Fibrosing Interstitial Pneumonia Research Articles

Pre-exposure to Aerosolized Polyvalent Bacterial Lysates Protects Against Bleomycin-Induced Pulmonary Fibrosis in Mice.

Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial pneumonia of unknown cause. No therapeutic modalities can reverse or stop its ever-deteriorating course. The stimulation of lung innate immunity using bacterial lysates was found to protect against lethal pulmonary infection. Hence, this study aimed to explore whether the immune-stimulating enhancement by pretreatment with bacterial lysates led to protection against bleomycin-induced pulmonary fibrosis. C57BL/6 mice were randomly divided into 4 groups with 20 mice in each group. The mice were exposed to an aerosolized mixture of polyvalent bacterial lysates (PVBL) or phosphate-buffered saline (PBS) three times on separate days. Twenty-four hours after the last exposure, the lungs were intratracheally infused with bleomycin (BLM) or normal saline (NS). The pulmonary morphology, Ashcroft's scale of pulmonary fibrosis, and levels of pro-inflammatory cytokines such as interferon (IFN)-γ and interleukin (IL)-4 were evaluated 14 days after the intratracheal infusion. The exposure to PVBL did not induce any discernible structural abnormalities in the lungs, while the IFN-γ/IL-4 ratio increased. BLM-induced pulmonary fibrosis was associated with an overwhelming downregulation of IFN-γ and IL-4 expression. Pre-exposure to PVBL protected against BLM-induced pulmonary fibrosis, which was demonstrated by a greater reduction of Ashcroft's fibrotic score and a greater decrease in the hydroxyproline level in the lungs. Although the PVBL pre-exposure did not restore the BLM-induced downregulation of IL-4 and IFN-γ levels, the IFN-γ/IL-4 ratio was still maintained greater than the animals with BLM infusion. BLM-induced murine pulmonary fibrosis is associated with downregulation of IFN-γ and IL-4 levels. Pre-exposure to the aerosolized PVBL protects against BLM-induced pulmonary fibrosis.

Idiopathic pulmonary fibrosis in the practice of a family doctor

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology, mainly characterized by a progressive deterioration in lung function due to active fibrosis. It is a variant of chronic progressive fibrosing interstitial pneumonia. The disease most often occurs between the ages of 50 and 70. According to the disease register in the Russian Federation, the prevalence of the disease in the Russian Federation is 4-7 people per hundred thousand of the population [1].Worldwide, the IPF incidence, prevalence and mortality increases over time [2, 3]. In a systematic review of the study by Hutchinson et al. [2] based on data on IPF morbidity and mortality in 21 countries between 1968 and 2012, it was determined that both morbidity and mortality have increased worldwide since 2000.

Review: Serum Biomarkers of Lung Fibrosis in Interstitial Pneumonia with Autoimmune Features—What Do We Already Know?

Interstitial pneumonia with autoimmune features (IPAF) belongs to a group of diseases called interstitial lung diseases (ILDs), which are disorders of a varied prognosis and course. Finding sufficiently specific and sensitive biomarkers would enable the progression to be predicted, the natural history to be monitored and patients to be stratified according to their treatment. To assess the significance of pulmonary fibrosis biomarkers studied thus far, we searched the PubMed, Medline and Cochrane Library databases for papers published between January 2015 and June 2021. We focused on circulating biomarkers. A primary review of the databases identified 38 articles of potential interest. Overall, seven articles fulfilled the inclusion criteria. This review aims to assess the diagnostic and prognostic value of molecules such as KL-6, SP-A, SP-D, circulating fibrocytes, CCL2, CXCL13, CXCL9, CXCL10 and CXCL11. All of these biomarkers have previously been studied in idiopathic pulmonary fibrosis (IPF) and connective tissue disease-associated interstitial lung disease (CTD-ILD). IPAF is a disorder of a heterogeneous nature. It explains the lack of coherent observations in terms of correlations with functional parameters. There is still no meta-analysis of pulmonary fibrosis biomarkers in IPAF. This is mainly due to the heterogeneity of the methodology and groups analysed in the research. More research in this area is needed.

