Effects of eradication of Helicobacter pylori infection in patients with immune thrombocytopenic purpura: a systematic review

Stasi, Roberto; Sarpatwari, Ameet; Segal, Jodi B; Osborn, John; Evangelista, Maria Laura; Cooper, Nichola; Provan, Drew; Newland, Adrian C.; Amadori, Sergio; Bussel, James B.

doi:10.1182/blood-2008-07-167155

Cited by 280 publications

(214 citation statements)

References 52 publications

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“…Due to variability in study methods and a lack of placebo-controlled studies, we conducted a proportion meta-analysis of fever rates using similar single-arm data from trials (StatsDirect statistical software version 2.7.9) to calculate pooled fever proportions. This method has been used previously in systematic reviews across different disciplines [16][17][18][19][20][21]. A random effects model with the DerSimonian-Laird method was used to account for variability in study design and results.…”

Section: Methodsmentioning

confidence: 99%

Systematic review of fever, febrile convulsions and serious adverse events following administration of inactivated trivalent influenza vaccines in children

et al. 2015

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In 2010, increased febrile convulsions (FC) occurred after administration of inactivated trivalent influenza vaccine (TIV) in Australia. We systematically reviewed the rates of fever, FC and serious adverse events (SAEs) after TIV, focussing on published and unpublished clinical trial data from 2005 to 2012, and performed meta-analysis of fever rates. From 4,372 records in electronic databases, 18 randomised controlled trials (RCTs), 14 non-randomised clinical trials, six observational studies and 12 registered trials (five RCTs and seven non-randomised) were identified. In published RCTs, fever ≥ 38 °C rates after first dose of non-adjuvanted TIV were 6.7% and 6.9% for children aged 6-35 months and ≥ 3 years, respectively. Analysis of RCTs by vaccine manufacturer showed pooled fever estimates up to 5.1% with Sanofi or GlaxoSmithKline vaccines; bioCSL vaccines were used in two non-randomised clinical trials and one unpublished RCT and were associated with fever in 22.5-37.1% for children aged 6-35 months. In RCTs, FCs occurred at a rate of 1.1 per 1,000 vaccinated children. While most TIVs induced acceptably low fever rates, bioCSL influenza vaccines were associated with much higher rates of fever in young children. Future standardised study methodology and access to individual level data would be illuminating.

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Section: Methodsmentioning

confidence: 99%

Systematic review of fever, febrile convulsions and serious adverse events following administration of inactivated trivalent influenza vaccines in children

et al. 2015

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“…24 The association between platelet count improvement and H. pylori eradication has since been corroborated in other studies. [1][2][3] However, an independent effect of H. pylori treatment has been hypothesized, since 1) macrolide antibiotics including clarithromycin (universally included in eradication regimens) possess anti-inflammatory properties which may improve platelet autoreactivity in ITP by blocking the production of proinflammatory cytokines; 4 and 2) antimicrobials used for H. pylori treatment may eradicate other commensal bacteria that stimulate cross reactive platelet antibodies. Using treated, H. pylori -negative patients as controls, this systematic review confirms that the effect of H. pylori treatment is indeed due to eradication of the bacteria and not to the treatment itself.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] However, eradication therapy may result in the improvement of thrombocytopenia by mechanisms independent of H. pylori including the immune modulating effects of the treatment itself 4 or the removal of other commensal bacteria. In support of these hypotheses is a recent meta-analysis showing an increase in platelet count following treatment in some patients with ITP regardless of the outcome of eradication therapy.…”

Section: Introductionmentioning

confidence: 99%

Platelet count response to H. pylori treatment in patients with immune thrombocytopenic purpura with and without H. pylori infection: a systematic review

