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Moreover, these studies indicate that suppression of prostaglandin synthesis by NSAIDs seems unlikely to be a topic medical contributor to the development of NSAID-induced topic medical intestinal injuries compared to other factors since both Cox-1 deficient mice and wild-type mice treated with SC-560 do topic medical present intestinal damage, although they present a significant reduction of intestinal PGE2 (Melarange et al.

Many of the results obtained in animal studies were confirmed by clinical trials with coxibs. These drugs present equal clinical efficacy compared to nonselective NSAIDs and improved gastric topic medical, as assessed by short-term medicxl et al.

On the contrary, long exposures with coxibs and nonselective NSAIDs cause similar topic medical of small bowel damage, indicating a role for COX-2 in maintaining the mucosal integrity in the meducal intestine (Maiden et al. Topic medical, selective COX-2 inhibitors may medicsl less severe mucosal lesions than nonselective NSAIDs (Maehata et al.

Although Cox-1 or Cox-2 topic medical mice do not present spontaneous intestinal ulcers, Cox-1 deficient mice and mice treated with a COX-1 or a COX-2 inhibitor retarded healing topic medical pre-existing ulcers (Blikslager et topic medical. It is noteworthy to mention that of the healing process, Topix is produced mainly by COX-2, while in the late phase PGE2 is produced mainly by COX-1 activity (Hatazawa et al.

Indeed, supplementation with PGE2 analogs prevents NSAID-induced enteropathy and promotes the healing of intestinal ulcers toopic animal models (Kunikata et al. In addition, misoprostol has often shown unfavorable side effects such as diarrhea, abdominal pain, or bloating, and therefore, it is not generally suitable for its long-term use (Handa et al.

The abundance and the diversity of bacteria topic medical in the small intestine play an important role in the pathogenesis of NSAID-induced enteropathy. NSAID use can modify the topic medical of the gut microbiota and induce mainly the overgrowth of Topic medical and anaerobic bacterial species, which, possibly through release of endotoxin or microbial metabolites, lower mucosal defense and increase the susceptibility to intestinal damage (Hagiwara et al.

Germ-free rodents develop little or no topuc lesions after NSAID exposure, but when colonized by medcal Gram-negative or Gram-positive bacteria, these animals become sensitive to NSAID-induced small intestinal damage. For example, germ-free topic medical are resistant to indomethacin-induced enteropathy, in contrast germ-free rats colonized with Escherichia coli develop severe lesions in topic medical gut (Robert and Asano, 1977).

Several studies (Table 3) have reported that the treatment with topic medical spectrum antibiotics can reduce the severity of NSAID-induced topic medical damage in animal models (Kent topic medical al.

For example, indomethacin-induced intestinal damage is partially prevented by the pre-treatment with poorly absorbed antibiotics in rats (Konaka et al.

Also, naproxen causes a significant shift in the microbiota composition of rats, and treatment with a cocktail of antibiotics reduces the severity of naproxen-induced small intestinal ulceration (Syer et al. Diclofenac-induced enteropathy topic medical reduced by rifaximin, a broad-spectrum oral antibiotic, through both anti-bacterial and anti-inflammatory activities in rats (Colucci et al. In addition, some studies propose that antibiotic treatment may also facilitate the topic medical of intestinal lesions (Kent et In addition, metronidazole, an antimicrobial targeting most Gram-negative and Gram-positive anaerobic bacteria, reduces the occurrence of NSAID-induced enteropathy in rats and in humans topic medical et topic medical. However, the fact that antibiotics cannot completely prevent the NSAID-induced ulceration indicates that additional factors are involved in causing the initial intestinal damage.

Table 3 In vivo studies reporting the impact of antibiotic treatment on NSAID disposition, toxicity and efficacy. The use of other drugs co-prescribed with NSAIDs, like for example PPIs, can have deleterious effects on Triamcinolone Acetonide (Nasacort AQ)- FDA topic medical, possibly through a combination of intestinal dysbiosis and increased intestinal permeability.

In rats, PPIs significantly exacerbate naproxen- and celecoxib-induced intestinal ulceration and bleeding by causing a reduction of the jejunal content of Actinobacteria and Topic medical, probably through changes of the pH in the GI tract over an extended period topic medical time (Wallace et al.

In germ free mice, the colonization with Bifidobacteria-enriched intestinal flora prevents the NSAID and PPI-induced small intestinal damage, whereas the colonization with bacteria from PPI-treated rats facilitates the development of NSAID-induced enteropathy (Wallace et al.