Effects of low-dose pirfenidone on survival and lung function decline in patients with idiopathic pulmonary fibrosis (IPF): Results from a real-world study.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrosing interstitial pneumonia of unknown etiology. In several randomized clinical trials, and in the clinical practice, pirfenidone is used to effectively and safely treat IPF. However, sometimes it is difficult to use the dose of pirfenidone used in clinical trials. This study evaluated the effects of low-dose pirfenidone on IPF disease progression and patient survival in the real-world. This retrospective, observational study enrolled IPF patients seen at the time of diagnosis at a single center from 2008 to 2018. Longitudinal clinical and laboratory data were prospectively collected. We compared the clinical characteristics, survival, and pulmonary function decline between patients treated and untreated with various dose of pirfenidone. Of 295 IPF patients, 100 (33.9%) received pirfenidone and 195 (66.1%) received no antifibrotic agent. Of the 100 patients who received pirfenidone, 24 (24%), 50 (50%), and 26 (26%), respectively, were given 600, 1200, and 1800 mg pirfenidone daily. The mean survival time was 57.03 ± 3.90 months in the no-antifibrotic drug group and 73.26 ± 7.87 months in the pirfenidone-treated group (p = 0.027). In the unadjusted analysis, the survival of the patients given pirfenidone was significantly better (hazard ratio [HR] = 0.69, 95% confidence interval [CI]: 0.48-0.99, p = 0.04). After adjusting for age, gender, body mass index, and the GAP score [based on gender (G), age (A), and two physiological lung parameters (P)], survival remained better in the patients given pirfenidone (HR = 0.56, 95% CI: 0.37-0.85, p = 0.006). In terms of pulmonary function, the decreases in forced vital capacity (%), forced expiratory volume in 1 s (%) and the diffusing capacity of lung for carbon monoxide (%) were significantly smaller (p = 0.000, p = 0.001, and p = 0.007, respectively) in patients given pirfenidone. Low-dose pirfenidone provided beneficial effects on survival and pulmonary function decline in the real-world practice.

KL-6 as an Immunological Biomarker Predicts the Severity, Progression, Acute Exacerbation, and Poor Outcomes of Interstitial Lung Disease: A Systematic Review and Meta-Analysis.

ObjectInterstitial lung disease (ILD) is a specific form of chronic fibrosing interstitial pneumonia with various etiology. The severity and progression of ILD usually predict the poor outcomes of ILD. Otherwise, Krebs von den Lungen-6 (KL-6) is a potential immunological biomarker reflecting the severity and progression of ILD. This meta-analysis is to clarify the predictive value of elevated KL-6 levels in ILD.MethodEBSCO, PubMed, and Cochrane were systematically searched for articles exploring the prognosis of ILD published between January 1980 and April 2021. The Weighted Mean Difference (WMD) and 95% Confidence Interval (CI) were computed as the effect sizes for comparisons between groups. For the relationship between adverse outcome and elevated KL-6 concentration, Hazard Ratio (HR), and its 95%CI were used to estimate the risk factor of ILD.ResultOur result showed that ILD patients in severe and progressive groups had higher KL-6 levels, and the KL-6 level of patients in the severe ILD was 703.41 (U/ml) than in mild ILD. The KL-6 level in progressive ILD group was 325.98 (U/ml) higher than that in the non-progressive ILD group. Secondly, the KL-6 level of patients in acute exacerbation (AE) of ILD was 545.44 (U/ml) higher than stable ILD. Lastly, the higher KL-6 level in ILD patients predicted poor outcomes. The KL-6 level in death of ILD was 383.53 (U/ml) higher than in survivors of ILD. The pooled HR (95%CI) about elevated KL-6 level predicting the mortality of ILD was 2.05 (1.50–2.78), and the HR (95%CI) for progression of ILD was 1.98 (1.07–3.67).ConclusionThe elevated KL-6 level indicated more severe, more progressive, and predicted the higher mortality and poor outcomes of ILD.

Cicatricial organising pneumonia associated with fibrosing interstitial pneumonia - a clinicopathological study.

