Background/Aims: Gastric dysrhythmias, loss of normal 3 cycles per minute (CPM) gastric myoelectrical activity (GMA), and variable loss of interstitial cells of Cajal are reported both in gastroparesis (GP) and functional dyspepsia (FD). We hypothesize that the patients with GP, and FD with normal gastric emptying (NGE) and delayed gastric emptying (DGE) may vary in symptom severity, and GMA profiles. Methods: Symptoms and their severity were evaluated by gastroparesis cardinal symptom index (GCSI), Abell scoring, short-form Nepean dyspepsia index (SF-NDI), the World Health Organization quality of life, and Rome IV subtyping for FD. Solid-meal gastric emptying was assessed by nuclear scintigraphy. Water load satiety test (WLST)-based electrogastrography determined GMA. Results: Patients with GP (n = 40) had higher GCSI than those with FD (n = 39; [12 DGE, 27 NGE] (2.79 [2.17-3.33] vs 1.67 [0.83-2.61] vs 0.83 [0.55-1.93]; P < 0.001, in GP vs FD-NGE vs FD-DGE, respectively), severe Abell grade (Grade III in 17 [43%] vs 0% vs 0%, in GP vs FD-NGE vs FD-DGE, respectively), severe SF-NDI (80.5 [63.5-102.5] vs 50 [27-91] vs 30 [21.25-45.5]); and poor QOL. Sixteen (40%) GP had impaired gastric accommodation (< 238 mL). Post-WLST 3 CPM normal/hypernormal GMA was observed in 17 (42%), 18 (67%), and 5 (42%) patients with GP, FD (NGE), and FD (DGE), respectively; and 3 CPM hyponormal in remaining patients in each group.Post-WLST dysrhythmia was comparable. Conclusions WLST-electrogastrography coupled with GE study may distinguish between normal/dysrhythmic GMA revealing pathophysiologicalphenotypes of GP and FD. Analysing extent of power change in normogastric, and dysrhythmic frequencies may comprehensively elucidate disease severity.

Background/Aims: Gastric dysrhythmias, loss of normal 3 cycles per minute (CPM) gastric myoelectrical activity (GMA), and variable loss of interstitial cells of Cajal are reported both in gastroparesis (GP) and functional dyspepsia (FD). We hypothesize that the patients with GP, and FD with normal gastric emptying (NGE) and delayed gastric emptying (DGE) may vary in symptom severity, and GMA profiles. Methods: Symptoms and their severity were evaluated by gastroparesis cardinal symptom index (GCSI), Abell scoring, short-form Nepean dyspepsia index (SF-NDI), the World Health Organization quality of life, and Rome IV subtyping for FD. Solid-meal gastric emptying was assessed by nuclear scintigraphy. Water load satiety test (WLST)-based electrogastrography determined GMA. Results: Patients with GP (n = 40) had higher GCSI than those with FD (n = 39; [12 DGE, 27 NGE] (2.79 [2.17-3.33] vs 1.67 [0.83-2.61] vs 0.83 [0.55-1.93]; P < 0.001, in GP vs FD-NGE vs FD-DGE, respectively), severe Abell grade (Grade III in 17 [43%] vs 0% vs 0%, in GP vs FD-NGE vs FD-DGE, respectively), severe SF-NDI (80.5 [63.5-102.5] vs 50 [27-91] vs 30 [21.25-45.5]); and poor QOL. Sixteen (40%) GP had impaired gastric accommodation (< 238 mL). Post-WLST 3 CPM normal/hypernormal GMA was observed in 17 (42%), 18 (67%), and 5 (42%) patients with GP, FD (NGE), and FD (DGE), respectively; and 3 CPM hyponormal in remaining patients in each group.Post-WLST dysrhythmia was comparable. Conclusions WLST-electrogastrography coupled with GE study may distinguish between normal/dysrhythmic GMA revealing pathophysiologicalphenotypes of GP and FD. Analysing extent of power change in normogastric, and dysrhythmic frequencies may comprehensively elucidate disease severity.

