&lt;i&gt;Helicobacter pylori&lt;/i&gt; Infection Increases Mucosal Permeability of the Stomach and Intestine

Fukuda, Yoshihiro; Bamba, Hiroko; Okui, Masanori; Tamura, Kouichi; Tanida, Noritoshi; Satomi, Masamichi; Shimoyama, Takashi; Nishigami, Takashi

doi:10.1159/000051918

Cited by 72 publications

(49 citation statements)

References 19 publications

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“…Latent celiac disease was excluded by measuring EMAs in the PBC cohort and the two positive patients were excluded. Helicobacter pylori infection with associated gastritis was not evaluated, however, this is unlikely to account for the differences observed [33]. A high rate of H. pylori infection has been documented in patients with hepatitis C [34], while studies of PBC have shown no increase in H. pylori prevalence [35,36].…”

Section: Discussionmentioning

confidence: 99%

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

2006

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Antimitochondrial antibodies (AMAs) found in patients with primary biliary cirrhosis (PBC) cross-react with bacterial proteins and hence molecular mimicry has been proposed as a mechanism for AMA development. Alterations in gastrointestinal permeability would provide a potential route for increased exposure of gut flora to the immune system. In this study we aimed to compare the measured gastrointestinal permeability in patients with PBC to that in patients with liver disease (hepatitis C) and healthy control populations. Subjects drank a mixture of sucrose, lactulose, and mannitol dissolved in water. Eight-hour urinary excretion of the sugars was measured to assess intestinal permeability. Antiendomysial antibody testing was performed to exclude subclinical celiac disease. Eighty-six patients with PBC were evaluated and compared to 69 hepatitis C patients and 155 healthy controls. The mean urinary excretion of sucrose in the PBC patients (133.89 +/- 72.56 mg) was significantly higher than that in hepatitis C patients (101.07+/-63.35) or healthy controls (89.46+/-41.76) (P=0.0001), suggesting abnormal gastric or proximal small intestinal permeability. Sucrose excretion was not increased among patients with hepatitis C compared to healthy controls. The ratio of lactulose:mannitol excretion, reflecting small bowel permeability, was also elevated in the PBC group (0.017+/-0.012) compared to healthy controls (0.012+/-0.007) (P=0.0001) but was equal to that found among patients with hepatitis C (0.016+/-0.011) (P=NS). We conclude that the permeability of both the stomach and the small bowel is increased in patients with PBC, however, it is unclear if it is a cause, consequence, or manifestation of the disease.

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Section: Discussionmentioning

confidence: 99%

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

2006

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“…This finding underscores that the minimal modifications in CYP-450 activity that occurred during treatment are completely reversible. Furthermore, since it is unlikely that H. pylori eradication may lead to an improvement in gastric emptying and/or increased absorption of aminopyrine (38)(39)(40), it should be interesting to evaluate in larger cohorts of patients whether H. pylori may affect CYP-450 activity as seems to happen in patients with chronic liver disease (41,42).…”

Section: Discussionmentioning

confidence: 99%

Influence of 1-Week Helicobacter pylori Eradication Therapy with Rabeprazole, Clarithromycin, and Metronidazole on 13C-Aminopyrine Breath Test

et al. 2005

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Helicobacter pylori eradication therapy is commonly prescribed in the general population. Treatment consists of drugs that are mainly metabolized by the liver cytochrome P-450 (CYP) enzymatic pool. Most H. pylori-infected patients often take drugs for comorbid illnesses, therefore increasing the potential for drug-drug interactions. We aimed to evaluate the interactions of rabeprazole, clarithromycin, and metronidazole 1-week H. pylori eradication therapy with CYP-dependent liver metabolic function in clinical practice. Ten patients referred to our unit for H. pylori infection underwent 1-week eradication therapy with rabeprazole (20 mg, b.i.d.), clarithromycin (500 mg, b.i.d.), and metronidazole (500 mg, b.i.d.). We chose the 13C-aminopyrine breath test (13C-ABT) to evaluate CYP-dependent liver function since it is noninvasive and nonharmful. All patients underwent 13C-ABT at three time points: before therapy (to), at the end of therapy (t8), and after 1 month of follow-up (t38). Mean 13C-ABT dose/hr (t0 = 14.0 +/- 5.4, t8 = 13.5 +/- 4.0, t38 = 16.1 +/- 5.6) as well as 13C-ABT cumulative dose (t0 = 2.4 +/- 1.1, t8 = 2.4 +/- 0.8, t38 = 2.6 +/- 1.0) were not statistically different at the three time points of the study. These results did not seem to be influenced by drugs being administered concomitantly. In everyday clinical practice rabeprazole-based H. pylori eradication therapy does not seem to display any significant interactions with CYP-dependent liver function, even in patients on multiple drugs.

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“…pylori infection is known to be associated with many gastrointestinal disorders such as gastritis, gastric ulcer, gastroesophageal reflux disease (GERD), gastric cancer, and NSAID/ aspirin-induced gastric injury [2,3,10,11]. Although H. pylori presence has also been detected in the small intestine [12], there are few reports on how H. pylori may affect the small intestinal mucosa. Until now, only small intestinal bacterial overgrowth (SIBO) [13][14][15][16] and the phenotype of Crohn's disease [17] have been reported to be associated with H. pylori in the small intestine.…”

Section: Discussionmentioning

confidence: 99%

Influence of Helicobacter pylori Infection on the Small Intestinal Mucosa

2013

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patients undergoing capsule endoscopy (CE) were tested for anti-H. pylori immunoglobulin G antibody (Hp-IgG) using an enzyme-linked immunosorbent assay (ELISA). None of the patients had been treated for H. pylori infection or diagnosed as having Crohn's disease or any other clinically apparent small intestinal disorders prior to the CE. Results. The overall Hp-IgG-positive rate was 26.3%. The incidence of enteritis, as diagnosed by CE, tended to be lower in the Hp-IgG-positive patients (23.1%) than in the Hp-IgG-negative patients (38.4%) ( = 0.140). When patients receiving aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs), well-known causes of enteritis, were excluded, the incidence of enteritis in the Hp-IgG-positive patients (11.7%) was significantly lower than that in the Hp-IgG-negative patients (43.7%) ( = 0.005). A binomial logistic regression analysis revealed a significant negative relationship between Hp-IgG positivity and the presence of enteritis in patients receiving neither aspirin nor NSAIDs ( = 0.017). Conclusions. Our data indicated that H. pylori positivity was inversely associated with the prevalence of enteritis.

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<i>Helicobacter pylori</i> Infection Increases Mucosal Permeability of the Stomach and Intestine

Cited by 72 publications

References 19 publications

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

Influence of 1-Week Helicobacter pylori Eradication Therapy with Rabeprazole, Clarithromycin, and Metronidazole on 13C-Aminopyrine Breath Test

Influence of Helicobacter pylori Infection on the Small Intestinal Mucosa

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