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PubMed2001

Clinicopathological characteristics of surgically resected lung cancer associated with idiopathic pulmonary fibrosis.

BACKGROUND AND OBJECTIVES: Idiopathic pulmonary fibrosis (IPF) is well known to be associated with lung cancer. It is important to clarify the clinical and pathological features of lung cancer with IPF in understanding the pathogenesis of lung cancer in IPF patients. We compared clinicopathological factors of lung cancer in patients with and without IPF. METHODS: A retrospective study was conducted in 711 surgically resected lung cancer patients. Medical records were compared of IPF and non-IPF patients. RESULTS: Of the 711 patients, 53 (7.5%) were IPF patients. Lung cancer in IPF patients was more frequent in elderly male smokers. Most lung cancers in IPF (79%) arose in peripheral areas involving fibrosis (P < 0.01). The incidence of squamous cell carcinoma in the IPF patients (46%) was significantly higher than that in non-IPF patients (22%) (P < 0.01). The incidence of multiple lung cancer in IPF cases (17%) was also significantly higher. CONCLUSIONS: These results suggest that IPF has the potential to develop into lung cancer, especially peripheral squamous cell carcinoma. Further molecular analyses are necessary to clarify the relationship between IPF and lung cancer.

Adenocarcinoma↗

PubMed1979

Bleomycin-induced pulmonary fibrosis in the rat: inhibition by indomethacin.

A model for pulmonary fibrosis in the rat has been developed using intratracheal administration of bleomycin. The histopathologic features of the reaction are similar to those reported in the hamster model. Increases in vascular permeability are seen in the lung within 24 hours and persist over a 2-month period. Extractable collagen, as measured by hydroxyproline, increases during this time by a factor greater than 1.5 times the reference control values of normal lung. During this same period, a prominent eosinophilia develops. The continued treatment of bleomycin-injected rats with indomethacin markedly diminishes the amount of extractable lung collagen at 60 days and the histopathologic evidence of pulmonary fibrosis. The eosinophilia over the first 3 weeks is also markedly suppressed. Less dramatic effects were seen with the permeability changes. These findings indicate that the rat is a reliable and useful model for the study of blemoycin-induced pulmonary fibrosis and that treatment with indomethacin ameliorates the lung changes.

Animals↗

PubMed2005

[Intractable pneumothorax successfully treated by talc slurry pleurodesis and video-assisted thoracoscopic surgery in a patient with idiopathic pulmonary fibrosis].

Pneumothorax associated with idiopathic pulmonary fibrosis (IPF) is intractable and often fatal because the patients are usually under a long-term steroid therapy, and are associated with severely impaired lung function. Further, pneumothorax itself recurs frequently, and acute exacerbation of IPF may develop after a surgical intervention. Here, we describe a case of intractable pneumothorax developed in a patient with IPF who was successfully treated with repeated talc pleurodesis combined with video-assisted thoracoscopic surgery under local anesthesia. A 67-year-old male with IPF who was under a long-term treatment with steroid, developed right-sided pneumothorax. A chest drainage tube was placed in the right pleural cavity, and repeated pleurodesis with minocycline or fibrinogen was challenged, but the outcome turned out to be unsuccessful. Then, talc slurry was applied repeatedly, resulting in a high-grade fever associated with reactive accumulation of pleural effusion. However, air leakage did not cease completely despite the eight-times pleurodesis with talc using 16 g in total. Finally, video-assisted thoracoscopic surgery under local anesthesia was undertaken and the pulmonary fistula was successfully closed.

Aged↗

PubMed1991

[Delayed nonspecific cutaneous hypersensitivity in extrinsic allergic alveolitis and idiopathic pulmonary fibrosis].

