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Posté : 30 mars 2007 09:22
par aud
Ah! VOUIII ! je me suis trompée ! C'est 40 mg l'inexium !
le clostridium, je l'ai fait chercher déjà 2 fois . la dernière c'était , il y a un un peu moins d'un an ... mais qui sait, cette fois, ça pourrait être ça.
Merci pour vos conseils. C'est bien de vous trouver là, dès le matin !
Bonne journée
Aud

Re: Lyme et problèmes gastro-intestinaux

Posté : 29 févr. 2008 11:54
par lea
Via Canalyme, puis le Deutsche Borréliose Bund, traduit en french par Manu... Il faut le faire, merci Manu

:ensemble

léa

LEAKY GUT SYNDROMES: BREAKING THE VICIOUS CYCLE
BY LEO GALLAND, M.D.
From the perspective of function, the contents of the gut lumen lie outside the body and contain a toxic/antigenic load from which the body needs to be protected. Protection is supplied by complex mechanisms which support one another: intestinal secretions (primarily mucus and secretory IgA), the mucosal epithelium, and intramural lymphocytes [1]. This primary, intestinal barrier is supported by the liver, through which all enterically-derived substances must pass before entering the arterial circulation for transport to other tissues and organs. Kupffer cells in the hepatic sinusoids remove absorbed macromolecules by phagocytosis. Hepatic microsomal enzymes alter gut-derived chemical substrates by oxidation and by conjugation to glycine and glutathione(GSH) for excretion into bile and for circulation to the kidneys. The cost of detoxification is high; reactive intermediates and free radicals are generated and anti-oxidants like GSH are consumed [2, 3]. Any compromise of intestinal barrier function increases the production of oxygen radicals and carcinogens by the liver's cytochrome P-450 mixed-function oxidase system. The excretion of oxidation by-products into bile and the reflux of this "toxic" bile into the pancreatic ducts may be the major cause of chronic pancreatic disease.[4, 5]
Compromised intestinal barrier function can also cause disease directly, by immunological mechanisms.[6-9] Increased permeability stimulates classic hypersensitivity responses to foods and to components of the normal gut flora; bacterial endotoxins, cell wall polymers and dietary gluten may cause "non-specific" activation of inflammatory pathways mediated by complement and cytokines. [10] In experimental animals, chronic low-grade endotoxemia causes the appearance of auto-immune disorders.[11-13]
Leaky Gut Syndromes are clinical disorders associated with increased intestinal permeability. They include inflammatory and infectious bowel diseases [14-19], chronic inflammatory arthritides [9, 20-24], cryptogenic skin conditions like acne, psoriasis and dermatitis herpetiformis [25-28], many diseases triggered by food allergy or specific food intolerance, including eczema, urticaria, and irritable bowel syndrome [29-37], AIDS [38-40], chronic fatigue syndromes [Rigden, Cheney, Lapp, Galland, unpublished results], chronic hepatitis [41], chronic pancreatitis [4, 5], cystic fibrosis [42] and pancreatic carcinoma. Hyperpermeability may play a primary etiologic role in the evolution of each disease, or may be a secondary consequence of it which causes immune activation, hepatic dysfunction, and pancreatic insufficiency, creating a vicious cycle. Unless specifically investigated, the role of altered intestinal permeability in patients with Leaky Gut Syndromes often goes unrecognized. The availability of safe, non-invasive, and inexpensive methods for measuring small intestinal permeability make it possible for clinicians to look for the presence of altered intestinal permeability in their patients and to objectively assess the efficacy of treatments. Monitoring the intestinal permeability of chronically ill patients with Leaky Gut Syndromes can help improve clinical outcomes.
TRIGGERS AND MEDIATORS OF THE LEAKY GUT
Leaky Gut Syndromes are usually provoked by exposure to substances which damage the integrity of the intestinal mucosa, disrupting the desmosomes which bind epithelial cells and increasing passive, para-cellular absorption. The commonest causes of damage are infectious agents (viral, bacterial and protozoan) [43-46], ethanol [47, 48], and non-steroidal anti-inflammatory drugs [20, 49, 50]. Hypoxia of the bowel (occurring as a consequence of open-heart surgery or of shock) [51, 52], elevated levels of reactive oxygen metabolites (biliary, food-borne or produced by inflammatory cells) [53], and cytotoxic drugs [54-56] also increase para-cellular permeability.
THE FOUR VICIOUS CYCLES
CYCLE ONE: ALLERGY
The relationship between food sensitivities and the leaky gut is complex and circular. Children and adults with eczema, urticaria or asthma triggered by atopic food allergy have baseline permeability measurements that are higher than control levels [57-59]. Following exposure to allergenic foods, permeability sharply increases. Most of this increase can be averted by pre-treatment with sodium cromoglycate [32, 34, 57-59], indicating that release from mast cells of atopic mediators like histamine and serotonin is responsible for the increase in permeability. It appears that an increase in intestinal permeability is important in the pathogenesis of food allergy and is also a result of food allergy.