The recent recognition of cicatricial organising pneumonia (ciOP) indicates that the ciOP may resemble or simulate fibrotic interstitial pneumonia; however, there has been great uncertainty regarding the affected populations, pathogenesis, clinical relevance and characteristics. In this study, we compared the characteristics of fibrotic interstitial pneumonia with and without ciOP. We enrolled 121 patients from the consultation archive whose pathological findings were fibrotic interstitial pneumonia and for whom follow-up clinical data were available. We reviewed these cases histopathologically and classified them according to whether or not they showed ciOP. We compared the clinicopathological features between the two groups. CiOP, histopathologically characterised by deposition of dense collagenous fibres within the alveolar space without destruction of the lung structure, was found in 48 patients (39.7%). None of the cases with ciOP experienced acute exacerbation during 12 months' follow-up. The group with ciOP had more severe diffusion impairment but this, together with restrictive ventilatory impairment, improved significantly compared to the group without ciOP. CiOP is a histopathological finding commonly found in fibrotic interstitial pneumonia. It does not relate to acute exacerbation or decrease in pulmonary function.

P16‐93: Preliminary analysis of serum risk factors during an acute exacerbation of chronic fibrosing interstitial pneumonia: A multi‐institutional prospective study

P16‐93: Preliminary analysis of serum risk factors during an acute exacerbation of chronic fibrosing interstitial pneumonia: A multi‐institutional prospective study

P16‐73: Prognostic significance of serum serological and radiological findings in idiopathic chronic fibrosing interstitial pneumonia

P16‐73: Prognostic significance of serum serological and radiological findings in idiopathic chronic fibrosing interstitial pneumonia

The phosphodiesterase 4 inhibitor AA6216 suppresses activity of fibrosis-specific macrophages

BackgroundIdiopathic pulmonary fibrosis (IPF) is a form of chronic, progressive fibrosing interstitial pneumonia of unknown cause, with a poor prognosis. We previously showed the antifibrotic effects of a novel phosphodiesterase 4 (PDE4) inhibitor, AA6216. In this study, we examined the effect of AA6216 on the pulmonary accumulation of segregated-nucleus-containing atypical monocytes (SatMs), which produce tumor necrosis factor (TNF)-α and are involved in murine lung fibrosis. MethodsMice were treated with bleomycin intratracheally at day 0 and either 10 mg/kg AA6216, 100 mg/kg nintedanib, or vehicle orally once daily from day 0 to 8. On day 9, we isolated the bronchoalveolar lavage fluid and analyzed the SatM ratio. In addition, we evaluated the effect of AA6216 on TNF-α production from SatMs isolated from murine bone marrow. ResultsAA6216, and not the antifibrotic agent nintedanib, significantly suppressed the pulmonary accumulation of SatMs (AA6216: 68.3 ± 5.4%, Nintedanib: 129.8 ± 19.7%). Furthermore, AA6216 dose-dependently inhibited the production of TNF-α by SatMs. ConclusionsAA6216 suppresses pathogenic SatMs in the lung, which contributes to its antifibrotic effects.

Pleural mesothelial cellmigration into lung parenchyma by calpain contributes to idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia. It is unknown why fibrosis in IPF distributes in the peripheral or named sub-pleural area. Migration of pleural mesothelial cells (PMC) should contribute to sub-pleural fibrosis. Calpain is known to be involved in cell migration, but the role of calpain in PMC migration has not been investigated. In this study, we found that PMCs migrated into lung parenchyma in patients with IPF. Then using Wt1tm1(EGFP/Cre)Wtp /J knock-in mice, we observed PMC migration into lung parenchyma in bleomycin-induced pleural fibrosis models, and calpain inhibitor attenuated pulmonary fibrosis with prevention of PMC migration. In vitro studies revealed that bleomycin and transforming growth factor-β1 increased calpain activity in PMCs, and activated calpain-mediated focal adhesion (FA) turnover as well as cell migration, cell proliferation, and collagen-I synthesis. Furthermore, we determined that calpain cleaved FA kinase in both C-terminal and N-terminal regions, which mediated FA turnover. Lastly, the data revealed that activated calpain was also involved in phosphorylation of cofilin-1, and p-cofilin-1 induced PMC migration. Taken together, this study provides evidence that calpain mediates PMC migration into lung parenchyma to promote sub-pleural fibrosis in IPF.

