ABSTRACT
INTRODUCTION: Patients often perceive flexible bronchoscopy as an unpleasant procedure. The aim of this study was to investigate the effect of virtual reality (VR) hypnosis on tolerance to flexible bronchoscopy. MATERIALS AND METHODS: We conducted a prospective, randomized, controlled, monocentric study comparing flexible bronchoscopy with VR-induced hypnosis to the usual procedure. Patient tolerance was evaluated using a visual analogue scale (VAS), the state-trait anxiety inventory (STAI) before and after the procedure and, finally, willingness to repeat the examination under the same conditions (WTR). RESULTS: Among the 70 patients included, 34 were randomized to the VR hypnosis group and 36 to the control group. There was no difference between the 2 groups in terms of modification of the pre-/post-bronchoscopy VAS for anxiety, pain, cough, choking, nausea and overall discomfort, or modification of the STAI score and WTR. Subgroup analysis among patients who were more anxious before the procedure revealed a trend toward reduced anxiety in the VR hypnosis group. CONCLUSION: This study did not observe any effect of VR hypnosis on the tolerance of patients during routine flexible bronchoscopy. However, VR hypnosis may be beneficial in patients with higher anxiety score before bronchoscopy, a hypothesis that needs to be confirmed by further studies with a larger number of subjects.
Subject(s)
Hypnosis , Virtual Reality , Humans , Bronchoscopy/adverse effects , Prospective Studies , Anxiety/etiology , Anxiety/prevention & controlABSTRACT
BACKGROUND: Nintedanib (Ofev®) and pirfenidone (Esbriet®) are recommended by international guidelines as treatment options for idiopathic pulmonary fibrosis (IPF). OBJECTIVES: To compare the cost-effectiveness of nintedanib with that of pirfenidone for the treatment of IPF from a Belgian healthcare payer perspective. METHODS: The economic analysis used a Markov model that calculated outcomes over patient lifetime. Overall survival was assumed to be the same for the two comparators. Data from a network meta-analysis were used for loss of lung function, acute exacerbation events, safety and treatment discontinuation (for any reason). The health-state utility estimates in the model were calculated from EQ-5D scores collected in nintedanib studies. The assumed resource use for background care was also based on patient-level data that were categorised to fit the health states in the model and synthesised with costs and tariffs from Belgian national databases. RESULTS: Treatment with nintedanib resulted in an estimated total cost of 102,315, which was less than the total cost of treatment with pirfenidone (113,313). Given the similarities in the survival and progression outcomes obtained with nintedanib and pirfenidone, the model predicted near equivalence in total QALYs (3.353 QALYs for the nintedanib arm and 3.318 for the pirfenidone arm). Results were largely driven by model assumptions underlying mortality, acute exacerbations and treatment discontinuation. CONCLUSIONS: After performing a synthesis of the most recently published evidence for IPF patients and assuming a Belgian healthcare payer perspective, we found nintedanib to be more cost-saving than pirfenidone.
ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disorder of unknown origin with a highly variable and unpredictable clinical course. Polymorphisms and environmentally induced epigenetic variations seem to determine individual susceptibility to the development of lung fibrosis. METHODS: We have studied circulating epitopes on cell-free nucleosomes (cfnucleosomes) in 50 IPF patients. We have compared untreated IPF (n = 23) with IPF receiving antifibrotic therapy (n = 27) and healthy subjects (HS) (n = 27). We analyzed serum levels of five cfnucleosomes including bound HMGB1 (nucleosomes adducted to high-mobility growth protein B1), mH2A1.1 (nucleosomes containing the histone variant mH2A1.1), 5mC (nucleosomes associated with methylated DNA), and H3K9Ac and H3K27Ac (nucleosomes associated with histone H3 acetylated at lysine 9 or 27 residue). RESULTS: Our findings showed that serum levels of bound HMGB1, mH2A1.1, 5mC, H3K9Ac, and H3K27Ac were significantly lower in IPF patients than in HS (p < 0.001, p < 0.001, p < 0.01, p < 0.001, and p < 0.0001, respectively). Moreover, we found differences in epigenetic profiles between untreated IPF patients and those receiving anti-fibrotic therapy with mH2A1.1 and 5mC being significantly lower in untreated than in treated patients (p < 0.01 and p < 0.05, respectively). Combination of four cfnucleosomes (HMGB1, 5mC, H3K9Ac, and H3K27Ac) allow to discriminate IPF vs HS with a good coefficient of determination (R2 = 0.681). The AUC for the ROC curve computed by this logistic regression was 0.93 (p < 0.001) with 91% sensitivity at 80% specificity. CONCLUSION: Our observations showed that cfnucleosomes (bound HMGB1, mH2A1.1, 5mC, H3K9Ac, and H3K27Ac) might have potential as biomarkers for diagnosis and treatment response. These results deserve further validation in longitudinal cohorts.
Subject(s)
5-Methylcytosine/blood , HMGB1 Protein/blood , Histones/blood , Idiopathic Pulmonary Fibrosis/genetics , Nucleosomes/genetics , Aged , Aged, 80 and over , Biomarkers/blood , DNA Methylation , Epigenesis, Genetic , Female , Humans , Idiopathic Pulmonary Fibrosis/blood , Male , Middle Aged , Nucleosomes/metabolismABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic lung disorder of unknown origin, which ultimately leads to death. Several growth factors such as IGFs (insulin-like-growth factor) and IGFBPs (insulin like growth factor binding proteins) seem to take part to the pathogenesis. We evaluated IGFs and IGFBPs in serum from patients with IPF and healthy subjects including 24 untreated IPF and 26 IPF receiving anti-fibrotic therapy and to compare them with healthy subjects. METHODS: Serum of 50 idiopathic pulmonary fibrosis and 55 healthy subjects (HS) were analysed by ELISA for IGFs and IGFBPs, TGF-ß and KL-6, the latter being tested as positive control in IPF. RESULTS: Serum levels of IGFBP-1 and IGFBP-2 and KL-6 were significantly higher in the IPF group than in the healthy subjects (p < 0.05, p < 0.001 and p < 0.0001 respectively) while the picture was inversed regarding IGFs. By contrast there was no significant difference between the groups with respect to TGF-ß. IGFBP-2 was significantly reduced in the patients with specific anti-fibrotic therapy pirfenidone and nintedanib compared to untreated patients (p < 0.05) but still significantly elevated in comparison to HS (p < 0.001). CONCLUSION: Serum IGFBP-1 and -2 are increased in idiopathic pulmonary fibrosis and IGFBP-2 may be reduced by anti-fibrosing therapy. IGFBPs may be promising biomarkers in IPF.