Claude Andre, the leading French research worker in this area, has proposed that measurement of gut permeability is a sensitive and practical screening test for the presence of food allergy and for following response to treatment [57]. In Andre's protocol, patients with suspected food allergy ingest 5 grams each of the innocuous sugars lactulose and mannitol. These sugars are not metabolized by humans and the amount absorbed is fully excreted in the urine within six hours. Mannitol, a monosaccharide, is passively transported through intestinal epithelial cells; mean absorption is 14% of the administered dose (range 5-25%). In contrast, the intestinal tract is impermeable to lactulose, a disaccharide; less than 1% of the administered dose is normally absorbed. The differential excretion of lactulose and mannitol in urine is then measured. The normal ratio of lactulose/mannitol recovered in urine is less than 0.03. A higher ratio signifies excessive lactulose absorption caused by disruption of the desmosomes which seal the intercellular tight junctions. The lactulose/mannitol challenge test is performed fasting and again after ingestion of a test meal. At the Hospital St. Vincent de Paul in Paris, permeability testing has been effectively used with allergic infants to determine which dietary modifications their mothers needed to make while breast feeding and which of the "hypoallergenic" infant formulas they needed to avoid in order to relieve their symptoms [60].
CYCLE TWO: MALNUTRITION.
Disruption of desmosomes increases absorption of macromolecules. If the epithelial cells themselves are damaged, a decrease in trans-cellular absorption may accompany the increased para-cellular absorption. Because nutrients are ordinarily absorbed by the trans-cellular route, malnutrition may occur, aggravating strucutural and functional disturbances [61]. Under normal conditions, intestinal epithelium has the fastest rate of mitosis of any tissue in the body; old cells slough and a new epithelium is generated every three to six days [62, 63]. The metabolic demands of this normally rapid cell turnover must be met if healing of damaged epithelium is to occur. When they are not met, hyperpermeability exacerbates [64, 65].
Correction of nutritional deficiency with a nutrient-dense diet and appropriate supplementation is essential for the proper care of patients with Leaky Gut Syndromes. Specific recommendations are made in the last section of this review. Because of the association between hyperpermeability and pancreatic dysfunction, pancreatic enzymes may also be required.
CYCLE THREE: BACTERIAL DYSBIOSIS
Dysbiosis is a state in which disease or dysfunction is induced by organisms of low intrinsic virulence that alter the metabolic or immunologic responses of their host. This condition has been the subject of a recent review article [66]. Immune sensitization to the normal gut flora is an important form of dysbiosis that has been implicated in the pathogenesis of Crohn's disease and ankylosing spondylitis[67-81]. Recent research findings suggest that bacterial sensitization is an early complication of altered permeability and exacerbates hyperpermeability by inducing an inflammatory enteropathy [82, 83]. This has been most studied in the response to NSAIDs. Single doses of aspirin or of indomethacin increase para-cellular permeability, in part by inhibiting the synthesis of protective prostaglandins [20, 49, 50, 84, 85]. Hyperpermeability is partially prevented by pre-treatment with the prostaglandin-E analogue, misoprosterol. Chronic exposure to NSAIDs produces a chronic state of hyper-permeability associated with inflammation, which can not be reversed by misoprosterol but which is both prevented and reversed by the administration of the antibiotic, metronidazole [83, 86]. The effectiveness of metronidazole in preventing NSAID-induced hyperpermeability probably reflects the importance of bacterial toxins in maintaining this vicious cycle. A single dose of bacterial endotoxin, administered by injection, increases the gut permeability of healthy humans [87]. Chronic arthritis can be induced in rats by injection of cell wall fragments isolated from normal enteric anaerobes[88]. Patients with rheumatoid arthritis receiving NSAIDs have increased antibody levels to Clostridium perfringens and to its alpha toxin, apparently as a secondary response to NSAID therap[89].
There is ample documentation for a therapeutic role of metronidazole and other antibiotics in Crohn's disease and rheumatoid arthritis[90-98]. The mechanism underlying the response has been in dispute. In the case of tetracyclines, one group has asserted that mycoplasma in the joints cause rheumatoid arthritis, others have countered this argument by demonstrating that minocycline is directly immunosuppressive in vitro [99]. Because all patients with arthritis have used NSAIDs, and because NSAID enteropathy is associated with bacterial senisitization, it is possible that the the antibiotic-responsiveness of some patients with inflammatory diseases is a secondary effect of NSAID-induced bacterial sensitization which then exacerbates the Leaky Gut Syndrome. Altering gut flora through the use of antibiotics, synthetic and natural, probiotics, and diet is a third strategy for breaking the vicious cycle in Leaky Gut Syndromes. With regard to diet, patients whose disease responds to vegetarian diets are those in whom the diet alters gut ecology; if vegetarian diets does not alter gut ecology, the arthritis is not improved[100].
CYCLE FOUR; HEPATIC STRESS
The liver of Leaky Gut patients works overtime to remove macromolecules and oxidize enteric toxins. Cytochrome P-450 mixed-function oxidase activity is induced and hepatic synthesis of free radicals increases. The results include damage to hepatocytes and the excretion of reactive by-products into bile, producing a toxic bile capable of damaging bile ducts and refluxing into the pancreas [4, 5]. In attempting to eliminate toxic oxidation products, the liver depletes its reserves of sulfur-containing amino acids [101]. These mechanisms have been most clearly demonstrated in ethanol-induced hepatic disease [47]. Sudduth [102] proposes that the initial insult is the ethanol-induced increase in gut permeability which creates hepatic endotoxemia. Endotoxemia can further increase permeability, alter hepatic metabolism, and stimulate hepatic synthesis of reactive species which are excreted in bile. This toxic bile, rich in free radicals, further damages the small-bowel mucosa, exacerbating hyperpermeability.

