The study on the role of inflammatory cells and mediators in post-infectious functional dyspepsia

Li, Xiaobo; Chen, Huimin; Lü, Hong; Li, Weiguang; Chen, Xiaoyu; Yansheng, Peng; Ge, Zhi‐Zheng

doi:10.3109/00365521003632576

Cited by 62 publications

(65 citation statements)

References 33 publications

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“…This finding is consistent with higher levels of GDNF in patients with functional dyspepsia 79 . Both duodenal and gastric biopsy samples showed mast cell hyperplasia and an increased release of histamine and tryptase (which indicates mast cell activation) 81 . Gastric biopsy samples also revealed a closer association between nerves and mast cells 81 , and these immune mediators are known to synergistically activate neurons 82 .…”

Section: Gastroduodenal Sensitivitymentioning

confidence: 99%

“…Both duodenal and gastric biopsy samples showed mast cell hyperplasia and an increased release of histamine and tryptase (which indicates mast cell activation) 81 . Gastric biopsy samples also revealed a closer association between nerves and mast cells 81 , and these immune mediators are known to synergistically activate neurons 82 . In the duodenal bulb, the number of chromogranin A (CGA)-positive enteroendocrine cells was reduced in duodenal biopsy samples from patients with functional dyspepsia, mostly in patients with EPS 83 .…”

Section: Gastroduodenal Sensitivitymentioning

confidence: 99%

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Functional dyspepsia

Enck¹,

Azpiroz

Boeckxstaens

et al. 2017

Nat Rev Dis Primers

260

247

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| Functional dyspepsia is one of the most prevalent functional gastrointestinal disorders. Functional dyspepsia comprises three subtypes with presumed different pathophysiology and aetiology: postprandial distress syndrome (PDS), epigastric pain syndrome (EPS) and a subtype with overlapping PDS and EPS features. Functional dyspepsia symptoms can be caused by disturbed gastric motility (for example, inadequate fundic accommodation or delayed gastric emptying), gastric sensation (for example, sensations associated with hypersensitivity to gas and bloating) or gastric and duodenal inflammation. A genetic predisposition is probable but less evident than in other functional gastrointestinal disorders, such as irritable bowel syndrome (IBS). Psychiatric comorbidity and psychopathological state and trait characteristics could also play a part, although they are not specific to functional dyspepsia and are less pronounced than in IBS. Possible differential diagnoses include Helicobacter pylori infection and peptic ulceration. Pharmacological therapy is mostly based on the subtype of functional dyspepsia, such as prokinetic and fundus-relaxing drugs for PDS and acid-suppressive drugs for EPS, whereas centrally active neuromodulators and herbal drugs play a minor part. Psychotherapy is effective only in a small subset of patients, whereas quality of life can be severely affected in nearly all patients. Future therapies might include novel compounds that attempt to treat the underlying gastric and duodenal inflammation. NATURE REVIEWS | DISEASE PRIMERS VOLUME 3 | ARTICLE NUMBER 17081 | 1 PRIMER © 2 0 1 7 M a c m i l l a n P u b l i s h e r s L i m i t e d , p a r t o f S p r i n g e r N a t u r e . A l l r i g h t s r e s e r v e d .standard therapy for gastro -oesophageal reflux disease. Paediatric dyspeptic symptoms are being addressed in a separate classification effort 10 . This Primer covers functional dyspepsia in adults only, although we sporadically refer to paediatric functional dyspepsia when similarities exist. EpidemiologyThe population prevalence of functional dyspepsia is quite variable across the globe, with overall high numbers (10-40%) in Western countries and low numbers (5-30%) in Asia, independent of the respective functional dyspepsia definitions 11 . A large-scale health and nutrition survey from France 12 (which involved >35,000 people) identified that 15% of individuals had suspected functional dyspepsia, 28% had irritable bowel syndrome (IBS) and 6% had both. The population of patients who are affected by both IBS and functional dyspepsia has been reported to range between 10% and 27% in previous studies 13 and to approach 30% in popu lation samples; it could be even higher in specific populations 14,15 . This observation has given rise to the term 'overlap syndrome' (REF. 13), which calls into question the sensitivity and specificity of the Rome criteria, at least for IBS and functional dyspepsia. This argument is also supported by the observation that patients with functional dyspepsia m...

