Detection of Helicobacter Pylori by Pcr in Idiopathic Pulmonary Fibrosis (ipf) Lung Biopsies

Objective: Increasing evidence suggests a role of gastroesophageal reflux (GER) in IPF pathogenesis. Recently, an association of serum Helicobacter pylori (HP) antibody positivity with more severe disease was described. Here, we report screening for HP in IPF lung tissue by PCR. Patients and methods: Our IPF data base (n=354) was screened for available lung biopsy material at IPF first diagnosis. Clinical and radiological data, especially the presence of GER and antacid medication were evaluated. Extraction of genomic DNA was performed by proteinase K digestion and fully automated purification using a QIASymphony SP (Qiagen, Hilden, Germany). HP specific PCR was carried out with the following primers: HP 16S rRNA (forward) 59- CTG GAG AGA CTA AGC CCT CC-39 and HP 16S rRNA (reverse) 59- ATT ACT GAC GCT GAT TGT GC-39. HP+ gastric biopsies served as positive controls. Results: 26 IPF patients (85% male, medians: age 70 years, FVC 77%pred, DLCO 60%pred, 73% surgical / 27% transbronchial lung biopsies) were identified. Comorbidities: GER 27% (n=7), diabetes mellitus 27%, sleep apnea 8%, hiatal hernia (HRCT) 4%. PPI were prescribed at time of biopsy in 15% (n=4). After a median follow up of 28 (range 6-69) months, 1 death, 1 lung transplantation and 23% acute exacerbations were recorded without relevant differences in the GER and non-GER subgroups. HP DNA was not detected in any of the IPF tissue samples. Conclusion: The negative findings of our study question the proposed relevance of HP in the pathogenesis of IPF, however, since only patients with mild-moderate IPF were included, a role of HP in more advanced IPF cannot be ruled out and needs further consideration.