Prevalence Of Pulmonary Fibrosis Research Articles

COVID-19 Chest Manifestation on CT Scan and Associated Risk Factors for Developing Pulmonary Fibrosis.

This retrospective study describes the imaging findings on chest computed tomography (CT) scans of coronavirus disease 2019 (COVID-19) patients as well as the prevalence of pulmonary fibrosis and the potential risk factors for the disease. One of the major COVID-19 centers in the western province of Saudi Arabia,the King Abdullah Medical Complex in Jeddah, was the site of this study. All adult COVID-19 patients who got a CT chest scan between January 2020 and April 2022 were included in the trial. The imaging findings and pulmonary severity scores (PSS) were obtained from the patients' CT chest. Patients were divided into two groups according to the evidence of fibrotic-like lung changes; clinical and radiological data between the two groups were subsequently compared. Data from the patients' electronic records was collected. The average patient age was 56.4 years, and most (73.5%) patients were men. Two-thirds of the patients had comorbidities (69.1%). CT scans revealed that diffuse lung infiltration is reported in 61% of cases, followed by lower lobes in 19.9%. Ground glass opacity (94.1%), consolidation (76.5%), septal thickening, and/or reticulation (24.4%) were the main chest findings during the initial CT scan. Fibrotic-like lung changes were developed in 9.6% of patients. Patients known to have a positive history of hypertension (p-value = 0.031) and coronary artery disease (CAD) (p-value = 0.011) were found to be significantly more likely to develop lung fibrosis. The patients' pneumonia severity score was significantly higher among the lung fibrotic patients (p-value = 0.026). Also, patients who were diagnosed with pulmonary fibrosis stayed longer in the hospital (p-value 0.001). Sex and age did not correlate significantly with risk of lung fibrosis. Pulmonary fibrosis was observed in 9.6% of COVID-19 patients. A close follow-up of patients with severe pneumonia, prolonged hospitalization, and pre-existing CAD and hypertension was necessary, as pulmonary fibrosis was more likely to occur as a result of these factors. There is a need for a thorough, long-term investigation with a large sample size.

FOXO4 peptide targets myofibroblast ameliorates bleomycin-induced pulmonary fibrosis in mice through ECM-receptor interaction pathway.

Pulmonary fibrosis (PF) is a progressive interstitial lung disease with limited treatment options. The incidence and prevalence of PF is increasing with age, cell senescence has been proposed as a pathogenic driver, the clearance of senescent cells could improve lung function in PF. FOXO4‐D‐Retro‐Inverso (FOXO4‐DRI), a synthesis peptide, has been reported to selectively kill senescent cells in aged mice. However, it remains unknown if FOXO4‐DRI could clear senescent cells in PF and reverse this disease. In this study, we explored the effect of FOXO4‐DRI on bleomycin (BLM)‐induced PF mouse model. We found that similar as the approved medication Pirfenidone, FOXO4‐DRI decreased senescent cells, downregulated the expression of senescence‐associated secretory phenotype (SASP) and attenuated BLM‐induced morphological changes and collagen deposition. Furthermore, FOXO4‐DRI could increase the percentage of type 2 alveolar epithelial cells (AEC2) and fibroblasts, and decrease the myofibroblasts in bleomycin (BLM)‐induced PF mouse model. Compared with mouse and human lung fibroblast cell lines, FOXO4‐DRI is inclined to kill TGF‐β‐induced myofibroblast in vitro. The inhibited effect of FOXO4‐DRI on myofibroblast lead to a downregulation of extracellular matrix (ECM) receptor interaction pathway in BLM‐induced PF. Above all, FOXO4‐DRI ameliorates BLM‐induced PF in mouse and may be served as a viable therapeutic option for PF.

Hyperbaric Oxygen Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Mice.

The prevalence of pulmonary fibrosis is increasing with an aging population and its burden is likely to increase following COVID-19, with large financial and medical implications. As approved therapies in pulmonary fibrosis only slow disease progression, there is a significant unmet medical need. Hyperbaric oxygen (HBO) is the inhaling of pure oxygen, under the pressure of greater than one atmosphere absolute, and it has been reported to improve pulmonary function in patients with pulmonary fibrosis. Our recent study suggested that repetitive HBO exposure may affect biological processes in mice lungs such as response to wounding and extracellular matrix. To extend these findings, a bleomycin-induced pulmonary fibrosis mouse model was used to evaluate the effect of repetitive HBO exposure on pulmonary fibrosis. Building on our previous findings, we provide evidence that HBO exposure attenuates bleomycin-induced pulmonary fibrosis in mice. In vitro, HBO exposure could reverse, at least partially, transforming growth factor (TGF)-β–induced fibroblast activation, and this effect may be mediated by downregulating TGF-β–induced expression of hypoxia inducible factor (HIF)-1α. These findings support HBO as a potentially life-changing therapy for patients with pulmonary fibrosis, although further research is needed to fully evaluate this.