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Section: Gastroduodenal Sensitivitymentioning

confidence: 99%

Section: Gastroduodenal Sensitivitymentioning

confidence: 99%

Functional dyspepsia

Enck¹,

Azpiroz

Boeckxstaens

et al. 2017

Nat Rev Dis Primers

260

247

View full text Add to dashboard Cite

show abstract

“…The report is sufficient to show that a nutritional and intestinal pathogenesis lies behind malnutrition, persistent diarrhea as well as behind overall subclinical inflammation that is in turn associated with overweight. These dysfunctions depend on a positive energy balance in the associated, parallel-alternative forms of insulin resistance and fattening [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. The intestinal pathogenesis consists of an overgrowth of immunogenic bacteria [1,9,12,14,19].…”

Section: Introductionmentioning

confidence: 99%

"Initial Hunger" for All? A Study on Undernourished Infants

Ciampolini¹

2014

JPNC

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Aim: A meal/satiety pattern dictated by the rhythmic arousal of Initial Hunger (IH and IHMP) is used by overweight people to decrease body weight. We however conceived IHMP to improve intestinal absorption and diminish immune involvement in intestinal mucosa as well as throughout the body (overall subclinical inflammation). The purpose of IHMP may be shown by its early employment in undernourished infants.Methods: Nine malnourished infants (weight per age lower than 70%) with diarrhea in the first 15 months of age were investigated in a controlled, randomized study. Organic diseases were excluded by conventional procedures, including intestinal biopsy. Six infants were assigned to the intervention and 3 to the control group. Compliance, intake, and anthropometry were recorded in hospital for 2 months, and then by frequent visiting and 7-day home diary under intervention for 5 total times in two years.Results: Six subjects under intervention and three controls were followed for at least 2 years. Energy intake decreased from 126±21 kcal/kg/d to 85±6 kcal/kg/d in treated infants and from 111±53 kcal/kg/d to 107±37 kcal/kg/d in the first 2 months of study (P<0.01 on longitudinal differences). Days with vomiting became null after 2 months of treatment, whereas in control subjects, 4 or 5 events every 60 days persisted for all follow-ups. Further longitudinal differences were significant on days with diarrhea after three months, and on plasma triglycerides at the two sampled times during treatment. The difference in the Chi square for trend was significant on energy intake and in the numbers of days with vomiting or diarrhea (P<0.002). Serum triglycerides decreased from 148±27 mg/dL to 70±10 mg/dL under intervention, and increased from 119±47 mg/dl to 139±59mg/dl in controls (P<0.002 on the difference). Values after two years of follow-ups were respectively: 73.2 ± 12.3 mg/dL and 89 ± 37 mg/dL (P<0.05). Toward the end of the study, anthropometric measurements increased per age from recruitment in treated infants with differences from control subjects that were not significant in the longitudinal comparisons between groups. Weight per age reached 88.8±8.7% under intervention, and 79.7±10.2% in controls after two years (not significant). Psychomotor development was normal except for one control infant. Conclusion:High triglycerides (and associated insulin resistance with an overall subclinical inflammation) are involved in the persistence of diarrhea and on malnutrition in these undernourished infants as in the development of functional bowel disorders and over weight in adults. IHMP was an actual solution also for malnourished infants.

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“…It is conceivable that these changes may contribute to symptom generation, either by direct interaction with nociceptive pathways or by infl uencing the normal physiology (including delayed gastric emptying and impaired gastric accommodation). On the other hand, low-grade lymphocytic and neutrophil infi ltration in the antral mucosa and increases in other infl ammatory components including enterochromaffi n-like cells and mast cells have been observed by others, suggesting that changes in histamine, tryptase, and 5-hydroxytryptamine (5-HT) could be biological mechanisms inducing gastro intestinal disturbances aft er gastrointestinal infections (38) . In addition, these investigators observed in postinfectious dyspepsia the numbers of activated mast cells and enterochromaffi ne cells in close proximity to the nerves to be signifi cantly higher than in those with nonspecifi c functional dyspepsia or controls.…”

Section: Pathophysiology Of Postinfectious Dyspepsiamentioning

confidence: 99%