A PRACTICAL APPROACH
Suspect a pathological increase in gut permeability when evaluating any patient with the diseases listed in Table 1 or the symptoms listed in Table 2. Measure permeability directly using the lactulose/mannitol challenge test. Indirect measures of gut permeability include titres of IgG antibody directed against antigens found in common foods and normal gut bacteria.
TABLE 1
DISEASES ASSOCIATED WITH INCREASED
INTESTINAL PERMEABILITY
Inflammatory bowel disease
Infectious enterocolitis
Spondyloarthropathies
Acne
Eczema
Psoriasis
Urticaria
HIV infection
Cystic fibrosis
Pancreatic insufficiency
AIDS, HIV infection
Hepatic dysfunction
Irritable bowel syndrome with food intolerance
CFIDS
Chronic arthritis/pain treated with NSAIDS
Alcoholism
Neoplasia treated with cytotoxic drugs
Celiac disease
Dermatitis herpetiformis
Autism
Childhood hyperactivity
Environmental illness
Multiple food and chemical sensitivities
These tests may be useful but cannot substitute for the direct permeability assay, especially when one is following the response to treatment.
IF ALL COMPONENTS OF THE LACTULOSE/MANNITOL TEST ARE NORMAL, repeat the challenge after a test meal of the patient's common foods. If the test meal produces an increase in lactulose excretion (signifying hyperpermeability) or a decrease in mannitol excretion (signifying malabsorption), specific food intolerances are likely and further testing for food allergy is warranted. Once the patient has been maintained on a stable elimination diet for four weeks, repeat the lactulose/mannitol challenge after a test meal of foods permitted on the elimination diet. A normal result assures you that all major allergens have been identified. An abnormal result indicates that more detective work is needed.
IF THE INITIAL FASTING MANNITOL ABSORPTION IS LOW, suspect malabsorption. This result has the same significance as an abnormal D-xylose absorption test. Look for evidence of celiac disease, intestinal parasites, ileitis, small bowel bacterial overgrowth and other disorders classically associated with intestinal malabsorption and treat appropriately. After eight weeks of therapy, repeat the lactulose/mannitol challenge. An improvement in mannitol excretion indicates a desirable increase in intestinal absorptive capacity. The lactulose/mannitol assay has been proposed as a sensitive screen for celiac disease and a sensitive test for dietary compliance [46, 103-106]. For gluten-sensitive patients, abnormal test results
demonstrate exposure to gluten, even when no intestinal symptoms are present. Monitoring dietary compliance to gluten avoidance by testing small bowel permeability is especially helpful in following those patients for whom gluten enteropathy does not produce diarrhea but instead causes failure to thrive, schizophrenia or inflammatory arthritis [107-115].
In the case of relatively mild celiac disease or inflammatory bowel disease, mannitol absorption may not be affected but lactulose absorption will be elevated. A recent study published in the Lancet found that the lactulose-mannitol ratio was an accurate predictor of relapse when measured in patients with Crohn's disease who were clinically in remission [116].