Pulmonary fibrosis in relation to genetic loci in an inception cohort of patients with early rheumatoid arthritis from northern Sweden.

ObjectivesPulmonary manifestations in RA are common comorbidities. Interstitial lung disease (ILD), both idiopathic and in RA, has been associated with several genetic variants. We assessed pulmonary fibrosis (PF) in an inception cohort of RA patients in relation to genetic variants and disease-related factors.MethodsA total of 1466 early RA patients were consecutively included and followed prospectively from the index date until death or 31 December 2016. Clinical and laboratory data and treatment were continuously registered according to the Swedish Rheumatology Quality Register. DNA was available from 1184 patients and 571 151 genome-wide single-nucleotide polymorphisms (SNPs) were analysed. Thirteen identified genetic variants were extracted. At follow-up, the patients answered a questionnaire regarding disease progression and lung involvement that was validated by reviewing medical records and analysing radiological examinations.ResultsThe prevalence of PF was 5.6% and the annualized incidence rate was 5.0/1000 (95% CI 3.80, 6.54). Four SNPs were associated with PF in RA: rs35705950 [MUC5B; OR 2.5 (95% CI 1.5, 4.0), adjusted P-value = 0.00016, q-value = 0.0021]; rs111521887 [TOLLIP; OR 1.9 (95% CI 1.3, 2.8), adjusted P-value = 0.0014, q-value = 0.0092]; rs2609255 [FAM13A; OR 1.7 (95% CI 1.1, 2.5), adjusted P-value = 0.013, q-value = 0.055] and rs2736100 [TERT; OR 1.5 (95% CI 1.0, 2.2), adjusted P-value = 0.046, q-value = 0.15]. Older age and RF positivity were associated with increased risk, while MTX treatment was associated with a lower risk of PF.ConclusionsDevelopment of PF in an inception cohort of RA patients was associated with 4 of 12 ILD risk genes. RA-related factors except for age at diagnosis and RF positivity were of limited importance in PF development.

The association of pulmonary fibrosis with diabetes mellitus.

The association between diabetes and pulmonary fibrosis is not well understood. This large study demonstrates that the prevalence of pulmonary fibrosis is lower in diabetic decedents compared to nondiabetic decedents. https://bit.ly/3gNgjeU

Epidemiology of Pulmonary Fibrosis: A Cohort Study Using Healthcare Data in Sweden.

IntroductionData on the epidemiology of idiopathic pulmonary fibrosis (IPF) in Sweden are lacking. This study estimates the incidence and prevalence of IPF in Sweden, and describes the demographic and clinical characteristics and the overall survival of patients with IPF.MethodsTwo cohorts were studied: a national cohort of 17,247 patients with pulmonary fibrosis (ICD-10 code J84.1 with no competing diagnosis) from the Swedish National Patient Register (cohort 1 [C1]); and an electronic medical record-based regional subset of C1 comprising 1755 patients having pulmonary fibrosis and a radiology procedure (C2).ResultsThe incidence of pulmonary fibrosis in C1 ranged from 10.4 to 15.4 cases per 100,000 population per year between 2001 and 2015. The prevalence increased from 15.4 to 68.0 cases per 100,000 population per year. Patients ≥ 70 years and men had a higher incidence and prevalence of pulmonary fibrosis. Common comorbidities included respiratory infections and cardiovascular disorders. Approximately one-third of patients in each cohort were hospitalised with pulmonary fibrosis within a year of diagnosis. The median survival time from disease diagnosis was 2.6 years in C1 and 5.2 years in C2. Older patients had a higher risk of hospitalisation and mortality. Women had a better prognosis than men.ConclusionThis study underscores the importance of pulmonary fibrosis as a cause of respiratory-related morbidity and mortality in Sweden. The stable incidence and increasing prevalence over time suggests longer survival. The higher morbidity and mortality in older patients highlights the importance of early case detection, diagnosis and management for better prognosis.FundingF. Hoffmann-La Roche, Ltd./Genentech, Inc.Electronic supplementary materialThe online version of this article (10.1007/s41030-019-0087-9) contains supplementary material, which is available to authorized users.

