Helicobacter pyloriseroprevalence in patients with idiopathic pulmonary fibrosis

Bennett, David; Bargagli, Elena; Refini, Rosa Metella; Campagna, Maria Stella; Gennari, Luigi; Nuti, Ranuccio; Figura, Natale; Rottoli, Paola

doi:10.1183/09031936.00104813

Cited by 17 publications

(11 citation statements)

References 13 publications

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“…The discrepancy between HP seroprevalence as shown in the report by Bennett et al [22] and our negative results is in line with findings in other chronic lung diseases [16,27,28,29]. This leads to the hypothesis that HP microaspiration may not be directly involved in the induction or progression of fibrotic lung disease in IPF, but that gastric infection with HP initiates a systemic immune response that has an impact on the pulmonary system in susceptible patients.…”

Section: Discussionsupporting

confidence: 61%

“…The possibility that GER with HP microaspiration is a later event in IPF and associated with disease progression should also be considered, since in the study by Bennett et al [22], HP seroprevalence was associated with more advanced disease and reduced lung function in patients with IPF, while the patients in our cohort had less advanced disease. In contrast to our results, Hogaboam [[23]; pers.…”

Section: Discussionmentioning

confidence: 99%

“…If there had been microaspiration at the time of diagnosis, it is unlikely that components of the aspirate would not have included HP based on seroprevalence data of up to 90% in males >65 years [21]. Furthermore, Bennett et al [22] showed that the seroprevalence of HP in the general population and in IPF patients was similar at 40-51.4% (mean age 65.7-66.8 years).…”

Section: Discussionmentioning

confidence: 99%

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Screening for Helicobacter pylori in Idiopathic Pulmonary Fibrosis Lung Biopsies

Kreuter¹,

Kirsten²,

Bahmer³

et al. 2015

Respiration

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Background: Increasing evidence suggests a role of gastro-oesophageal reflux (GER) in idiopathic pulmonary fibrosis (IPF) pathogenesis. Recently, an association between serum Helicobacter pylori (HP) antibody positivity and more severe disease was described, but HP has not been directly analysed in lung tissue so far. Objective: To investigate the presence of HP in the lung tissue of IPF patients. Methods: Two tertiary interstitial lung disease care centre databases were screened for available lung biopsy material from IPF patients. Clinical and radiological data, including presence of GER and antiacid medication, were evaluated. HP-specific PCR was carried out on the IPF lung biopsy specimens. Results: A total of 39 IPF patients were included, of whom 85% were male. The patients' median age was 66 years, their vital capacity was 79% predicted, and their diffusing capacity for carbon monoxide was 53% predicted. In all, 82% of the lung biopsies were surgical and 18% transbronchial. Comorbidities were GER disease in 23% (n = 9), sleep apnoea in 13% (n = 5) and hiatal hernia in 38% of the cases (n = 15). Proton pump inhibitors were prescribed at the time of biopsy in 21% of the cases (n = 9). After a median follow-up of 25 months (range 6-69), there were 1 death, 1 lung transplantation and 8 acute exacerbations without relevant differences between the GER and non-GER subgroups. HP DNA was not detected in any of the lung tissue samples. Conclusion: The fact that no HP DNA was detected in the lung tissues calls into question the proposed relevance of HP to the direct pathogenesis of IPF.

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Screening for Helicobacter pylori in Idiopathic Pulmonary Fibrosis Lung Biopsies

Kreuter¹,

Kirsten²,

Bahmer³

et al. 2015

Respiration

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“…Moreover MET phosphorylation can also occur through transactivation by other membrane receptors, including adhesive receptors such as CD44, integrins, signal transducing receptors (RON, EGFR family members, FAS, plexin B9) [for a detailed review see 11, 13]. In addition, it has been demonstrated that MET activation can be mediated by an interaction between MET and microbes, including H. Pylori , associated with gastro-esophageal reflux disease which, in turn, is known to be implicated in the development of IPF, giving rise to recurrent lung insult [14, 15]. Notably, MET is expressed in stem and committed progenitor cells and the MET-driven invasive growth is usurped by cancer stem cells (CSC) [7].…”