BACKGROUND: A study of delayed nonspecific cutaneous hypersensitivity in extrinsic allergic alveolitis and in idiopathic pulmonary fibrosis. METHODS: 13 patients with extrinsic allergic alveolitis, 10 with idiopathic pulmonary fibrosis, 34 with sarcoidosis and a control group of 110 subjects without respiratory disease or apparent defects in cell immunity were evaluated. The skin tests of delayed hypersensitivity were carried out with five antigenic extracts (candidin, staphylococcal toxoid, tuberculin-PPD, trichophyllin, streptokinase-streptodornase). The reactions were read after 48 hours. Delayed nonspecific cutaneous hypersensitivity was globally calculated, both quantitatively (sum of the mean diameters) and quantitatively (overall average of positive reactions). RESULTS: No significant differences were found between the group of patients with idiopathic pulmonary fibrosis and the control group, nor between those with extrinsic allergic alveolitis and those with sarcoidosis. However, differences were found between the control group and the patients with extrinsic allergic alveolitis, both in the quantitative and the qualitative analysis. CONCLUSIONS: Delayed nonspecific cutaneous hypersensitivity in extrinsic allergic alveolitis is depressed in a similar way as in sarcoidosis, whereas it appears to be preserved in idiopathic pulmonary fibrosis. Therefore, extrinsic allergic alveolitis should be considered as another cause of reduction of delayed nonspecific cutaneous hypersensitivity as it is the case with sarcoidosis.

Adult↗

PubMed1998

Recognition and treatment of idiopathic pulmonary fibrosis.

The diagnosis of idiopathic pulmonary fibrosis can be made only after exclusion of other entities such as neoplasm, toxic treatments, collagen vascular diseases, occupational exposure or granulomatous diseases, such as sarcoidosis. The repercussions on gas exchanges are the most reliable indications of the severity of the disease, the measure of lung volume or chest x-rays alone often being misleading. Biopsies obtained during transbronchial procedures by thoracoscopies or thoracotomy are of great help, but mainly to rule out other diseases. In many cases, only a high resolution computerised tomography (CT) scan and bronchoalveolar lavage are performed to rule out infection or tumour and to assess the inflammatory state of the disease. Due to the fact that barely a quarter of patients respond to corticosteroids alone, cytostatics (in particular azathioprine) are often prescribed simultaneously with low dose corticosteroids, either initially or after an unsuccessful trial of corticosteroids. Cyclosporin has been useful for only a limited number of patients. Colchicine has been shown useful in an open trial but its role still needs to be assessed. Anticytokine therapy and the role of substances such as relaxin are still at the experimental stage. Lung transplantation is now a therapeutic option for selected patients.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Lung cytokine production in bleomycin-induced pulmonary fibrosis.

In bleomycin-induced pulmonary fibrosis, lung injury is accompanied with inflammation and subsequent fibrosis. In this study, lung mRNA for several cytokines was measured in bleomycin-treated mice to evaluate their roles in lung fibrosis. Significant increases in tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta (TGF-beta) mRNA were found in lungs of bleomycin-treated responder CBA mice but not in nonresponder BALB/c mice. Increases in responder animals peaked on day 7 after bleomycin administration, and subsequently returned toward control levels. This time course paralleled that for the increase in beta-actin mRNA, but preceded the peak increase in mRNA for collagens I and III. When lung macrophages were analyzed for cytokine secretion, differences were observed between alveolar macrophages and interstitial cells, and between cells from bleomycin-responsive CBA and nonresponsive BALB/c mice. Only alveolar macrophages from CBA mice secreted increased amounts of IL-1. TNF-alpha activity was increased in conditioned media of alveolar and interstitial cells of CBA mice, while only alveolar macrophages of nonresponder BALB/c mice secreted any activity. The kinetics of the increased secretion of TNF-alpha was dissimilar for these different cells. These results are consistent with the conclusion that increased production of TNF-alpha and TGF-beta is an important component of the fibrotic process.

Animals↗

PubMed2002

A rearranged form of Epstein-Barr virus DNA is associated with idiopathic pulmonary fibrosis.

An association between idiopathic pulmonary fibrosis (IPF) and productive Epstein-Barr virus (EBV) infection has been found previously. Productive EBV replication can be associated with a rearrangement in EBV genomes termed WZhet. We hypothesized that WZhet genomes might be present in patients with IPF. Thirty-nine patients with IPF, 26 lung transplant recipients, and 24 normal subjects were studied. When EBV DNA-positive lung tissue biopsies from IPF patients were analyzed, 11 of 18 (61%) were positive for WZhet. Buffy coat DNA analysis showed that 75-85% were EBV DNA-positive in both IPF and control groups. Buffy coat analysis for WZhet was positive in 16 of 27 (59%) IPF patients, compared with none of 32 lung transplant recipients and 1 of 24 (4%) normal blood donors (p < or = 0.001). There was thus a good correlation between the presence of WZhet in lung tissue and peripheral blood. However, there was no significant association between the presence of WZhet and immunosuppressive therapy. These data further confirm the association between active EBV infection and IPF and provide a potential marker in the peripheral blood for the tracking of EBV in this disease.