TABLE 2
SYMPTOMS ASSOCIATED WITH INCREASED INTESTINAL PERMEABILITY
Fatigue and malaise
Arthralgias
Myalgias
Fevers of unknown origin
Food intolerances
Abdominal pain
Abdominal distension
Diarrhea
Skin rashes
Toxic feelings
Cognitive and memory deficits
Shortness of breath
Poor exercise tolerance
IF THE INITIAL FASTING LACTULOSE IS ELEVATED, OR IF THE INITIAL FASTING LACTULOSE/MANNITOL RATIO IS ELEVATED, consider the possibility of mild inflammatory bowel disease or gluten enteropathy. There are four other primary considerations:
(A) Exposures. Does the patient drink ethanol, take NSAIDs or any potentially cytotoxic drugs? If so, discontinue them and have the lactulose/mannitol challenge repeated three weeks later. If it has become normal, drug exposures were the likely cause of leaky gut. If it has not, bacterial sensitization may have occurred. This may be treated with a regimen of antimicrobials and probiotics. My preference is a combination of citrus seed extract, berberine and artemisinin (the active alkaloid in Artemisia annua), which exerts a broad spectrum of activity against Enterobacteriaceae, Bacteroides, protozoa and yeasts [117-120].
If the patient has no enterotoxic drug exposures, inquire into dietary habits. Recent fasting or crash dieting may increase permeability. Counsel the patient in consuming a nutritionally sound diet for three weeks and repeat the test.
Patients with chronic arthritis may have difficulty stopping NSAIDs. Alternative anti-inflammatory therapy should be instituted, including essential fatty acids, anti-oxidants or mucopolysaccharides[121-125]. Changing the NSAID used may also be helpful. NSAIDs like indomethacin, which undergo enteroheaptic recirculation, are more likely to damage the small intestine that NSAIDs that are not excreted in bile, like ibuprofen [126]. Nabumetone (relafen) is a pro-NSAID that is activated into a potent NSAID by colonic bacteria; the active metabolite is not excreted in bile. Nabumetone is the only presently available NSAID that does not increase small intestinal permeability.
(B) Infection. The possibilities include recent acute viral or bacterial enteritis, intestinal parasitism, HIV infection and candidosis. Stool testing is useful in identifying these. Repeat the permeability test six weeks after initiating appropriate therapy.
(C) Food allergy. Approach this probability as described in the section above on food allergy in patients with normal fasting test results. The difference lies in degree of damage; food intolerant patients with abnormal fasting permeability have more mucosal damage than patients with normal fasting permeability and will take longer to heal.
(D) Bacterial overgrowth resulting from hypochlorhydria, maldigestion, or stasis [41, 127, 128]. This is confirmed by an abnormal hydrogen breath test. Most of the damage resulting from bacterial overgrowth is caused by bacterial enzyme activity. Bacterial mucinase destroys the protective mucus coat; proteinases degrade pancreatic and brush border enzymes and attack structural proteins. Bacteria produce vitamin B12 analogues and uncouple the B12-intrinsic factor complex, reducing circulating B12 levels, even among individuals who are otherwise asymptomatic [129, 130]. In the absence of intestinal surgery, strictures or fistulae, bacterial overgrowth is most likely a sign of hypochlorhydria resulting from chronic gastritis due to Helicobacter pylori infection. Triple therapy with bismuth and antibiotics may be needed, but it is not presently known whether such treatment can reverse atrophic gastritis or whether natural, plant-derived antimicrobials can achieve the same results as metronidazole and ampicillin, the antibiotics of choice.
Bacterial overgrowth due to hypochlorhydria tends to be a chronic problem that recurs within days or weeks after antimicrobials are discontinued. Keith Eaton, a British allergist who has worked extensively with the gut fermentation syndrome, finds that administration of L-histidine, 500 mg bid, improves gastric acid production in allergic patients with hypochlorhydria, probably by increasing gastric histamine levels [personal communication]. Dietary supplementation with betaine hydrochloride is usually helpful but intermittent short courses of bismuth, citrus seed extract, artemisinin, colloidal silver and other natural antimicrobials are often needed. The first round of such treatment, while the patient is symptomatic, should last for at least twelve weeks, to allow complete healing to occur. Repeat the lactulose/mannitol assay at the end of twelve weeks, while the patient is taking the antimicrobials, to see if complete healing has been achieved. The most sensitive test for recurrence of bacterial overgrowth is not the lactulose/mannitol assay but the breath hydrogen analysis.
TROPHIC THERAPIES
Many naturally occurring substances help repair the intestinal mucosal surface or support the liver when stressed by enteric toxins. Basic vitamin and mineral supplementation should include all the B vitamins, retinol, ascorbate, tocopherol, zinc, selenium, molybdenum, manganese, and magnesium. More specialized nutritional, glandular and herbal therapies are considered below. These should not be used as primary therapies. Avoidance of enterotoxic drugs, treatment of intestinal infection or dysbiosis, and an allergy elimination diet of high nutrient density that is appropriate for the individual patient are the primary treatment strategies for the Leaky Gut Syndromes. The recommendations that follow are to be used as adjuncts:
(1) Epidermal Growth Factor (EGF) is a polypeptide that stimulates growth and repair of epithelial tissue. It is widely distributed in the body, with high concentrations detectable in salivary and prostate glands and in the duodenum. Saliva can be a rich source of EGF, especially the saliva of certain non-poisonous snakes. The use of serpents in healing rituals may reflect the value of ophidian saliva in promoting the healing of wounds. Thorough mastication of food may nourish the gut by providing it with salivary EGF. Purified EGF has been shown to heal ulceration of the small intestine [131].
(2) Saccharomyces boulardii is a non-pathogenic yeast originally isolated from the surface of lichee nuts. It has been widely used in Europe to treat diarrhea. In France it is popularly called "Yeast against yeast" and is thought to help clear the skin in addition to the gut. Clinical trials have demonstrated the effectiveness for S. boulardii in the treatment or prevention of C. difficile diarrhea, antibiotic diarrhea and traveler's diarrhea[132, 133]. Experimental data suggest that the yeast owes its effect to stimulation of SIgA secretion[134]. SIgA is a key immunological component of gut barrier function.
Passive elevation of gut immunoglobulin levels can be produced by feeding whey protein concentrates that are rich in IgA and IgG. These have been shown to be effective in preventing infantile necrotizing enterocolitis[135].
(3) Lactobacillus caseii var GG is a strain of lactobacillus isolated and purified in Finland. Like S.boulardii, Lactobacillus GG has been shown effective in the prevention of traveller's diarrhea and of antibiotic diarrhea and in the treatment of colitis caused by C. difficile. Lactobacillus GG limits diarrhea caused by rotavirus infection in children and in so doing improves the hyperpermeability associated with rotavirus infection.[136-139] The mechanism of action is unclear. The ability of other Lactobacillus preparations to improve altered permeability has not been directly tested, but is suggested by the ability of live cultures of L. acidophilus to diminish radiation-induced diarrhea, a condition directly produced by the loss of mucosal integrity.
(4) Glutamine is an important substrate for the maintenance of intestinal metabolism, structure and function. Patients and experimental animals that are fasted or fed only by a parenteral route develop intestinal villous atrophy, depletion of SIgA, and translocation of bacteria from the gut lumen to the systemic circulation. Feeding glutamine reverses all these abnormalities. Patients with intestinal mucosal injury secondary to chemotherapy or radiation benefit from glutamine supplementation with less villous atrophy, increased mucosal healing and decreased passage of endotoxin through the gut wall[140-143].
(5) Glutathione (GSH) is an important component of the anti-oxidant defense against free radical-induced tissue damage. Dietary glutathione is not well absorbed, so that considerable quantities may be found throughout the gut lumen following supplementation[144]. Hepatic GSH is a key substrate for reducing toxic oxygen metabolites and oxidized xenobiotics in the liver. Depletion of hepatic glutathione is a common occurence in Leaky Gut Syndromes contributing to liver dysfunction and liver necrosis among alcoholics and immune impairment in patients with AIDS. The most effective way to raise hepatic glutathione is to administer its dietary precursors, cysteine or methionine. Anti-oxidant supplementation for Leaky Gut Syndromes should therefore include both GSH and N-acetyl cysteine. Because protozoa are more sensitive to oxidant stress than are humans and because most anti-parasitic drugs and herbs work by oxidative mechanisms, high dose anti-oxidant supplementation should be witheld during the treatment of protozoan infection, especially during treatment with Artemisia. (6) Flavonoids are potent, phenolic anti-oxidants and enzyme inhibitors with varied effects depending on the tissues in which they act. Quercetin and related flavonoids inhibit the release of histamine and inflammatory mediators. Taken before eating, they may block allergic reactions which increase permeability. Catechins have been used in Europe to treat gastric ulcerations. The flavonoids in milk thistle (silymarin) and in dandelion root (taraxacum) protect the liver against reactive oxygen species[145].
(7) Essential fatty acids (EFAs) are the substrates for prostaglandin synthesis. Differential feeding of EFAs can profoundly affect prostanoid synthesis and the systemic response to endotoxin. In experimental animals, fish oil feeding ameliorates the intestinal mucosal injury produced by methotrexate and, additionally, blunts the systemic circulatory response to endotoxin[146]. The feeding of gamma-linolenic acid (GLA), promotes the synthesis of E-series prostaglandins, which decrease permeability. EFAs should be consumed in the most concentrated and physiologically active form to avoid exposure to large quantities of polyunsaturated fatty acids from dietary oils. Consumption of vegetable oils tends to increase the free radical content of bile and to exacerbate the effects of endotoxin[147].
(8) Fiber supplements have complex effects on gut permeability and bacterial composition. Low fibre diets increase permeability. Dietary supplementation with insoluble fibre, such as pure cellulose, decreases permeability. Dietary supplementation with highly soluble fibre sources, such as fruit pectin or guar gum, has a biphasic effect. At low levels they reverse the hyperpermeability of low residue diets, probably by a mechanical bulking effect which stimulates synthesis of mucosal growth factors. At high levels of supplementation, they produce hyperpermeability, probably by inducing synthesis of bacterial enzymes which degrade intestinal mucins[148-151]. For maximum benefit with regard to intestinal permeability, dietary fibre supplementation should therefore contain a predominance of hypoallergenic insoluble fibre.
(9) Gamma oryzanol, a complex mixture of ferulic acid esters of phytosterosl and other triterpene alcohols derived from rice bran, has been extensively researched in Japan for its healing effects in the treatment of gastric and duodenal ulceration, thought to be secondary to its potent anti-oxidant activity[152, 153].