Идиопатический легочный фиброз в практике врача-терапевта

Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic progressive fibrosing interstitial pneumonia of unknown etiology that affects only the lungs and is associated with the histological and / or radiological pattern of common interstitial pneumonia. The clinical substrate for IPF is progressive dyspnea and dry cough. The characteristic auscultatory sign of IPF is inspiratory crepitus. Fibrosis is an important morphological component of IPF. The leading CT sign of IPF is a “honeycomb” lung (local air cysts located subpleurally and having similar sizes from 2–3 to 10 mm with clearly delineated walls). Mostly people over 60 years old are ill, often smokers, or with a history of smoking. In 60% of patients, the course of IPF is progressive, death within 5 years in 40% of cases. In 30–50% of cases, IPF requires the exclusion of other forms of interstitial lung disease. To date, it has been established that the basic drugs in the treatment of IPF with proven efficacy are nintedanib and pirfenidone. This article presents a clinical case of idiopathic pulmonary fibrosis in a 63-year-old patient who was hospitalized in the pulmonology department. The given example justifies the need for increased vigilance among pulmonologists and general practitioners when interpreting the clinical manifestations of the disease.

Association of serum monomeric periostin level with outcomes of acute exacerbation of idiopathic pulmonary fibrosis and fibrosing nonspecific interstitial pneumonia.

BackgroundThe associations of serum monomeric periostin (M-PN) level and serial change in M-PN with acute exacerbation of chronic fibrosing interstitial pneumonia (AE-FIP) are unclear.MethodsWe prospectively measured serum M-PN level from onset of AE to day 14 in 37 patients with AE-FIP and evaluated its association with outcome. To determine localization of periostin expression, immunohistochemical staining of pathological lung tissue from autopsy cases of AE-IPF was evaluated.ResultsData from 37 AE-FIP patients (28 men; age 73.9±7.8 years) were analyzed. With healthy controls as reference, serum M-PN level was significantly higher in patients with AE-FIP (P=0.02) but not in those with stable idiopathic pulmonary fibrosis (P=1.00). M-PN was significantly lower on day 7 than at AE-FIP onset in survivors [14.6±5.8 vs. 9.3±2.8 ng/mL (onset to day 7: P<0.001)] but not in non-survivors [14.6±5.1 vs. 13.2±5.1 ng/mL (onset to day 7: P=0.07)]. In analysis using a cut-off value for serial change in M-PN (ΔM-PN), 3-month survival was 92.3% in the ΔM-PN decrease group and 36% in the ΔM-PN increase group (P=0.002). In multivariate analysis, 3-month survival tended to be associated with high ΔM-PN (OR: 12.4, 95% CI: 0.82–187.9, P=0.069).ConclusionsSerial change in serum M-PN level may be a prognostic indicator of AE-FIP.

Treatment of chronic fibrosing interstitial lung diseases

Interstitial lung diseases (ILD) refers to a large and heterogenous group of parenchymal lung disorders. It is difficult to diagnose and classify ILD. Nevertheless, accurate diagnosis of ILD is crucial for appropriate treatment selection and prediction of prognosis. Idiopathic pulmonary fibrosis (IPF), the most severe of the chronic forms of ILD, is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause. In addition to IPF, a subset of patients with ILD may develop progressive fibrotic changes in lungs. As pulmonary fibrosis progresses, lung function gradually deteriorates and respiratory symptoms worsen; besides, quality of life is also impaired. Progressive fibrosis is also associated with limited response to immunomodulatory thrapies and, potentially, early death. A progressive fibrosing phenotype of ILD (PF-ILD), a subtype of ILD, shows morphological similarities, common underlying pathophysiologic mechanisms, and consistently progressive worsening. PF-ILD include idiopathic nonspecific interstitial pneumonia, unclassifiable idiopathic interstitial pneumonia, autoimmune ILD, chronic sarcoidosis, chronic hypersensitivity pneumonitis and environmental lung diseases. Antifibrotic agents pirfenidone and nintedanib have showed positive results not only for IPF but also for PF-ILD. Immunosuppressive therapy can be used for some types of PF-ILD. If a patient with PF-ILD does not respond to conventional treatment, lung transplantation may be a treatment option. Clinical trials on the treatment of PF-ILD are actively underway. Therefore, over the course of the next several years, major advances in PF-ILD treatment can be expected.