Section: Introductionmentioning

confidence: 99%

Ockham’s razor for the MET-driven invasive growth linking idiopathic pulmonary fibrosis and cancer

et al. 2016

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Background: Idiopathic pulmonary fibrosis (IPF) identifies a specific lung disorder characterized by chronic, progressive fibrosing interstitial pneumonia of unknown etiology, which lacks effective treatment. According to the current pathogenic perspective, the aberrant proliferative events in IPF resemble those occurring during malignant transformation. Main body:Receptor tyrosine kinases (RTK) are known to be key players in cancer onset and progression. It has been demonstrated that RTK expression is sometimes also altered and even druggable in IPF. One example of an RTK-the MET proto-oncogene-is a key regulator of invasive growth. This physiological genetic program supports embryonic development and post-natal organ regeneration, as well as cooperating in the evolution of cancer metastasis when aberrantly activated. Growing evidence sustains that MET activation may collaborate in maintaining tissue plasticity and the regenerative potential that characterizes IPF. Conclusion:The present work aims to elucidate-by applying the logic of simplicity-the bio-molecular mechanisms involved in MET activation in IPF. This clarification is crucial to accurately design MET blockade strategies within a fully personalized approach to IPF.

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“…Il RGE è associato sia alle riacutizzazioni acute, che alla mortalità [43] e sembra essere coinvolto sia nell'induzione dell'IPF, che nella sua progressione. Un trattamento appropriato del RGE è comunque giustificabile [44], poiché è stato dimostrato che l'utilizzo di farmaci anti-RGE è un fattore indipendente predittivo della maggiore sopravvivenza nei pazienti con IPF [45,46]. La dispnea al baseline, l'enfisema e l'ipertensione polmonare sono spesso considerate tra i più rilevanti predittori di outcome clinici nella IPF [6].…”

Section: Comorbiditàunclassified

[Nintedanib for the treatment of idiopathic pulmonary fibrosis in Italy]

Belisari¹,

Bettoni

Cortesi

et al. 2017

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To date, there are few therapeutic answers for Idiopathic pulmonary fibrosis (IPF) and only two pharmacological treatments have a marketing authorization for this disease. Recently nintedanib (Ofev®) has been authorized as a new therapeutic option and its economic profile has been evaluated by international Health Technology Assessment (HTA) bodies. IPF has important implications for everyday life of patients and their carers, negatively influencing their quality of life and bringing heavy economic burden to the NHS and to the entire society. It is, therefore important to consider these aspects for the Italian environment and to perform a pharmacoeconomic evaluation to define the efficiency of nintedanib in IPF by means of a Cost-Utility Analysis (CUA). As IPF is a chronic and progressive disease, a lifetime Markov model has been therefore developed with health states describing the patient’s condition as a combination of lung function and exacerbation history. The cohort entered in the model at different Forced Vital Capacity (FVC%) predicted health states, without exacerbation. The Clinical data used to perform this CUA were derived from clinical trials and the relative efficacy of nintedanib versus the comparator (pirfenidone) was then obtained from a Network Meta-Analysis (NMA) combining data reported in each primary study (INPULSIS 1-2 and TOMORROW trials for nintedanib, and CAPACITY and ASCEND trials for pirfenidone, respectively). At base-case, treatment with nintedanib resulted in a slightly lower estimated total cost vs pirfenidone, better safety profile and lower risk of acute exacerbations with an advantage in Quality Adjusted Life years (QALYs) gained. These results were confirmed by the sensitivity analysis. Although nintedanib appears to be a valuable option for the NHS to treat IPF patients, future data evidence, as long-term or real-life data, will help to confirm these results.[In Italian]

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Helicobacter pyloriseroprevalence in patients with idiopathic pulmonary fibrosis

Cited by 17 publications

References 13 publications

Screening for <b><i>Helicobacter pylori</i></b> in Idiopathic Pulmonary Fibrosis Lung Biopsies

Screening for <b><i>Helicobacter pylori</i></b> in Idiopathic Pulmonary Fibrosis Lung Biopsies

Ockham’s razor for the MET-driven invasive growth linking idiopathic pulmonary fibrosis and cancer

[Nintedanib for the treatment of idiopathic pulmonary fibrosis in Italy]

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