SUMMARY
Altered intestinal permeability is a key element in the pathogenesis of many different diseases. Hyperpermeability initiates a vicious cycle in which allergic sensitization, endotoxic immune activation, hepatic dysfunction, pancreatic insufficiency and malnutrition occur; each of these increases the leakiness of the small bowel. Effective treatment of the Leaky Gut Syndromes requires several components: avoidance of enterotoxic drugs and allergic foods, elimination of infection or bacterial overgrowth with antimicrobials and probiotics, and dietary supplementation with trophic nutrients. Direct measurement of intestinal permeability allows the clinician to plan appropriate strategies and to gauge the effectiveness of treatment, using objective parameters.


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Re: Lyme et problèmes gastro-intestinaux

Posté : 29 févr. 2008 11:58
par lea
Bon, comme un message n'accepte que 60000 caractères....
la traduction içi :

léa

Pour comprendre: l'hyperperméabilité intestinale
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source: http://www.mdheal.org/leakygut.htm" onclick="window.open(this.href);return false;
traduction / Manu
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Ce concept n'est pas bien connu par le grand publique, ni très documenté en Français, mais, chez les anglo-saxons, l'idée a été développée et des moyens d'y remédier ont été testé.
Si vous avez compris que l'intestin est un filtre, mais que la qualité du filtre peut aller de très bon (sujet sain) à la passoire (nous, les malades souffrant d'inflammation intestinale souvent méconnue). Et si vous avez compris que l'intestin est probablement au centre de la Spondylarthrite, Alors, vous serez intéressés par cette petite traduction....
Syndrome d’hyper perméabilité intestinale

D’un point de vue fonctionnel, le contenu de la lumière intestinale est éliminée à l’extérieur du corps, il est chargé de déchets toxiques et d’antigènes desquels le corps doit se protéger. Cette protection fait intervenir des mécanismes interdépendants : les sécrétions intestinales (principalement le mucus et les IgA sécrétoires), la muqueuse épithéliale et des lymphocytes [1]. Après cela, le foie est la barrière intestinale à travers laquelle les substances provenant de l’intestin doivent passer avant de pouvoir rejoindre le flux sanguin qui les mènera aux différents tissus et organes. Les cellules de Kupffer situées dans le sinus hépatique enlèvent par phagocytose les macromolécules absorbées. Les enzymes des microsomes hépatiques s’attaquent aux substances chimiques provenant de l’intestin par des phénomènes d’oxydation et par conjugaison à la glycine et au glutathion (GSH) avant une excrétion dans la bile ou un passage dans les reins. Le coût de cette détoxication est élevé, des intermédiaires réducteurs et des radicaux libres sont produits tandis que les anti-oxydants comme le glutathion sont consommés [2, 3]. Toute atteinte à ces fonctions de barrière intestinale augmente la production d’oxydants et de substances carcinogènes par les cytochrome P450 hépatiques (mixed fonction oxydase system) . l’excrétion des sous-produits d'oxydation dans la bile et le reflux de cette bile "toxique" dans les conduits pancréatiques peuvent être la cause principale de la pancréatite chronique.[4 , 5]
L’atteinte de la fonction de barrière intestinale peut aussi causer des maladies directement, par des mécanismes immunologiques. [6-9] Une perméabilité augmentée des réponses classiques d’hypersensibilité aux aliments et aux composants normaux de la flore intestinale ; les endotoxines bactériennes, les polymères membranaires et le gluten alimentaire peuvent être responsables dune activation « non-spécifique » des voies inflammatoires relayées par le complément et les cytokynes . [10] Chez les animaux de laboratoire, de passages sanguins chroniques d’endotoxines provoquent des troubles auto-immuns. [11-13]
Les syndromes d’hyper perméabilité intestinale sont des désordres cliniques associés à une perméabilité intestinale exacerbée. Ils incluent les maladies infectieuses et inflammatoires de l’intestin [14-19], les rhumatismes inflammatoires chroniques [9, 20-24], des atteintes cutanées telles que l’acné, le psoriasis et la dermite herpétiforme [25-28], beaucoup de maladies aggravées par des allergies alimentaires ou des intolérances alimentaires spécifiques, comme l’eczéma, l’urticaire, et le syndrome de l’intestin irritable [29-37], les déficits immunitaires [38-40], le syndrome de fatigue chronique, les hépatites chroniques [41], les pancréatites chroniques [4, 5], la fibrose cystique [42] et le carcinome pancréatique. L’hyper perméabilité pourrait jouer un rôle étiologique primordiale dans l’évolution de chaque maladie, ou pourrait en être une conséquence secondaire ce qui cause l’’activation immunitaire, le dysfonctionnement hépatique et l’insuffisance pancréatique, créant un cercle viscieux. A moins d’investigation spécifiques, le rôle de la perméabilité intestinale altérée chez les patients ayant un « syndrome d’hyper perméabilité intestinale » reste souvent méconnu. La disponibilité de techniques sûres, non invasives, et peu coûteuses pour mesurer la perméabilité de l’intestin grèle donne la possibilité aux cliniciens d’observer la présence d’une perméabilité intestinale altérée chez leur patients et pour évaluer objectivement l’efficacité des traitements. Surveiller la perméabilité intestinale chez les patients atteints de maladies chroniques associé au « syndrome d’hyper perméabilité intestinale » pourrait aider à améliorer les résultats cliniques.
DÉCLENCHEMENTS ET MÉDIATEURS DE L'INTESTIN HYPER PERMÉABLE
Les syndromes d’hyper perméabilité intestinale sont souvent provoqués par des substances qui endommagent l’intégrité de la muqueuse intestinale, déconnectant les desmosomes qui sont attachés à la membrane épithéliale, augmentant ainsi l’absorption para cellulaire passive. La cause la plus sommune de ce type de dommage est représenté par les agents infectieux (viraux, bactériens, protozoaires..) [43-46], l’éthanol (l’alcool) [47-48] et les anti-inflammatoires non stéroïdiens [20, 49, 50]. L’hypoxie de l’intestin (apparaissant lors des chirurgies à cœur ouvert ou des états de choc) [51, 52], des taux élevés de métabolites oxydants (biliaire, d’origine alimentaire ou produits par des cellules inflammatoires) [53], les médicaments cytotoxiques (chimiothérapie) [54-56] augmentent aussi la perméabilité para-cellulaire.
LES 4 CERCLES VISCIEUX