Background/Aims: Gastric dysrhythmias, loss of normal 3 cycles per minute (CPM) gastric myoelectrical activity (GMA), and variable loss of interstitial cells of Cajal are reported both in gastroparesis (GP) and functional dyspepsia (FD). We hypothesize that the patients with GP, and FD with normal gastric emptying (NGE) and delayed gastric emptying (DGE) may vary in symptom severity, and GMA profiles. Methods: Symptoms and their severity were evaluated by gastroparesis cardinal symptom index (GCSI), Abell scoring, short-form Nepean dyspepsia index (SF-NDI), the World Health Organization quality of life, and Rome IV subtyping for FD. Solid-meal gastric emptying was assessed by nuclear scintigraphy. Water load satiety test (WLST)-based electrogastrography determined GMA. Results: Patients with GP (n = 40) had higher GCSI than those with FD (n = 39; [12 DGE, 27 NGE] (2.79 [2.17-3.33] vs 1.67 [0.83-2.61] vs 0.83 [0.55-1.93]; P < 0.001, in GP vs FD-NGE vs FD-DGE, respectively), severe Abell grade (Grade III in 17 [43%] vs 0% vs 0%, in GP vs FD-NGE vs FD-DGE, respectively), severe SF-NDI (80.5 [63.5-102.5] vs 50 [27-91] vs 30 [21.25-45.5]); and poor QOL. Sixteen (40%) GP had impaired gastric accommodation (< 238 mL). Post-WLST 3 CPM normal/hypernormal GMA was observed in 17 (42%), 18 (67%), and 5 (42%) patients with GP, FD (NGE), and FD (DGE), respectively; and 3 CPM hyponormal in remaining patients in each group.Post-WLST dysrhythmia was comparable. Conclusions WLST-electrogastrography coupled with GE study may distinguish between normal/dysrhythmic GMA revealing pathophysiologicalphenotypes of GP and FD. Analysing extent of power change in normogastric, and dysrhythmic frequencies may comprehensively elucidate disease severity.

Background/Aims: Systemic sclerosis (SSc) often is complicated by small intestinal bacterial overgrowth (SIBO). A systematic review and meta-analysis thus examined the prevalence of SIBO in SSc (SSc-subtypes), identify risk factors for SIBO in SSc and the effects of concomitant SIBO on gastrointestinal symptoms in SSc. Methods: We searched electronic databases until January-2022 for studies providing prevalence rates of SIBO in SSc. The prevalence rates, odds ratio (OR) and 95% confidence intervals (CI) of SIBO in SSc and controls were calculated. Results: The final dataset comprised 28 studies with 1112 SSc-patients and 335 controls. SIBO prevalence in SSc-patients was 39.9% (95% CI, 33.1-47.1; P= 0.006), with considerable heterogeneity, (I 2 = 76.00%, P < 0.001). As compared to controls, there was a 10-fold increased SIBO prevalence in SSc-patients (OR, 9.6; 95% CI, 5.6-16.5; P< 0.001). The prevalence of SIBO was not different in limited cutaneous SSc as compared to diffuse cutaneous SSc (OR, 1.01; 95% CI, 0.46-2.20; P = 0.978). Diarrhea (OR, 5.9; 95% CI, 2.9-16.0; P = 0.001) and the association between SIBO in SSc and proton pump inhibitor use (OR, 2.3; 95% CI, 0.8-6.4; P = 0.105) failed statistical significance. Rifaximin was significantly more effective as compared to rotating antibiotic in eradicating SIBO in SSc-patients (77.8% [95% CI, 64.4-87.9]) vs 44.8% [95% CI, 31.7-58.4]; P < 0.05). Conclusions There is a 10-fold increased prevalence of SIBO in SSc, with similar SIBO prevalence rates in SSc-subtypes. Antimicrobial therapy of SIBO-positive SSc-patients with diarrhea should be considered. However, the results must be interpreted with caution due to substantial unexplained heterogeneity in the prevalence studies, and the low sensitivity and specificity of the diagnostic tests suggesting that the reliability of the evidence may be low.

Disorders of gut-brain interaction (DGBIs) are common conditions in community and clinical practice. As specialized enteroendocrine cells, enterochromaffin (EC) cells produce up to 95% of total body serotonin and coordinate luminal and basolateral communication in the gastrointestinal (GI) tract. EC cells affect a broad range of gut physiological processes, such as motility, absorption, secretion, chemo/mechanosensation, and pathologies, including visceral hypersensitivity, immune dysfunction, and impaired gastrointestinal barrier function. We aim to review EC cell and serotonin-mediated physiology and pathophysiology with particular emphasis on DGBIs. We explored the knowledge gap and attempted to suggest new perspectives of physiological and pathophysiological insights of DGBIs, such as (1) functional heterogeneity of regionally distributed EC cells throughout the entire GI tract; (2) potential pathophysiological mechanisms mediated by EC cell defect in DGBIs; (3) cellular and molecular mechanisms characterizing EC cells and gut microbiota bidirectional communication; (4) differential modulation of EC cells through GI segment-specific gut microbiota; (5) uncover whether crosstalk between EC cells and (i) luminal contents; (ii) enteric nervous system; and (iii) central nervous system are core mechanisms modulating gut-brain homeostasis; and (6) explore the therapeutic modalities for physiological and pathophysiological mechanisms mediated through EC cells. Insights discussed in this review will fuel the conception and realization of pathophysiological mechanisms and therapeutic clues to improve the management and clinical care of DGBIs.

no abstract available.