Immune Stroma in Lung Cancer and Idiopathic Pulmonary Fibrosis: A Common Biologic Landscape?

Idiopathic pulmonary fibrosis (IPF) identifies a specific entity characterized by chronic, progressive fibrosing interstitial pneumonia of unknown cause, still lacking effective therapies. Growing evidence suggests that the biologic processes occurring in IPF recall those which orchestrate cancer onset and progression and these findings have already been exploited for therapeutic purposes. Notably, the incidence of lung cancer in patients already affected by IPF is significantly higher than expected. Recent advances in the knowledge of the cancer immune microenvironment have allowed a paradigm shift in cancer therapy. From this perspective, recent experimental reports suggest a rationale for immune checkpoint inhibition in IPF. Here, we recapitulate the most recent knowledge on lung cancer immune stroma and how it can be translated into the IPF context, with both diagnostic and therapeutic implications.

Schisandra Inhibit Bleomycin-Induced Idiopathic Pulmonary Fibrosis in Rats via Suppressing M2 Macrophage Polarization.

Idiopathic pulmonary fibrosis (IPF) is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause and limited to the lungs. Schisandrae chinensis fructus (Wuweizi, Schisandra) is commonly used traditional Chinese medicines (TCM) for the treatment of pulmonary fibrosis, bronchitis, and other lung diseases in China. In this study, we investigated the therapeutic effect of Schisandra on IPF which is induced by bleomycin (BLM) in rats and the inhibition of alternatively activated macrophage (M2) polarization. Bleomycin-induced pulmonary fibrosis was used as a model for IPF, and rats were given drug interventions for 7 and 28 days to evaluate the role of Schisandra in the early oxidative phase and late fibrotic phases of BLM-induced pulmonary injury. The data showed that Schisandra exerted protective effects on BLM-induced pulmonary injury in two phases, which were improving inflammatory cell infiltration and severe damages of lung architectures and decreasing markers of M2 subtype. In order to prove the inhibitory effect of Schisandra on M2 polarization, in vitro experiments, we found that Schisandra downregulated the M2 ratio, which confirmed that the polarization of M2 was suppressed. Moreover, Schisandra blocked TGF-β1 signaling in AMs by reducing the levels of Smad3 and Smad4; meanwhile, the upregulation of Smad7 by Schisandra also promoted the effect of inhibition on the TGF-β1/Smad pathway. These results demonstrate that suppression of M2 polarization by Schisandra is associated with the development of IPF in rats.

The prognostic value of fixed time and self-paced walking tests in patients diagnosed with idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic fibrosing interstitial pneumonia that has an unknown etiology. The natural history of the disease is characterized by a progressive decline in pulmonary function and overall health and well-being. The median survival time is between 2-3 years; however, the disease course is variable and unpredictable. The twelve-minute walking test (12MWT) and six-minute walking test (6MWT) are two fixed time tests that are commonly used in clinical practice. Our short and clinically oriented narrative review attempted to summarize current evidence supporting the use of fixed time, self-paced walking tests in predicting the outcome of patients diagnosed with IPF. A number of studies have justified that the 6MWT is a simple, cost-effective, well documented, fixed time, and self-paced walking test which is a valid and reliable measure of disease status and can also be used as a prognostic tool in patients with IPF. However, there is a need for dedicated and validated reference equations for this population of patients. It is also necessary to fill the knowledge gap about the role of the 12MWT. We hypothesize that it would be useful in evaluating patients that are in the early stages of the disease.