CERCLE 1 : L’ALLERGIE
La relation entre la sensibilité aux aliments et le syndrome d’hyper perméabilité intestinale est complexe et circulaire. Les enfants et adultes avec de l’eczéma, de l’urticaire ou de l’asthme déclenchées par une allergie alimentaire sur terrain atopic ont des taux de base de perméabilité intestinale qui sont plus élevés que chez les sujets témoins [57-59].
Suite à l’exposition à des aliments allergéniques, la perméabilité augmente brusquement. La plus grande partie de cette augmentation peut être prévenue par l’administration préventive de cromoglycate de sodium [32, 34, 57-59], cela indique que la libération depuis les mastocytes de médiateurs de l’atopie tels que l’histamine et la sérotonine sont responsables de l’augmentation de la perméabilité. Il apparaît donc qu’une augmentation de la perméabilité intestinale est important dans la pathogénèse de l’allergie alimentaire mais est aussi une conséquence de l’allergie alimentaire.
Claude André, le principale chercheur français dans ce domaine, a proposé la mesure de la perméabilité intestinale comme un test d’évaluation sensible et pratique pour diagnostiquer une allergie alimentaire et pour suivre la réponse au traitement [57]. Dans le protocole du chercheur André, les patients suspects d’allergies alimentaires ingurgitent respectivement 5 g. de sucre lactulose et de mannitol . Ces sucres ne sont pas métabolisés par les humains et toute les quantités ingurgitées sont complètement éliminées par les urines dans les 6 heures. Le mannitol, un monosaccharide, est passivement transporté par les cellules épithéliales intestinales ; l'absorption moyenne est 14% de la dose administrée (marge : 5-25%). En revanche, la barrière intestinale est imperméable au lactulose, un disaccharide ; moins de 1% de la dose administrée est normalement absorbé. L'excrétion différentielle du lactulose et du mannitol dans l’urine est alors mesurée. Le rapport normal du rappot lactulose/mannitol récupéré dans l’urine est inférieur à 0.03. Un rapport plus élevé signifie l'absorption excessive du lactulose causée par la rupture des desmosomes qui scellent les jonctions serrées intercellulaires. Le test d’absorption lactulose/mannitol est exécuté à jeun et encore après l'ingestion d'un repas test. À l'hôpital St Vincent de Paul à Paris, l'essai de perméabilité a été efficacement employé avec les enfants en bas âge allergiques pour déterminer quelles modifications diététiques leurs mères devaient faire tout en allaitant au sein et déterminer quelles formules infantiles "hypoallergéniques" elles devaient éviter afin de soulager leurs symptômes [ 60 ].
CYCLE DEUX : MALNUTRITION
La déconnexion des desmosomes augmente l’absorption des macro-molécules. Si les cellules épithéliales sont elles aussi endommagées, une diminution de l’absorption trans-cellulaire peut accompagner l’augmentation de l’absorption para-cellulaire. Parce que les nutriments normalement absorbés par la voie trans-cellulaire, une malnutrition peut intervenir, aggravant les perturbations structurelles et fonctionnelles [61]. En condition normale, l’épithélium intestinale a la fréquence de mitose (multiplication cellulaire) le plus rapide de l’organisme ; les vielles cellules muent et un nouvel épithélium est généré en 3 à 6 jours [62, 63]. Les demandes métaboliques d’un tel remplacement cellulaire physiologiquement rapide doivent être réunis pour éventuellement réparer des dommages. S’ils ne sont pas réunis, l’hyper perméabilité s’aggrave [64, 65].
La correction des déficiences nutritionnelles avec un régime approprié et des compléments alimentaires est essentiel dans le cas particulier des patients avec le syndrome d’hyper perméabilité intestinale. Des recommandations spécifiques seront formulées dans la dernière section de ce document. Parce qu’il y a association entre hyper perméabilité et un dysfonctionnement pancréatique, une supplémentation en enzyme pancréatique peut aussi être nécessaire.
CYCLE TROIS : DYSBIOSE INTESTINALE
La dysbiose est un état dans lequel une maladie ou un dysfonctionnement est provoqué par des micro-organismes à pauvre potentiel virulent intrinsèque qui altèrent la réponse métabolique et immunologique chez leurs hôtes. Cette condition a fait l’objet d’un article récent [66]. La sensibilisation immunitaire envers la flore normale de l’intestin est une forme importante de dysbiose , qui serait impliquée dans la pathogénèse de la maladie de Crohn et la Spondylarthrite Ankylosante [67-81]. Des résultats de recherche récentes suggèrent que la sensibilisation soit une complication précoce d’une perméabilité altérée et augmente l’hyperperméabilité en induisant une entéropathie inflammatoire[82, 83]. Ce phénomène a été bien étudié dans le cas des anti inflammatoires non stéroïdiens (AINS). Des doses uniques d’aspirine ou d’indométhacine augmentant la perméabilité trans-cellulaire , en partie en diminuant les prostaglandines protectrices [20, 49, 50, 84, 85]. L’hyper perméabilité peut être prévenue en partie en administrant un traitement à base de prostaglandine E analogues, le Misoprosterol DCI (en France, on le trouve sous le nom de CYTOTEC° ).
L’exposition chronique aux AINS produit un état d’hyper perméabilité chronique associé à l’inflammation, qui ne peux pas être renversé par l’utilisation du misoprosterol mais qui peut être à la fois prévenu et renversé par l’administration d’un anti-biotique : le metronidazole (en France : FLAGYL°) [83, 86]. L’efficacité du metronidazole dans la prévention des hyper perméabilités induites par les AINS reflète le röle très probable des toxines bactériennes dans le maintient de ce cercle vicieux. Une seule dose d’endotoxine bactérienne , administrée par injection, augmente la perméabilité intestinale chez les sujets sains [87]. Des arthrites chroniques peuvent être induites chez les rats par l’injection de fragments de membranes cellulaires isolés à partir d’entéro-bactéries anaérobies (bactéries intestinales qui survivent dans les milieux sans oxygène) [88]. Les patients souffrants de polyarthrite rhumatoïde recevant des AINS ont des taux d’anticorps contre Clostridium Perfringens et contre son alpha-toxine, ce qui apparait comme un effet secondaire des AINS [89].
Il existe une documentation très fournie sur le rôle thérapeutique du metronidazole et d’autres antibiotiques dans la maladie de Crohn et la polyarthrite rhumatoïde [90-98]. Les mécanismes qui sous-tendent la réponse font encore l’objet de discussion. Dans le cas des tetracycliques, un groupe affirme que la présence de mycoplasme dans l’articulation est à l’origine de la polyarthrite, les autres ont contré cet affirmation en démontrant que la monocycline était directement immunosuppressive in-vitro [99]. Parce ce que tous les patients souffrant d’arthrites ont utilisé des AINS, et parce que les entéropathies aux AINS sont associés à une sensibilisation aux bactéries intestinales, il est possible que la réponse aux anti-biotiques de certains patients souffrant de maladies inflammatoires soit un effet secondaire des sensibilisation bactériennes induites par les AINS et qui viendraient aggraver le syndrome d’hyper perméabilité intestinale.
Modifier la flore intestinale avec des anti-biotiques naturels ou synthétiques, des pro biotiques, un régime est le triptyque de la stratégie pour lutter contre le syndrome d’hyper perméabilité intestinale.
En regardant du côté des régimes alimentaires, on constate que les patients dont la maladie est améliorées par un régime végétarien sont ceux chez qui le régime a modifié la flore intestinale. Si le régime végétarien n’arrive pas à modifier l’écosystème intestinale, l’arthrite ne s’améliore pas [100].
CERCLE QUATRE : LE STRESS HEPATIQUE
Les foies de patients à l’intestin hyper perméable travaille en sur régime pour éliminer les macromolécules et les toxines oxydantes intestinales. L'activité à fonctions mixtes d'oxydase du cytochrome P-450 est induite et la synthèse hépatique de radicaux libres augmente. Il en résulte des dommages causés aux hépatocytes et l’excrétion de sous-produits réactifs dans la bile, en produisant une bile toxique capable d’endommager les voies biliaires et de refluer dans le pancréas [4, 5]. En essayant d'éliminer les produits toxiques d'oxydation, le foie épuise ses réserves en acides aminés contenant du soufre [ 101 ]. Ces mécanismes les plus clairs ont été démontrés dans la maladie hépatique alcoolique [ 47 ]. Sudduth [ 102 ] propose que l'acte initiale soit l'augmentation sous l’effet de l’alcool de la perméabilité de l’intestin qui crée l’intoxication hépatique. L’intoxication hépatique augmentera ensuite la perméabilité, altèrera le métabolisme hépatique, et stimulera la synthèse hépatique d’espèces réactives qui seront excrétées dans la bile. Cette bile toxique, riche en radicaux libres, ira endommager la muqueuse de l’intestin grêle, exacerbant l’hyper perméabilité.
UNE APPROCHE PRATIQUE
Test au mannitol/lactulose

