Somatization in patients with predominant diarrhoea irritable bowel syndrome: the role of the intestinal barrier function and integrity.

BACKGROUND: Irritable bowel syndrome (IBS) is characterised by gastrointestinal (GI) and psychological symptoms (e.g., depression, anxiety, and somatization). Depression and anxiety, but not somatization, have already been associated with altered intestinal barrier function, increased LPS, and dysbiosis. The study aimed to investigate the possible link between somatization and intestinal barrier in IBS with diarrhoea (IBS-D) patients. METHODS: Forty-seven IBS-D patients were classified as having low somatization (LS = 19) or high somatization (HS = 28) according to the Symptom Checklist-90-Revised (SCL-90-R), (cut-off score = 63). The IBS Severity Scoring System (IBS-SSS) and the Gastrointestinal Symptom Rating Scale (GSRS) questionnaires were administered to evaluate GI symptoms. The intestinal barrier function was studied by the lactulose/mannitol absorption test, faecal and serum zonulin, serum intestinal fatty-acid binding protein, and diamine oxidase. Inflammation was assessed by assaying serum Interleukins (IL-6, IL-8, IL-10), and tumour necrosis factor-α. Dysbiosis was assessed by the urinary concentrations of indole and skatole and serum lipopolysaccharide (LPS). All data were analysed using a non-parametric test. RESULTS: The GI symptoms profiles were significantly more severe, both as a single symptom and as clusters of IBS-SSS and GSRS, in HS than LS patients. This finding was associated with impaired small intestinal permeability and increased faecal zonulin levels. Besides, HS patients showed significantly higher IL-8 and lowered IL-10 concentrations than LS patients. Lastly, circulating LPS levels and the urinary concentrations of indole were higher in HS than LS ones, suggesting a more pronounced imbalance of the small intestine in the former patients. CONCLUSIONS: IBS is a multifactorial disorder needing complete clinical, psychological, and biochemical evaluations. TRIAL REGISTRATION: https://clinicaltrials.gov/ct2/show/NCT03423069 .

Helicobacter pylori Primary and Secondary Genotypic Resistance to Clarithromycin and Levofloxacin Detection in Stools: A 4-Year Scenario in Southern Italy.

Antibiotic resistance has become an emerging problem for treating Helicobacter pylori (H. pylori) infection. Clarithromycin and levofloxacin are two key antibiotics used for its eradication. Therefore, we reviewed our experience with genotypic resistance analysis in stools to both clarithromycin and levofloxacin in the last four years to evaluate time trends, both in naive and failure patients. Patients collected a fecal sample using the THD fecal test device. Real-time polymerase chain reaction was performed to detect point mutations conferring resistance to clarithromycin (A2142C, A2142G, and A2143G in 23S rRNA) and levofloxacin (substitutions at amino acid position 87 and 91 of gyrA). One hundred and thirty-five naive patients were recruited between 2017-2020. Clarithromycin resistance was detected in 37 (27.4%). The time trend did not show any significant variation from 2017 to 2020 (p = 0.33). Primary levofloxacin resistance was found in 26 subjects (19.2%), and we observed a dramatic increase in rates from 2017 (10%) to 2018 (3.3%), 2019 (20%), and 2020 (37.8%). Ninety-one patients with at least one eradication failure were recruited. Secondary resistance to clarithromycin and levofloxacin was found in 59 (64.8%) and 45 patients (59.3%), respectively. In conclusion, our geographic area has a high risk of resistance to clarithromycin. There is also a progressive spreading of levofloxacin-resistant strains.

Improved Symptom Profiles and Minimal Inflammation in IBS-D Patients Undergoing a Long-Term Low-FODMAP Diet: A Lipidomic Perspective.