Blotting, Southern↗

PubMed2005

Health-related quality of life among patients with idiopathic pulmonary fibrosis.

The hallmark of idiopathic pulmonary fibrosis (IPF) is relentless and progressive breathlessness culminating in respiratory failure and death. Clinicians and investigators are increasingly aware that many patients with chronic diseases, like IPF, value the quality of their lives as much or more than their length of survival. Despite this growing awareness, little research has focused on quality of life (QOL) in IPF patients. Nevertheless, the few studies that have been performed uniformly show the negative impacts of IPF on QOL, particularly in the areas of physical health, energy, and symptoms. To fill important knowledge gaps, more research is needed. For example, future studies in well-defined IPF patient populations should rigorously assess the psychometric properties of different measures of QOL. Currently, there is no disease-specific instrument for use in patients with IPF. A carefully developed, IPF-specific instrument that includes items most relevant to IPF patients should be more sensitive to change than existing generic or non-IPF respiratory disease-specific instruments. Longitudinal assessments are needed to map the trajectory of QOL in relation to disease progression and to reveal whether different aspects of QOL become impaired over time. Addressing these research opportunities will markedly improve our knowledge of this outcome, which is highly valued by patients. These endeavors will also help clinicians who care for patients with IPF to develop a better understanding of its profound negative impact, and it will help future IPF clinical investigators to select the most valid, reliable, and appropriate QOL instrument to fill the roles their studies require.

Disease Progression↗

PubMed2005

Induction of epithelial-mesenchymal transition in alveolar epithelial cells by transforming growth factor-beta1: potential role in idiopathic pulmonary fibrosis.

The hallmark of idiopathic pulmonary fibrosis (IPF) is the myofibroblast, the cellular origin of which in the lung is unknown. We hypothesized that alveolar epithelial cells (AECs) may serve as a source of myofibroblasts through epithelial-mesenchymal transition (EMT). Effects of chronic exposure to transforming growth factor (TGF)-beta1 on the phenotype of isolated rat AECs in primary culture and a rat type II cell line (RLE-6TN) were evaluated. Additionally, tissue samples from patients with IPF were evaluated for cells co-expressing epithelial (thyroid transcription factor (TTF)-1 and pro-surfactant protein-B (pro-SP-B), and mesenchymal (alpha-smooth muscle actin (alpha-SMA)) markers. RLE-6TN cells exposed to TGF-beta1 for 6 days demonstrated increased expression of mesenchymal cell markers and a fibroblast-like morphology, an effect augmented by tumor necrosis factor-alpha (TNF-alpha). Exposure of rat AECs to TGF-beta1 (100 pmol/L) resulted in increased expression of alpha-SMA, type I collagen, vimentin, and desmin, with concurrent transition to a fibroblast-like morphology and decreased expression of TTF-1, aquaporin-5 (AQP5), zonula occludens-1 (ZO-1), and cytokeratins. Cells co-expressing epithelial markers and alpha-SMA were abundant in lung tissue from IPF patients. These results suggest that AECs undergo EMT when chronically exposed to TGF-beta1, raising the possibility that epithelial cells may serve as a novel source of myofibroblasts in IPF.

Actins↗

PubMed2003

Cyclosporin A followed by the treatment of acute exacerbation of idiopathic pulmonary fibrosis with corticosteroid.