si le test à jeun initial au lactulose est élevé, ou si le rapports à jeun initial du test lactulose/mannitol est élevé, il faut considérer la possibilité d’une maladie inflammatoire intestinale intermédiaire ou d’une entéropathie au gluten. Il y a quatre autres consédirations à prendre en compte :
(a) exposition : alcool, AINS, chimio….
(b) Infection : parasitose, candidose, VIH, gastro entérite virale ou bactérienne
(c) Allergies alimentaires
(d) Croissance trop importante de la flore intestinale causée par l’hypo chlorhydrie gastrique, mauvaise digestion, stase
TRAITEMENT LOCAL
(1) epidermal groth factor : facteur de croissance epidermique : la salive apporte ce facteur : mastiquez vos aliments
(2) saccharomyces boulardii : (en France :ULTRA LEVURE)
(3) lactobacillus casei var GG (en France : Ergyphilus du labo nutergia)
(4) la glutamine, pour nourrir les entérocytes
(5) du glutathion , important anti oxydant
(6) des flavonoïdes : par exemple la quercitine qui inhiberait l’espression de l’hidtamine et d’autres médiateurs de l’inflammation
(7) des acides gras essentiels, biensûr l’acide gamma linolenique (omega 3)
(8) une alimentation riche en fibre
(9) gamma oryzanol : une mixture complexe d’esters d’acide ferulique et de triterpene-alcool dérivés de fibre de riz

maladies associées à une augmentation de la perméabilité intestinale

-Maladies inflammatoires de l'intestin
-Gastro entérites infectieuses
-Spondylarthropathies
-Acné
-Eczema
-Psoriasis
-Urticaire
-infection à HIV
-Fibrose cystique
-Insuffisance pancréatique
-Syndrome de l'intestin irritable avec intolérance alimentaire
-syndrome de fatigue chronique et de dysfonctionnement immunologique (voir http://www.cfids.org" onclick="window.open(this.href);return false; )
-arthrite chronique traitée par anti inflammatoires non stéroïdiens
-alcoolisme
-cancer traité par chimiothérapie
-maladie coeliaque
-dermite herpétiforme
-Autisme
-hyper activité infantile
-maladie environementale
-sensibilité chimique ou alimentaire multiple



symtomes associés à l'augmentation de la perméabilité intestinale

-fatigue, malaise
-arthralgie
-myalgie
-fièvre d'origine inconnue
-intolérance alimentaire
-douleurs abdominales
-distension abdominale
-diarrhée
-rougeurs cutanées
-sensation d'intoxication
-déficit cognitif et troubles de la mémoire
-soufle coupé
-faible tolérance à l'exercice physique
Posté par manudk à 15:07 - sciences - Commentaires [1] - Rétroliens [0] - Permalien [#]

Re: Lyme et problèmes gastro-intestinaux

Posté : 29 févr. 2008 12:41
par Françoise
Merci Léa pour ce document important pour les lymés ou non !
le foie est la barrière intestinale à travers laquelle les substances provenant de l’intestin doivent passer avant de pouvoir rejoindre le flux sanguin
il faudrait simplement dire plutôt "le foie est un filtre"....
La relation entre la sensibilité aux aliments et le syndrome d’hyper perméabilité intestinale est complexe et circulaire.
ça me rappelle ce que j'ai lu concernant l'EPP et les pb qu'il semble occasionner au niveau de la muqueuse intestinale mais je ne reviens pas sur un sujet qui fâche
Léa : je te souhaite beaucoup de courage :mouak
et encore merci pour ce travail de documentation et traduc mais où vas tu pêcher tout ça ?
Françoise

Re: Lyme et problèmes gastro-intestinaux

Posté : 29 févr. 2008 13:20
par lea
Françoise a écrit : il faudrait simplement dire plutôt "le foie est un filtre"..
Francoise, chui d'accord.. mais je ne "touche pas" à la traduction des autres :P
C'est un principe.. et j'en ai beaucoup.. et cela ne rend pas forcément heureux!!!

