Biomedical subjects

Bruno Bonaz

Publications and source records attributed to Bruno Bonaz.

22 records · Page 2Linked to original sources

PubMed2004

Irritable bowel syndrome: a model of the brain-gut interactions.

Brain-gut interactions are increasingly recognized as underlying pathomechanisms of functional gastrointestinal disorders. Bi-directional communication between the central nervous system (CNS) and the enteric nervous system (ENS) occurs both in health and disease. Various CNS- and gut-directed stressors stimulate the brain-gut axis. Processes modulating responsiveness to stressors along the brain-gut axis involve neural pathways, the immunological, and endocrinological mechanisms. Disturbances at every level of neural control of the gastrointestinal tract can affect modulation of gastrointestinal motility, secretion, immune functions as well as perception and emotional response to visceral events. ENS function, central processing, and autonomic regulation play an important role in the brain-gut dialogue. Stress and emotions may trigger neuroimmune and neuroendocrine reactions via the brain-gut axis. Various non-site specific neurotransmitters influence gastrointestinal, endocrine and immune function, as well as human behavior and emotional state, depending on their location. The physiology of the digestive tract, the subjective experience of symptom, health behavior, and treatment outcome are strongly affected by psychosocial factors. Recently, a biopsychosocial model of IBS containing physiological, emotional, cognitive and behavioral components has been proposed. Rapid progress in neurogastroenterology, using new brain imaging techniques, should bring better understanding of the brain-gut axis and open new therapeutic perspectives.

Brain↗

PubMed2003

[Correction of insulin resistance syndrome does not cause normalisation of hyperferritinaemia].

UNLABELLED: The consequences of iron overload from dysmetabolic hyper-ferritinaemia are a strong motivation for an active medical care program. Venesection therapy is known to be effective in controlling iron overload parameters although no study has evaluated the impact of the normalization of metabolic dysfunction on iron overload. AIMS: To evaluate the impact of normalization of metabolic dysfunction on iron overload. METHODS: Sixty consecutive patients with dysmetabolic hepatosiderosis were included in a prospective study. Patients with hyper-ferritinaemia above 1000 microg/l were excluded. Multidisciplinary care was offered to all patients to normalize metabolic disorders (body mass index, arterial hypertension, fasting and postprandial hyperglycemia, hyperuricemia, hypercholesterolemia and hypertriglyceridemia) every three months. All patients were followed for one year. At clinical examinations, ferritinaemia concentrations were measured and all dysmetabolic parameters evaluated. MRI was performed at the beginning of the study and at the one year follow-up, to measure hepatic iron load. RESULTS: Despite efficient medical care of insulin resistance syndrome, ferritinaemia remained stable. In two thirds of the study population, hyper-ferritinaemia reached at least one and a half times the baseline value, although the dysmetabolic disorders of 40% of the patients were strictly normalized. In this group of 44 patients with strict normalization of metabolic functions, 24 (54%) had hyper-ferritinaemia at one year follow-up whereas 16 other (36%) normalized this parameter. Only 4 patients who had a ferritinaemia below 450 microg/l at baseline, normalized this value at one year. Intra-hepatic iron overload, evaluated by MRI imaging remained stable except for 2 patients who normalized ferritinaemia. CONCLUSION: Although efficient handling of dysmetabolic disorders is essential, it is not sufficient to normalize dysmetabolic hyper-ferritinaemia. Only patients with a ferritinaemia value below a baseline of 450 microg/l had normalization of iron overload. Therefore venesection must be offered to all patients with a hyper-ferritinaemia above this value.

Adult↗

PubMed2002

Oesophageal motor and sensitivity abnormalities in non-obstructive dysphagia.

OBJECTIVES: To evaluate oesophageal sensitivity to balloon distension in patients with non-obstructive dysphagia (NOD), and to determine its relationship with the motility pattern in response to food ingestion. PATIENTS AND METHODS: Twenty-one healthy volunteers and 19 consecutive patients complaining of NOD with normal standard manometry were included. An oesophageal sensitivity test was carried out before the manometry study with liquid and solid swallows. RESULTS: The median threshold to distension was 9 ml in control subjects and 5 ml in patients (P < 0.002). Dysphagia or odynophagia were reproduced in 15/19 (78.9%) patients during manometry with solid swallows only. The percentage of swallows with abnormal motility patterns was higher in patients than control subjects (P < 0.001). Compared with control values, sensitivity abnormality was defined by a distension threshold of < 6 ml. Motor abnormality was defined by > 19% of swallows occurring with one or more abnormal motor profiles. A total of 8/19 (42%) patients presented with the association of an abnormal sensitivity threshold and an abnormal motor pattern; 5/19 (26%) presented with isolated motor abnormalities; 4/19 (21%) patients presented with isolated abnormal sensitivity thresholds; and 2/19 (11%) patients presented without any abnormality. CONCLUSION: Manometry with solid swallows and oesophageal balloon distension are useful in characterizing NOD.

Adult↗

PubMed2002

Increased urinary F2-isoprostanes in patients with Crohn's disease.

OBJECTIVES: Reactive oxygen metabolites have been suggested to participate in the pathogenesis of Crohn's disease, but the evidence supporting this contention in vivo is incomplete. Isoprostaglandin F2alpha type III (iPF2alpha-III, or 15-F2t-IsoP) is a prostaglandin F2alpha isomer produced in vivo by free radical-catalyzed peroxidation of arachidonic acid. We aimed to investigate urinary iPF2alpha-III concentrations as an index of lipid peroxidation in 23 patients with Crohn's disease compared with 23 healthy controls, and to test whether lipid peroxidation correlates to clinical relapse and inflammation. METHODS: Urinary iPF2alpha-III was measured by gas chromatography/electronic impact mass spectrometry. RESULTS: Urinary iPF2alpha-III concentrations were significantly higher in patients with Crohn's disease than in healthy controls (median [range] = 130 [38-622] vs 91 [35-152] pmol/mmol of creatinine, respectively; p < 0.01). There was a trend toward significance for patients with clinical relapse versus patients with clinical remission (median [range] = 155 [38-622] vs 96 [64-253] pmol/mmol of creatinine, respectively; p = 0.09). A significant correlation was found between urinary iPF2alpha-III and plasma C-reactive protein concentrations, suggesting a link between lipid peroxidation and inflammation. CONCLUSION: This study provides evidence of increased lipid peroxidation in patients suffering from Crohn's disease, especially in patients with clinical relapse. iPF2alpha-III quantification has to be investigated as a prognosis biomarker in patients suffering from Crohn's disease.

Adolescent↗