OBJECTIVE: Idiopathic pulmonary fibrosis (IPF) is a slowly progressive disease with a poor prognosis. Acute exacerbation is the worst stage in the clinical course of IPF, as the condition is unresponsive to most conventional therapies. Corticosteroids and other immunosuppressive drugs have been attempted for the treatment of acute exacerbation, but only with very limited effectiveness. This study was performed to examine the effect of cyclosporin A (CsA) on acute exacerbation of IPF. PATIENTS AND METHODS: Thirteen patients with acute exacerbation of IPF were retrospectively studied. All 13 patients received pulse-therapy with methylprednisolone (1,000 mg per day for 3 days), followed by oral prednisolone (40-60 mg per day). Seven patients were received CsA (1.0-2.0 mg/kg per day) after the treatment with corticosteroids. We attempted to keep the blood trough level of CsA between 100 and 150 ng/ml. RESULTS: Among the 7 patients treated with CsA, 4 patients have survived for 60, 120, 276 and 208 weeks, respectively; 2 did not respond to pulse-therapy with methylprednisolone and died within 8 weeks after the start of CsA treatment. The other patient experienced re-exacerbation and died 87 weeks after the discontinuation of CsA due to the development of viral encephalitis. In contrast, all 6 patients treated without CsA died within 66 weeks after the onset of acute exacerbation. Four of these patients responded to pulse-therapy with methylprednisolone, but their condition deteriorated again while the subsequent prednisolone was being tapered. CONCLUSION: CsA seems to prevent re-exacerbation of IPF and improve the patients' chances for long-term survival.

Acute Disease↗

PubMed1991

[Proliferative characteristics of fibroblast lines derived from open lung biopsy specimens of patients with the usual interstitial pneumonia form of idiopathic pulmonary fibrosis].

One form of idiopathic pulmonary fibrosis (IPF), usual intersitial pneumonia (UIP) is characterized pathologically by patchily distributed fibrotic areas in apparently normal parenchyma. Excessive accumulation of collagen and fibroblasts in fibrotic areas are shown histologically. Fibroblast proliferation is generally evaluated as a process following alveolitis. However, substantial alveolitis with increased inflammatory and immune cells were not observed in our UIP cases. To evaluate the possibility that fibroblasts in UIP are controlled by mechanisms other than normal paracrine regulation, proliferative features of lung fibroblast lines from UIP lung with regular growth medium, platelet derived growth factor (PDGF) and prostaglandin E2 (PGE2) were investigated. Ten fibroblast lines from open lung biopsy specimens of patients with IPF (UIP) and 10 control fibroblast lines from surgically resected lung tissues of patients with limited lung disease were established. The doubling time of fibroblast lines with regular growth medium was UIP:32.0 +/- 6.0 hrs. (mean +/- S.D.), normal control: 33.2 +/- 10.4 hrs. There was no difference between the groups. To examine growth promotion activity by PDGF and growth inhibition by PGE2, lung specimens from 4 patients with IPF were subdivided into tissue with high intensity fibrotic lesion (H) and low intensity fibrotic lesion (L), and the fibroblast lines were established separately. 3H-thymidine uptake with or without PDGF and PGE2 was examined, and results were expressed as the stimulation index. Growth promotion by PDGF was H: 1.97 +/- 1.19, L: 1.89 +/- 0.78, normal control: 2.29 +/- 0.55. There were no differences between groups. Growth inhibition by PGE2 was H: 0.88 +/- 0.24, L: 0.69 +/- 0.49, normal control: 0.44 +/- 0.33. Growth inhibition for H was significantly lower than control (p less than 0.05). Growth inhibition for L was lower than controls, but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2002

The distribution and number of Leu-7 (CD57) positive cells in lung tissue from patients with pulmonary fibrosis.

Leu-7 positive lymphocytes, including natural killer cells, play an important role in the immune system's surveillance function to prevent the development of cancer. The incidence of lung cancer is significantly high in patients with end-stage pulmonary fibrosis. We hypothesized that the number of Leu-7 positive cells may be decreased in areas of severe pulmonary fibrosis. To demonstrate this, Leu-7 positive cells were immunohistochemically stained in 41 lung specimens obtained from patients with idiopathic pulmonary fibrosis and pulmonary fibrosis associated with collagen vascular disorders. The number of Leu-7 positive cells was evaluated according to the pathological findings. In pathologically normal lung, Leu-7 positive cells were mostly found within the capillaries of the septa and rarely in the alveolar space or the stroma. The number of Leu-7 positive cells was 0.69 +/- 0.15 in areas of advanced fibrosis (n = 41), 2.39 +/- 0.60 in areas that had newly developeing fibrosis (n = 41), 1.14 +/- 0.57 in bronchiolitis obliterans organizing pneumonia (n = 9), and 1.35 +/- 0.87 in diffuse alveolar damage (DAD) (n = 11). The number of Leu-7 positive cells in areas of newly developing fibrosis (2.39 +/- 0.60) was significantly higher than that in areas of established fibrosis (0.69 +/- 0.15, P < 0.05). Our present study demonstrates a significant decrease in the number of Leu-7 positive cells in areas of advanced fibrosis. This evidence may partly explain the high incidence of lung cancer associated with pulmonary fibrosis.