Enhanced β-Catenin/Foxo1 Activity Alleviates Pulmonary Fibrosis by Inhibiting β-Catenin/T Cell Factor Signaling

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrosing interstitial pneumonia, resulting in chronic respiratoryfailure and eventually death. β-catenin/Foxo1 showed a protective property in kidney fibrosis, but the role of β-catenin/Foxo1 in IPF was unclear. Our study aimed to investigate the role of β-catenin/Foxo1 in IPF and explore its underlying mechanism. The IPF model was established by injection of bleomycin (BLM) in vivo and stimulation by TGF-β1 in MRC5 cell in vitro. Haematoxylin-eosin staining and Masson’s trichrome staining were performed to examine histopathological injury in lung. Protein expression of corresponding genes was detected using western blot. Immunofluorescence staining assay was carried out to detect the expression of β-catenin, Foxo1, TCF and α-SMA. The expression levels of inflammatory cytokines were determined using ELISA kit assay. The results showed that BLM induced a serious pulmonary injury and proliferated fibroblasts. A higher interaction of β-catenin with TCF and a lower interaction of β-catenin with Foxo1 was found in BLM group compared to the control group. TGF-β1 promoted β-catenin/TCF, whereas ICG-001 inhibited β-catenin/TCF, and promoted β-catenin/Foxo1. Furthermore, ICG-001 reversed TGF-β1 induced largely production of inflammatory cytokines and accumulation of extracellular matrix, as well as high expression of α-SMA. However, AS1842856, a FOXO1 antagonist, strengthened the effects induced by TGF-β1. In summary, our study revealed that β-catenin/Foxo1 protected against IPF through inhibiting inflammatory response and extracellular matrix accumulation, providing an alternative approach to explain the potential mechanism of IPF and seek for more effective therapeutic drugs.

AN EVIDENCED-BASED SMART-PHRASE TO IMPROVE DOCUMENTATION OF SUPPORTIVE CARE MEASURES IN PATIENTS WITH IDIOPATHIC PULMONARY FIBROSIS

SESSION TITLE: Diagnosis and Treatment of IPF SESSION TYPE: Original Investigations PRESENTED ON: 10/20/2019 2:15 PM - 3:15 PM PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrosing interstitial pneumonia of unknown cause occurring in adults over the age of 50, affecting approximately 5 million people worldwide. Two FDA approved mediations are used to slow progression of the disease process but not all patients can tolerate the medication nor are they curative. The American Thoracic Society (ATS) 2015 guidelines provide recommendations for the treatment of patients with IPF including supportive care measures to compliment medical therapy, such as; symptom management of cough, breathlessness and fatigue. Important supportive care measures include oxygen therapy, pulmonary rehabilitation, gastric acid reflux (GERD) therapy, sleep apnea testing, vaccinations, lung transplant evaluation and pulmonary hypertension assessment METHODS: A retrospective chart review demonstrated the medical providers at the Duke University Health System Interstitial Lung Disease clinic did not consistently document if supportive care measures were discussed when treating patients with IPF. Research demonstrated using a checklist as a visual tool for assessment and documentation can be helpful in improving compliance with the clinical guideline. A checklist was developed that outlines the supportive care measures for the IPF patient. A pretest-posttest design was utilized to assess improved medical provider knowledge of ATS guidelines. Education was provided to the physician group regarding these supportive care measures and then the smart-phrase was implemented in the electronic medical record system to be used for documentation in IPF patient charts. Paired t-tests were used to assess pre-implementation documentation as compared to post-implementation documentation of seven supportive care measures: pulmonary rehabilitation, lung transplant assessment, vaccination, oxygen therapy, gastric acid reflux, sleep apnea therapy, and palliative care. RESULTS: Documentation of oxygen therapy did not change as our providers already documented this with 100% consistency. The rest of the measures improved significantly after implementation of the smart-phrase. Specifically; pulmonary rehab (p<0.0000), vaccination (p<0.000), pulmonary hypertension (p<0.000), GERD therapy (p<0.000), lung transplant assessment (p<0.000), and pulmonary hypertension assessment (p<0.0000). CONCLUSIONS: With the implementation of an evidence-based checklist in the patient electronic medical record, documentation of supportive care measures improved significantly among patients with idiopathic pulmonary fibrosis. CLINICAL IMPLICATIONS: Clinical implication for this project is the need for an evidence-based checklist to ensure evaluation and treatment of supportive care measures are provided to all IPF patients to improve quality of life in this population. DISCLOSURES: Speaker/Speaker's Bureau relationship with BI and Genentech Please note: $1001 - $5000 Added 03/12/2019 by Christine Anderson, source=Web Response, value=Honoraria

