. CIPO seems to be strongly associated with low serum levels of 25-hydroxy-vitamin D.

O126: Non-invasive vagus nerve stimulation to reduce ileus after colorectal surgery: randomised feasibility trial and efficacy assessment

Abstract Objective Ileus is characterised by intestinal dysmotility after surgery. In preclinical models, vagus nerve stimulation reduces intestinal inflammation, preventing smooth muscle dysfunction and accelerating the return of gut function. This study explored the efficacy and feasibility of a definitive trial and implementation of non-invasive, electrical, vagus nerve stimulation (nVNS). Design A participant-blinded, multi-centre, feasibility trial of self-administered nVNS was performed. Patients undergoing colorectal surgery were randomised to four groups of pre- and post-operative treatment (A: nVNS/nVNS; B: nVNS/Sham; C: Sham/nVNS; D: Sham/Sham). Feasibility outcomes were participant recruitment, compliance, and blinding. Clinical outcomes were intestinal function and adverse events. Interviews with patients and clinicians explored barriers to feasibility and implementation. In an independent cohort, the effects of nVNS on serum IL-1b, IL-6, and TNFa were quantified at baseline, 24-hours, and 72-hours after surgery. Results Ninety-seven out of 125 (77.6%) eligible patients took part. The median compliance was 19 out of 20 stimulations (IQR: 17-20). The median time to pass stool was 4 (3-5), 3 (2-4), 2.5 (2-3.5), and 3 (2-4) days for groups A-D, respectively. The incidence of adverse events was similar across groups. Trends toward reduced pro-inflammatory mediators were observed after nVNS. Interviews with patients (n=19) demonstrated their motivation to contribute actively to their recovery and interviews with clinicians (n=10) revealed strong reciprocal support. Conclusion This study confirms the safety, feasibility, and support for nVNS after surgery. Research on nVNS should progress from its current focus on pre-clinical models to powered, dedicated assessments of clinical effectiveness.

Safety of prolonged use of metoclopramide and domperidone as treatment for chronic gastrointestinal dysmotility disorders in patients with systemic sclerosis

BackgroundMetoclopramide and domperidone are prokinetic agents commonly used to treat gastrointestinal dysmotility disorders. This study aimed to evaluate the safety and associated side effects of prolonged-use metoclopramide and domperidone as treatment for chronic gastrointestinal dysmotility disorders in patients with systemic sclerosis (SSc). MethodsA quantitative observational survey was conducted by interview questionnaire in rheumatology outpatients at a tertiary teaching hospital in Riyadh, Saudi Arabia. The study included all patients aged 25–80 years diagnosed with SSc. All patients were on metoclopramide or domperidone for the treatment of chronic gastrointestinal dysmotility symptoms over at least 12 weeks. ResultsEighteen eligible patients were included. Most study participants were diagnosed with SSc complicated by interstitial lung disease (n = 13; 72.2 %). The most frequently reported side effect that occurred while taking prokinetic drugs was shortness of breath (n = 12; 66.7 %). None of the participants reported experiencing depression, galactorrhea, or syncope. CNS side effects were reported in 5.6 %. There were no differences in side effects based on the type and dosage of prokinetic drug used. ConclusionsUse of metoclopramide and domperidone for the treatment of chronic gastrointestinal dysmotility in SSc patients for 12 weeks or longer was not associated with any troublesome side effects. Further studies with more participants are needed to confirm our findings.

Clinical validation of the VIPUN™ gastric monitoring system versus manometry for the evaluation of gastric motility.

Gastrointestinal dysmotility is frequently suspected in patients with gastroparesis, functional dyspepsia, and ileus, and in the intensive care unit. Monitoring of gastric motility in clinical practice remains challenging. A novel technology was developed to meet the medical need for a widely available bedside tool to monitor gastric motility continuously. The VIPUN™ Gastric Monitoring System (GMS) comprises a nasogastric feeding tube with intragastric balloon to allow for measuring gastric contractions. To compare the performance of the VIPUN GMS versus a reference technique (manometry). In this validation study in healthy subjects, the investigational catheter and a solid-state manometry catheter were placed in the stomach concomitantly. Motility was recorded for 2.5 h: 2 h in a fasting state, followed by a 400-kcal liquid meal, and monitoring of the fed state for the remaining half hour. The performance of both systems was compared by automated recognition and manual identification of the contractile activity. Data are presented as mean (standard deviation). The analysis set comprised 13 healthy subjects (6 women, age: 27.5 (8.1) years, BMI: 22.2 (2.46) kg/m2). Automatically-recognized contractility was strongly correlated between the two techniques (endpoint: contraction duration; Spearman ρ = 0.96, p < 0.001). A correlation was also observed between the number of individual contractions identified by expert gastroenterologists on both technologies independently (ρ = 0.71, p = .007) and between the contractions identified by the experts and by the GMS software (ρ = 0.87, p = 0.001). No serious or unanticipated adverse events occurred. The observed strong correlations with the gold standard, manometry, validate the performance of the VIPUN GMS as a gastric monitoring system.