Given the link between the minimal inflammation underlying irritable bowel syndrome (IBS) and dietary treatments, considerable attention has focused on diets low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs). In this context, inflammatory patterns and lipidomic investigations may shed light on the pathophysiological mechanisms whereby a low-FODMAP diet (LFD) improves the IBS diarrhoea (IBS-D) variant. Thus, we investigated whether a long-term LFD induced changes in symptom profiles, anthropometric characteristics, inflammatory markers (C-reactive protein, cyclooxygenase-2, and prostaglandin E2) and erythrocyte-membrane fatty acid (FA) composition in IBS-D patients. Twenty IBS-D patients underwent a 90 day personalised LFD programme, and were regularly evaluated at scheduled visits. At the diet's end, both IBS symptoms and anthropometric parameters were significantly improved. A significant decrease in prostaglandin E2 also accompanied these reductions. As for FAs, the putative inflammatory indicators, arachidonic acid (AA) levels and the AA/eicosapentaenoic acid ratio were significantly decreased. In conclusion, IBS-D patients following a controlled long-term LFD experienced improved symptom profiles and decreased inflammatory markers linked to FAs. Lipidomic data may be insightful for unravelling the molecular mechanisms associated with IBS-D pathophysiology.

Gastric Activity and Gut Peptides in Patients With Functional Dyspepsia: Postprandial Distress Syndrome Versus Epigastric Pain Syndrome.

GOALS: The goals of the study were to investigate in both postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS) the gastric electrical activity and the gastric emptying (GE) time together with the circulating concentrations of motilin, somatostatin, corticotrophin-releasing factor, and neurotensin, and to establish whether the genetic variability in the neurotensin system genes differs between these 2 categories of functional dyspepsia (FD). BACKGROUND: The current FD classification is based on symptoms and it has been proven not to be completely satisfying because of a high degree of symptom overlap between subgroups. STUDY: Gastric electrical activity was evaluated by cutaneous electrogastrography: the GE time by C-octanoic acid breast test. Circulating concentrations of gut peptides were measured by a radioimmunoassay. NTS 479 A/G and NTSR1 rs6090453 SNPs were evaluated by PCR and endonuclease digestion. RESULTS: Fifty-four FD patients (50 female/4 male) were studied. Using a symptom questionnaire, 42 patients were classified as PDS and 12 as EPS, although an overlap between the symptom profiles of the 2 subgroups was recorded. The electrogastrographic parameters (the postprandial instability coefficient of dominant frequency, the dominant power, and the power ratio) were significantly different between the subgroups, whereas the GE time did not differ significantly. In addition, EPS was characterized by a different gut peptide profile compared with PDS. Finally, neurotensin polymorphism was shown to be associated with neurotensin levels. This evidence deserves further studies in consideration of an analgesic role of neurotensin. CONCLUSIONS: Analysis of gut peptide profiles could represent an interesting tool to enhance FD diagnosis and overcome limitations due to a distinction based solely on symptoms.

Lipidomic analysis of fatty acids in erythrocytes of coeliac patients before and after a gluten-free diet intervention: a comparison with healthy subjects.

Coeliac disease (CD) patients may exhibit a pro-inflammatory profile and fatty acids (FA) can influence inflammation through a variety of cellular pathways in them. The aims of the present study were to (1) evaluate the FA composition of erythrocytes obtained from newly diagnosed CD patients by lipidomic analysis and compare it with that in healthy subjects and (2) determine the effects of 1-year gluten-free diet (GFD) intervention. A total of twenty CD patients (five men and fifteen women; mean age 34.0 (sem 1.7) years) were evaluated at diagnosis and after 1 year of GFD intervention. A total of twenty healthy subjects (seven men and thirteen women; mean age 40.2 (sem 2.5) years) served as controls. CD patients on an unrestricted diet exhibited a significant 2.08-fold higher concentration of arachidic acid when compared with healthy subjects, suggesting that it can be considered as a putative marker of CD. Besides, the arachidonic acid (AA):dihomo-γ-linolenic acid ratio was 2.01-fold significantly lower in CD patients than in healthy subjects (P< 0.01), underlying an inefficient synthesis of PUFA from their precursors in terms of desaturase activity. In addition, mainly due to lower concentrations of docosahexaenoic acid, the inflammation marker AA:docosahexaenoic acid ratio was 1.40-fold significantly higher in CD patients than in healthy subjects. After 1 year of GFD intervention, FA concentrations in CD patients were still different from those observed in healthy subjects. The lipidomic analysis of erythrocyte membranes confirmed the presence of an altered FA composition in CD patients and the GFD's ability to modify FA profile, even if 1-year GFD intervention seems to be not sufficient to restore FA concentrations to normality. This procedure, being easier and non-invasive compared with the evaluation of the FA pattern of the intestinal mucosa, could offer more potentiality for also evaluating therapeutic interventions in CD patients by using FA supplementation.