Arnold¹,

Bernotas²,

Nazi³

et al. 2009

Haematologica

122

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Eradication of H. pylori improves thrombocytopenia in some patients with immune thrombocytopenic purpura by mechanisms that remain obscure. Platelet count responses may occur independently of H. pylori infection as a result of the immune modulating effects of macrolide antimicrobials or the removal of other commensal bacteria. We performed a systematic review of the literature to determine the effect of H. pylori eradication therapy in patients with immune thrombocytopenic purpura by comparing the platelet response in patients who were, and who were not infected with H. pylori. MEDLINE, EMBASE, Cochrane central registry and abstracts from the American Society of Hematology (from 2003) were searched in duplicate and independently without language or age restrictions. Eleven studies, 8 from Japan, were included enrolling 282 patients with immune thrombocytopenic purpura who received eradication therapy; 205 were H. pylori-positive and 77 were H. pylori-negative. The odds of achieving a platelet count response following eradication therapy were 14.5 higher (95% confidence interval 4.2 to 83.0) in patients with H. pylori infection (51.2% vs. 8.8%). No study reported bleeding or quality of life. Adverse events were reported in 12 patients. H. pylori eradication therapy was of little benefit for H. pylori-negative patients. These findings strengthen the causal association between H. pylori infection and immune thrombocytopenia in some patients. Randomized trials are needed to determine the applicability of H. pylori eradication therapy across diverse geographical regions.Key words: helicobacter, autoimmunity, purpura, platelets. Citation

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“…1,2 As H. pylori was first cultivated from human gastric biopsy specimens in 1982, it has been recognized as a causative agent in most of the gastroduodenal diseases, including peptic ulcer, gastric cancer, and gastric mucosa lymphoid tissue lymphoma. [3][4][5][6][7] Furthermore, chronic H. pylori infection is related to various other gastric diseases, though the precise role of H. pylori is unknown in these diseases and there is still controversy regarding this association, including idiopathic thrombocytopenic purpura 8 and cardiovascular disease. 9 Elevated levels of C-reactive protein and IL-6 that are systemic inflammatory markers have been reported to predict the development of type 2 diabetes mellitus (DM).…”

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confidence: 99%

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

Goo

Park

et al. 2010

Laboratory Investigation

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Our earlier report has shown that Helicobacter pylori promoted hepatic fibrosis in a murine model. Herein, in order to elucidate the mechanism by which H. pylori accelerate liver fibrosis, the authors investigated the changes in expression levels of mitogen-activated protein kinases (MAPKs), p53-related proteins, antioxidants, and proinflammatory cytokines in liver samples. H. pylori infection enhanced CCl 4 -induced MAP kinase activation and p53 signaling pathway as well as Bax-and proliferating-cell nuclear antigen expressions, whereas H. pylori alone induced neither of these expressions nor hepatic fibrosis. Moreover, mRNA expressions of inflammatory cytokines, glutathione peroxidase expression, and the proliferative index were strongly augmented in livers of the H. pylori with CCl 4 treatment group compared with those of the CCl 4 -alone treatment group, whereas there was no difference in apoptotic index between the two groups. Interestingly, H. pylori treatment increased the number of a-fetoprotein-expressing hepatocytes independently of CCl 4 intoxication. In vitro analyses, using an immortalized rat hepatic stellate cell (HSC) line, revealed that H. pylori lysates increased the proliferation of HSCs, which was boosted by the addition of transforming growth factor-beta1 (TGF-b1). Furthermore, the treatment of H. pylori lysates promoted the translocation of nuclear factor kappa-light-chain enhancer of activated B cells (NF-kB) into the nucleus based on an increase in the degradation of NF-kB inhibitor alpha, in the presence of TGF-b1, as did H 2 O 2 treatment. In conclusion, H. pylori infection along with an elevated TGF-b1 may accelerate hepatic fibrosis through increased TGF-b1-induced pro-inflammatory signaling pathways in HSCs. Moreover, H. pylori infection might increase the risk of TGF-b1-mediated tumorigenesis by disturbing the balance between apoptosis and proliferation of hepatocytes.

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Effects of eradication of Helicobacter pylori infection in patients with immune thrombocytopenic purpura: a systematic review

Cited by 280 publications

References 52 publications

Systematic review of fever, febrile convulsions and serious adverse events following administration of inactivated trivalent influenza vaccines in children

Systematic review of fever, febrile convulsions and serious adverse events following administration of inactivated trivalent influenza vaccines in children

Platelet count response to H. pylori treatment in patients with immune thrombocytopenic purpura with and without H. pylori infection: a systematic review

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

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