CT Findings in People Who Were Environmentally Exposed to Asbestos in Korea.

Asbestos related pleuropulmonary disease has been emerging health problem for recent years. It can cause variable clinical symptoms and radiological abnormalities. However, there has been no report for their characteristics in subjects who were environmentally exposed to asbestos. We reviewed the CT images of 35 people who were environmentally exposed to asbestos in Chungnam province, Korea. The study result showed high incidence of pleural plaque and pulmonary fibrosis on chest CT (94% and 77%, respectively). The common CT findings of lung parenchymal lesions were as follows: centrilobular opacities (94%), subpleural dot-like or branching opacities (80%), interlobular septal thickening (57%), intralobular interstitial thickening (46%), parenchymal bands (43%) and subpleural curvilinear line (29%). There were no significant differences in the prevalence of pulmonary fibrosis and pleural plaques according to sex, age and duration of exposure. In conclusion, pleural plaque and pulmonary fibrosis are common asbestos-related CT finding in the exposed people. Asbestos related lung parenchymal CT findings in the participants with environmental exposure show similar to those observed in the occupational exposure.

Prevalence of pulmonary fibrosis in Puerto Rico 2000-2010: Phenotype correlations

Prevalence of pulmonary fibrosis in Puerto Rico 2000-2010: Phenotype correlations

Serum levels of soluble CD21 in patients with systemic sclerosis

Systemic sclerosis (SSc) is a systemic disorder that typically results in fibrosis of the skin and multiple internal organ systems. Although the precise mechanism is unknown, overproduction of extracellular matrix proteins, including collagens and fibronectins, and aberrant immune activation might be involved in the pathogenesis. The soluble cluster of differentiation 21 (sCD21) represents the extracellular portion of the CD21 glycoprotein that is released by shedding from the cell surfaces into plasma. sCD21 binds complement fragments and activates monocytes through binding to membrane CD23. The present study was undertaken to investigate the serum levels of sCD21 in patients with SSc. Serum sCD21 levels were reduced with age both in patients with SSc and normal controls. Serum sCD21 levels in patients with SSc were significantly decreased compared to those in control subjects. When we divided patients with SSc into limited cutaneous SSc (lcSSc) and diffuse cutaneous SSc (dcSSc), patients with lcSSc had lower levels of serum sCD21 than those with dcSSc. Moreover, the prevalence of pulmonary fibrosis in the patients with dcSSc inversely correlated with serum sCD21 levels. Our finding may support the notion that B-cell activation is involved in the mechanism for pulmonary fibrosis and skin sclerosis.

Adenosine-Dependent Pulmonary Fibrosis in Adenosine Deaminase-Deficient Mice

Pulmonary fibrosis is a common feature of numerous lung disorders, including interstitial lung diseases, asthma, and chronic obstructive pulmonary disease. Despite the prevalence of pulmonary fibrosis, the molecular mechanisms governing inflammatory and fibroproliferative aspects of the disorder are not clear. Adenosine is a purine-signaling nucleoside that is generated in excess during cellular stress and damage. This signaling molecule has been implicated in the regulation of features of chronic lung disease; however, the impact of adenosine on pulmonary fibrosis is not well understood. The goal of this study was to explore the impact of endogenous adenosine elevations on pulmonary fibrosis. To accomplish this, adenosine deaminase (ADA)-deficient mice were treated with various levels of ADA enzyme replacement therapy to regulate endogenous adenosine levels in the lung. Maintaining ADA-deficient mice on low dosages of ADA enzyme therapy led to chronic elevations in lung adenosine levels that were associated with pulmonary inflammation, expression of profibrotic molecules, collagen deposition, and extreme alteration in airway structure. These features could be blocked by preventing elevations in lung adenosine. Furthermore, lowering lung adenosine levels after the establishment of pulmonary fibrosis resulted in a resolution of fibrosis. These findings demonstrate that chronic adenosine elevations are associated with pulmonary fibrosis in ADA-deficient mice and suggest that the adenosine functions as a profibrotic signal in the lung.