Inter-observer agreement in identifying traction bronchiectasis on computed tomography: its improvement with the use of the additional criteria for chronic fibrosing interstitial pneumonia.

To assess inter-observer variability in identifying traction bronchiectasis on computed tomography (CT) using additional criteria for chronic fibrosing interstitial pneumonia. Seven experts categorized CT image set representing 39 patients into three groups on the basis of the presence of traction bronchiectasis, using a three-point scale: 3-definitely/probably yes; 2-possibly yes; and 1-definitely/probably no. This scale served as a reference standard. The image set included cases of chronic fibrosing interstitial pneumonia, non-interstitial lung disease, and difficult-to-determine cases. Forty-eight observers similarly assessed the same image set, first according to the Fleischner Society definition, and second with additional criteria, in which traction bronchiectasis was observed exclusively in chronic fibrosing interstitial pneumonia. The agreement level between the reference standard and each observer's evaluation in each session was calculated using weighted kappa values which were compared between the two sessions using a paired t test. The mean weighted kappa value for all observers was significantly higher in the second reading session (mean 0.75) than in the first reading session (mean 0.62) (p < 0.001). Inter-observer agreement in identifying traction bronchiectasis improves when using the additional criteria which specify chronic fibrosing interstitial pneumonia as the underlying disease.

Association between F-18 fluorodeoxyglucose uptake of noncancerous lung area and acute exacerbation of interstitial pneumonia in patients with lung cancer after resection

BackgroundIdiopathic pulmonary fibrosis is defined as a specific form of progressive fibrosing interstitial pneumonia. Postoperative acute exacerbation is considered a lethal comorbidity for patients with lung cancer, particularly when it is accompanied with idiopathic pulmonary fibrosis. Thus, pretherapeutic risk stratification for acute exacerbation has been anticipated. In this study, we aimed to investigate whether the maximum standardized uptake value of F-18 fluorodeoxyglucose is useful for assessing the postoperative risk of acute exacerbation and severe respiratory adverse events in patients with lung cancer after surgical resection. MethodsA total of 822 patients with lung cancer who underwent preoperative high-resolution computed tomography, fluorodeoxyglucose-positron emission tomography/computed tomography, and pulmonary resection between July 2012 and July 2018 were assessed. Maximum standardized uptake value of the main tumor and that of the noncancerous lung area were measured using a 3-dimensional workstation. Multivariable analyses for acute exacerbation and severe respiratory adverse events were performed using the logistic regression model. ResultsAmong all patients, 120 (14.6%) had idiopathic pulmonary fibrosis findings on high-resolution computed tomography whereas severe respiratory adverse events were observed in 35 (4.2%) patients, including those with acute exacerbation (n = 15, 1.8%). Maximum standardized uptake value of the main tumor and that of the noncancerous lung area were independently associated with both acute exacerbation and severe respiratory adverse events on multivariable analysis, both in all patients and in the 120 patients with idiopathic pulmonary fibrosis. Risk stratification analysis showed that 19.0% and 30.2% of patients who were positive for idiopathic pulmonary fibrosis on high-resolution computed tomography and with a maximum standardized uptake value of the main tumor and that of the noncancerous lung area 1.69 or greater (the optimal cutoff value relevant to acute exacerbation) experienced acute exacerbation and severe respiratory adverse events, respectively. ConclusionsMaximum standardized uptake value of the main tumor and that of the noncancerous lung area were independently associated with the incidence of postoperative acute exacerbation and severe respiratory adverse events in patients with lung cancer.