:oops:
:mouak

léa

Re: Lyme et problèmes gastro-intestinaux

Posté : 29 févr. 2008 20:02
par aud
Merci Léa . C'est vraiment trés interessant ! Je comprends mieux mon ventre grace à toi !
Aud

Re: Lyme et problèmes gastro-intestinaux

Posté : 01 mars 2008 09:49
par christine
Léa,
merci, j'ai imprimé pour lire tranquillement et faire partager cette lecture.

Bises

christine

Re: Lyme et problèmes gastro-intestinaux

Posté : 30 nov. 2009 14:00
par Titine
Merci Léa pour cette mine de renseignements.

J'ai des douleurs au ventre depuis plusieurs années, plus ou moins violentes, des gargouillements, je fais de l'aérophagie :? , j'ai des problèmes de digestion, très souvent des brûlures d'estomac et parfois la bile qui remonte, sans parler des rots :beurk . Des diarrhées vraiment très souvent. La plupart du temps à vrai dire.

Il y a quatre ans, j'ai fais une colite, il y a deux ans, j'avais des calculs dans les reins, dont un a eu beaucoup de mal à descendre et est resté coincé juste avant la vessie. C'est une horreur ces trucs-là :mrgreen: .

Depuis quatre ans (et même depuis plus longtemps mais moins fortement) j'ai toujours des douleurs au ventre. Je n'en ai pas parlé aux médecins. Ca fait partie des douleurs récurentes mais avec lesquelles j'ai appris à vivre. J'ai l'impression que mes intestins parfois se gonflent, d'autres fois se dégonflent. A d'autres moments ça fait comme lors de la grossesse quand mon fils donnait des coups de pieds.

Et aujourd'hui, sous amoxicilline, ça c'était accentué un peu au début du traitement, mais depuis quelques jours les symptômes diminuent.

Bonne continuation à tous.

Re: Lyme et problèmes gastro-intestinaux

Posté : 30 nov. 2009 14:08
par fobitic
Coucou Titine,

un régime strict sans caséine, ni gluten pourrait te soulager.

Re: Lyme et problèmes gastro-intestinaux

Posté : 30 nov. 2009 14:39
par Titine
Fobitic merci,

je vais m'y mettre dès que j'aurai regardé ce qu'est exactement la caséine et dans quoi on la trouve! :oops:

Merci merci

reflux

Posté : 02 juil. 2013 15:04
par lymette47
bonjour,

je fais une fibroscopie jeudi prochain pour explorer mon système digestif a cause de reflux gastro oesophagien.
Ce serait donc une manifestation de la maladie de lyme ?

merci pour vos réponses.

Re: Lyme et problèmes gastro-intestinaux

Posté : 03 juil. 2013 13:26
par Lisa B
C'est un des symptômes de Lyme, bien connus notamment chez les enfants (mais aussi les adultes).

Mais, il y a aussi pleins d'autres causes au reflux gastro-oesophagien, donc il faut aussi investiguer un peu partout avant d'accuser Lyme : un train peut en cacher un autre...

Re: Lyme et problèmes gastro-intestinaux

Posté : 03 juil. 2013 15:16
par vanchou
Gaviscon marche bien contre les reflues.
Quand je suis en chute libre avec Lyme, je fais des diarrhées très liquides avec parfois du sang.
Je prend de la glutamine riche en acide aminés et des probiotiques çà marche bien en général, les antibiotiques m'ont aussi été d'une grande aide pour éliminer ce symptôme.
Et le sans gluten aide bien aussi, quand je fais des écarts j'en paye les conséquences...

Re: Lyme et problèmes gastro-intestinaux

Posté : 05 juil. 2013 00:30
par KLAATU
si c'est un ulcère gastro, faut voir :
La bactérie Helicobacter pylori (H. Pylori), une bactérie qui survit à l’acidité, est la principale cause d’ulcères : elle causerait approximativement de 60 % à 80 % des ulcères de l’estomac et de 80 % à 85 % des ulcères duodénaux;

La prise d’anti-inflammatoires non stéroïdiens ou AINS (par exemple, l’aspirine, l’Advil® et le Motrin®), est la seconde cause la plus fréquente d’ulcère au tube digestif.

Comme calmant et cicatrisant antiulcère : jus de pomme de terre(bio) cru (j'ai eu un crohn: recto colite hémorragique( très) !, je sais de quoi je parle, guerri par Flagil- métronidazole!) et aussi l'argile verte surfine à boire ( le fameux Smecta n'en est qu'une fraction purifiée) .

Sinon une inflammation des canaux et de la vésicule biliaire ,lithiase , donnes des douleur "gastrique", aussi siégeant dans l'hypochondre droit, irradiant vers l'omoplate .droite. ( les antibio et autre médicament mettent le foie à rude épreuve, et donc tout le système digestif et empêche la détoxification) .

Pour détox le foie, vésicule et canaux: j'ai expérimenté : ca fonctionne !!
Faire une cure de Magnésium sulfate( le chlorure fatigue les reins) : http://phytotherapie-homeopathie.blogsp ... sicule.htm

l(Teinture-mère de brou de noix noire n'est pas obligatoire) le souffre est éliminé par les intestins ( boire beaucoup)

- Et le chardon Marie( Sylibum Marianus- principe actif Silymarine ( Legalon en pharma) , c'est reconnu comme un contre poison ;( inhibe le cytochrome P450, donc certains toxiques, médicaments, et abx métabolisé par le foie)
la silymarine peut régénérer les tissus abîmés du foie en plus de protéger cet organe contre les effets des toxines naturelles (champignons, morsures de serpents, piqûres d'insectes, alcool, etc.) ou synthétiques (solvants, produits de nettoyage, médicaments, etc.). La silybine semble efficace dans le cas d'intoxication par de l'amanite phalloïde

- echographie du foie et vésicule

Lyme et perméabilité intestinale

Posté : 16 avr. 2014 02:46
par litana
Pensez vous que la borreliose / maladie de Lyme crée de la perméabilité intestinale?
Avez des articles scientifiques qui tendraient vers cette hypothèse?



Si c'est le cas, cela expliquerai les symptômes de
- dépression (crée par l'intolérance au gluten)
- tendinite (si résistante aux anti-inflammatoire, elles sont crées par un encrassage de l'organisme par les molécules de caséine)