Rheumatoid factor isotypes and anti-agalactosyl IgG antibodies in systemic sclerosis

Rheumatoid factor isotypes and anti-agalactosyl IgG antibodies (anti-AG IgG) have been reported to be detected and correlated with the disease activity in some collagen diseases. To study the frequency and the clinical significance of IgM, IgG and IgA rheumatoid factor (IgM-RF, IgG-RF and IgA-RF) and anti-AG IgG in patients with systemic sclerosis (SSc). Seventy-nine serum samples from patients with SSc were examined by specific enzyme-linked immunosorbent assays. The levels of IgM-, IgG-, IgA-RF and anti-AG IgG were significantly higher in SSc patients than in normal healthy controls. The levels of IgM- and IgA-RF were significantly higher in patients with diffuse cutaneous SSc than in those with limited cutaneous SSc. IgM-, IgG- and IgA-RF and anti-AG IgG were significantly elevated in 39%, 32%, 23% and 35% of 79 SSc patients, respectively. The prevalence of pulmonary fibrosis, oesophageal involvement and cutaneous telangectasias in patients with elevated IgA-RF levels was significantly higher than in those with normal levels. The incidence of pitting scars of digits in those with elevated IgG-RF levels and the incidence of contracture of phalanges in those with elevated IgM-RF levels were significantly higher than in those with normal levels. The frequency of increased erythrocyte sedimentation rate in patients with elevated IgG-RF and the frequency of increased C-reactive protein in those with elevated IgM-RF were significantly greater than in those with normal levels. IgM-, IgG-, IgA-RF and anti-AG IgG can be serum indicators of specific clinical manifestations in SSc patients.

Pulmonary diffusion capacity in patients with systemic lupus erythematosus.

The aim of this study was to clarify the characteristics of pulmonary function tests (PFT), especially carbon monoxide diffusion capacity (DLCO), and their correlation with clinical features and immunological findings in patients with systemic lupus erythematosus (SLE). Vital capacity (VC) and DLCO were analysed retrospectively in 110 sequential Japanese SLE patients with active disease between 1985 and 1999. In 38 patients, serial measurements of PFT were also assessed during high-dose corticosteroid therapy. DLCO was reduced in 52 patients (47%) and a restrictive impairment of PFT was observed in nine patients (8%). The prevalence of pulmonary fibrosis was 13%. Reduced DLCO was frequently observed, even in patients with neither pulmonary fibrosis nor a restrictive pattern. No correlation between immunological data and reduced DLCO was found, except for the presence of anti-RNP. Patients with Raynaud's phenomenon showed a higher prevalence of DLCO impairment than those without this phenomenon. Although immunological parameters improved significantly after the corticosteroid therapy, no significant change in the level of DLCO was observed. Impairment of DLCO was frequently observed in patients with SLE who had no clinical respiratory abnormalities. DLCO impairments were correlated with Raynaud's phenomenon clinically, and the presence of anti-RNP immunologically. No significant correlation was found between impairment of DLCO and disease activity of SLE.

Exposure to Asbestiform Minerals and Radiographic Chest Abnormalities in a Talc Mining Region of Upstate New York

A radiologist in New York reported a high prevalence of pulmonary fibrosis in St. Lawrence and Jefferson counties. The New York State Department of Health responded by conducting a case history study of radiographic abnormalities found in the lung parenchyma and pleura of residents in Lawrence and Jefferson counties, where tremolitic talc has been mined for many years. During a 1-y period, all radiographs from 6 hospitals in the region were reviewed. A B-reader confirmed that 355 of 9,442 patients who were at least 40 y of age (3.8%) had a relevant abnormality; 60% of them reported occupational exposure to asbestiform minerals, and another 15% had a chest condition or injury that could have accounted for the abnormal radiograph. The results should be interpreted cautiously, but there was no evidence of widespread radiographic abnormalities resulting from ambient dust exposure. The data, however, support earlier studies that indicate that talc miners and millers experience excess parenchymal fibrosis and pleural changes. The data also suggest that individuals in the paper industry and construction trades may be at risk.

Cigarette smoking, asbestos, and pulmonary fibrosis.

A group of 100 asbestos textile workers was examined by chest roentgenogram and a questionnaire concerning age, sex, smoking habits, and duration of occupational exposure to asbestos. The roentgenograms were examined for evidences of pulmonary fibrosis without knowing the results of the questionnaire. Seventy-five workers were cigarette smokers and 25 were nonsmokers. The prevalence of pulmonary fibrosis was 40 per cent in the smokers and 24 per cent in the nonsmokers. The factors of age, sex, and duration of exposure to asbestos did not account for this difference. The prevalence of pulmonary fibrosis increased with increasing amount and duration of cigarette smoking and with increasing duration of exposure to asbestos.