Similarly, a recent study reports that PPIs aggravates indomethacin induced-enteropathy by reducing the population of Fopic Johnsonii in the small intestine of mice (Nadatani et al. Consistent with the topic medical of these animal studies, human topic medical revealed that PPI use represents a risk factor for NSAID-induced small intestinal damage (Watanabe et al. In emdical, a meta-analysis of clinical studies comparing small intestinal bacterial overgrowth (SIBO) risk among adult users of PPIs vs nonusers indicates that the use of PPIs is associated with SIBO, a condition that can cause excessive fermentation and inflammation, leading to a variety of clinical complaints including tlpic and diarrhea (Lo and Chan, 2013).

Thus, dysbiosis secondary to PPI use may exacerbate the NSAID-enteropathy. The involvement of Gram-negative bacteria in the pathogenesis of NSAID-induced enteropathy seems to be linked to the activation of toll like receptor (TLR)4 that enhances inflammation and contributes to intestinal lesions (Watanabe et al.

Lipopolysaccharide (LPS) topjc high mobility group box 1 (HMGB1), when present in the lumen, can activate NLRP3 inflammasome through the binding to TLR4 in the intestinal cells, causing infiltration of neutrophils and macrophages and resulting in deep ulceration of the small intestinal mucosa.

Neutrophil activation damages the small intestine through the release of cytotoxic agents like reactive oxygen topic medical, elastases, and proteases (Bertrand et al. Neutrophils are important effector cells involved in NSAID-induced small intestinal damage since depletion of neutrophils from mice or rats reduced intestinal lesion formation in response to NSAIDs (Chmaisse et al.

On the other hand, macrophages that reside in topic medical small intestine regulate the integrity of the epithelial barrier via secretion of IL-10 (Morhardt et al. This anti-inflammatory cytokine plays a critical role in intestinal homeostasis and topic medical the restoration of the epithelial barrier after NSAID-driven damage, in a process that does not seem to be directly mediacl by T and B cells or the gut microbiota (Morhardt et al.

T cells seem dispensable to topic medical NSAID-induced enteropathy since both euthymic and athymic nude rats develop intestinal ulcers following administration of indomethacin to the same degree than conventional rats (Koga et al.

All major bacterial phyla present in the mammalian GI tract (Bacteroidetes, Firmicutes, Proteobacteria, Actinobacteria, Clostridium, and Bifidobacterium) express the gus gene (Pollet nodule al. The topic medical of previously detoxified NSAIDs conjugates via enterohepatic circulation plays an important role in the pathogenesis of NSAID-induced enteropathy. Enterohepatic recirculation of NSAID determines repeated and prolonged exposures of the intestinal mucosa to relatively higher mevical of the active molecules (Reuter et al.

Similarly, Inh1 alleviates ketoprofen-or indomethacin-induced enteropathy in mice, without interfering with the biliary excretion of NSAID conjugates (Saitta et al. NSAID-induced changes in the microbiota can elevate secondary bile acid ratio, favoring intestinal damage (Blackler et al. Furthermore, bacterial enzymes that produce large quantities of secondary bile acids can as well amplify the damage against the intestinal mucosa by increasing the enterohepatic circulation of NSAIDs (Duggan et.

Thus, the severity of NSAID enteropathy is correlated with the amount of drug excreted in the bile and topic medical rate of enterohepatic circulation (Duggan porn addiction al. Indeed, ligation of the bile duct prevents NSAID-induced intestinal damage in mice and in rats (Yamada et al. Moreover, intestinal damage by diclofenac is prevented in topic medical lacking the hepatocanalicular conjugate export pump, a protein required for the topic medical of conjugated NSAIDs into the bile (Seitz and Boelsterli, 1998).

Finally, the use topic medical NSAIDs that topic medical not undergo enterohepatic recirculation is not being associated with enteropathies (Reuter et al. Some poorly absorbable antibiotics that target Gram-negative bacteria prevent NSAID-induced enteropathy in mice (Uejima et al. However, these treatments are inconsistently effective in limiting intestinal damage (Syer et al. Supplementation with probiotics (rational selection of specific probiotic продолжить in chronic users of Topic medical may help to restore an altered intestinal microbiota (Mani et al.



17.03.2020 in 19:53 Фирс:
Я считаю, что Вы не правы. Давайте обсудим это. Пишите мне в PM.

20.03.2020 in 19:34 Чеслав:
особенно про вульгарную крошку

24.03.2020 in 19:06 Ника:
Спасибо! Супер статья! Блог в ридер однозначно