Archive for ottobre, 2012
Reazioni avverse agli alimenti – Reflusso esofageo e Sindrome da colon irritabile
ECIM 2012 – 5th European Congress for Integrative Medicine – “The Future of Comprehensive Patient Care” – 21-22 September 2012 – Palazzo dei Congressi, Florence
CLINICAL AUDIT ON FOOD ADVERSE REACTIONS AND ELIMINATION DIET. A RETROSPECTIVE STUDY
Francesco Cosentino, PhD Gastroenterology and Hepatology Department Milton Keynes General Hospital NHS –Milton Keynes – UK Francesco.Cosentino@mkhospital.nhs.uk
Maria Concetta Giuliano, PhD General Practice Gravina di Catania, NHS Italy mcstudio@hotmail.it
Download presentazione: http://www.asf.toscana.it/images/stories/pubblicazioni/ecim2012/22/m-c-giuliano.pdf
Recent insights into the role of innate immunity in the intestinal tract underline that role of specific receptors and specialized immunity cells is the basis of tolerance to a food and microrganism. Food adverse reactions can be quite often the cause of reflux acid symptoms and IBS. Recently eosinophilic oesophagitis has been recognized as cause of chronic GORD symptoms despite PPI therapy. On our experience, we have been recognizing reflux acid symptoms and chronic diarrhoea due to food adverse reactions when every specific diagnostic exam has been unable to demonstrate any remarkable abnormality. Food adverse reactions is responsible for increase in cytokines and histamine, serotonin and nitric oxide production. Nitric oxide is also neuromediator of TLOR and participates in regulating interdigestive motility complex phase III. In many cases of IBS syndrome does exist evidence of triptase increase; further in large bowel mucosa we notice many mastocites which contain many granules rich in histamine and are near to the intestinal nerves. We report retrospective study conducted in the last two years about elimination diet in fifty patients (25 patients with acid reflux symptoms; 25 patients with chronic diarrhoea). The elimination diet was formulated on the basis of food adverse reactions emerged by IGG4 Food Intolerance. None of the 25 GERD patients was on proton pump inhibitor or antiacid therapy either at the time of the test or during three months of exclusion diet (GERD control group13 pts). IBS patients were taking at the time of test metoclopramide or loperamide tablets without any good improvement. IBD and particularly microscopic colitis had been excluded by colonoscopy and histological colonic biopsies. The specific exclusion diet proved to be effective for ameliorating symptoms in Gerd and IBS patients. After three months, going on elimination diet, we used reintroduction diet to assess any symptomatology recurrence and then specific SLIT for other three months. After one meal without dietary restriction was allowed once a week.We increased one meal, without dietary restriction, a week for every month till to reach six meals a week. Rarely we stopped our schedule. A total period of 12 months was necessary to recover food tolerance. Food adverse reaction is more often mediated by IGG antibodies than IGE; IGG4 food intolerance test should be requested every time we don’t improve patient’s symptoms by therapy and realize the exact nature of symptomatology.
http://www.europeanintegrativemedicinejrnl.com/article/S1876-3820(12)00720-2/fulltext
Patologie Ambientali – stress ossidativo e polimorfismi genetici
ECIM 2012 – 5th European Congress for Integrative Medicine – “The Future of Comprehensive Patient Care” – 21-22 September 2012 – Palazzo dei Congressi, Florence
ENVIRONMENTAL DISEASES, OXIDATIVE STRESS AND GENETIC POLYMORFISM
F. Cosentino1, M.C. Giuliano2 , F. Bisicchia3
1Gastroenterology and Hepatology Department Milton Keynes General Hospital NHS – UK, Milton Keynes – 2Ph GP NHS Italy, Gravina di Catania –3Ph GP Trainee NHS Italy, Catania
download presentazione: http://www.asf.toscana.it/images/stories/pubblicazioni/ecim2012/22/f-bisicchia.pdf
The increasing industrialization and globalization have led to an increasing of volatile organic compounds (VOC an increasing of the concentration of heavy metals (lead, mercury, arsenic, cadmium) that in the past were not at concentrations not harm, and an aggravating electromagnetic pollution. All that is the cause of environmental illness. The way in which environmental disease are expressed depends on how the environmental agent enters the body, how it is metabolized, and route of excretion. L ‘increased load of xenobiotics and the consequent increase in oxidative stress would be behind the rise of allergic diseases and in many cases of neoplastic diseases. In particular, some genetic polymorphisms (CYP2D6, PON1, MnSOD, SOD3, GSTP1, GSTM1 GSTT1) or epigenetic alterations through a reduced or absent elimination of superoxide and the subsequent production of peroxynitrite and hydroxyl groups could be responsible for worsening chronic degenerative diseases such as SBS (Sick BuildingSyndrome), CFS (Crhonic Fatigue Syndrome), FMS (Fibromyalgia Syndrome) and MCS (Multi Chemical Sensitivity). Some of these diseases are often diagnosed in the same individual, would suggest that they may represent an epiphenomenon of a common denominator across the nuclear membrane lipid peroxidation damage. DNA damage (epigenetic alteration) and relative decrease of the enzymatic functions of superoxide dismutase, catalase, glutathione peroxidase and transferase justify the low threshold of sensitivity to xenobiotics. The purpose of this research is to perform a retrospective analysis of patients who have already been given the diagnosis of environmental disease, but where neurological symptoms of acute respiratory or may instead be related to somatoform disorders. All patients will undergo tests at the first level, to verify the actual presence of increased oxidative stress, possible involvement of the immune system, presence of neoplastic diseases. Confirmed the presence of increased oxidative stress, are subjected to subsequent investigations (second level) such as the dosages of these enzyme activities in leukocyte and therefore searched for genetic polymorphisms.
http://www.europeanintegrativemedicinejrnl.com/article/S1876-3820(12)00844-X/fulltext
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