Aged↗

PubMed2001

Heterogeneity of pulmonary fibrosis: interstitial pneumonias and sarcoidosis.

This review focuses on two representatives of pulmonary fibrosis. One is usual interstitial pneumonia lesion, typically seen in patients with idiopathic pulmonary fibrosis. The other is parenchymal fibrosis along the bronchovascular bundles, observed in patients with sarcoidosis. Both are intractable fibrosis amenable only to lung transplantation. The authors trace the historical classification of idiopathic interstitial pneumonia, discuss interstitial pneumonia associated with collagen vascular diseases and occupational exposure, and review the most important issues to clarify both types of pulmonary fibrosis.

Animals↗

PubMed1998

Bleomycin-induced pulmonary fibrosis in rat is associated with increased expression of collagen-binding heat shock protein (HSP) 47.

Increased accumulation of collagens in extracellular matrix (ECM) is mainly responsible for bleomycin-induced pulmonary fibrosis in rats. This study was designed to assess whether increased collagen accumulation in bleomycin-induced pulmonary fibrosis is associated with heat shock protein (HSP) 47, a molecular chaperone for collagen biosynthesis. We investigated the expression of type I and type III collagens and HSP47 in bleomycin-induced pulmonary fibrosis. Fifteen male Wistar rats were divided into two groups; group I: bleomycin-induced pulmonary fibrosis; group II: PBS-treated age-matched control rats. Pulmonary fibrosis was induced by injecting a single dose of bleomycin sulphate (5 U/kg body weight) intratracheally. Three bleomycin-treated rats and two age-matched control rats were sacrificed at the end of each of the 1st, 2nd and 4th weeks of the experiment. In bleomycin-treated rats, histological examination revealed pulmonary fibrosis, which increased with time. Increased type I and type III collagen desposition was observed in the lungs of all the bleomycin-treated rats. Weak immunostaining of HSP47 was noted in the control lungs. In contrast, strong immunostaining for HSP47 was seen in all the bleomycin-treated fibrotic lungs. In addition, increased numbers of phenotypically altered myofibroblasts (alpha-smooth muscle actin immunopositive) and fibroblast (vimentin immunopositive) were seen in bleomycin-treated lungs and found to express HSP47. Parallel increase of collagens and their molecular chaperone HSP47 expression was found in the bleomycin-treated lungs, and their co-localization could be detected by double immunostaining. Overexpression of HSP47 may play a significant part in the excessive assembly of collagens and could contribute in this way to the fibrosis found in bleomycin-treated rat lungs.

Animals↗

PubMed1988

Effects of buthionine sulfoximine on the development of ozone-induced pulmonary fibrosis.

The capacity of reduced glutathione (GSH) to protect lung tissue against ozone-induced pulmonary fibrosis was investigated. Male B6C3F1 mice were exposed to 0, 0.2, 0.5, and 1.0 ppm ozone for 23 hr/day for 14 days. During exposures and/or for a period of 90 days after exposures, subgroups of mice at each exposure level were given drinking water containing 30 mM L-buthionine-S,R-sulfoximine (BSO) to lower in vivo levels of GSH. These BSO treatments reduced blood glutamylcysteine synthetase (GCS) activity (regulatory enzyme for GSH biosynthesis) and lung nonprotein sulfhydryl (NPSH) levels in nonexposed animals by approximately half. In contrast, ozone exposures increased blood GCS activity and lung NPSH levels in a concentration-dependent manner, with smaller increases in the BSO-treated mice. Immediately after exposures, an ozone-related inflammatory response was seen in lungs, but no histopathological signs of developing fibrosis were evident. Ninety days later, mice exposed to 1 ppm ozone and not treated with BSO had modest evidence of pulmonary fibrosis. Mice exposed to 1 ppm ozone and treated with BSO during this post-exposure period (regardless of BSO treatment during exposures) showed histopathological evidence of exacerbated pulmonary fibrosis, compared to similarly exposed mice not treated with BSO postexposure. These results indicated that interference with the body's normal defense mechanisms against oxidant damage, including suppression of GSH biosynthesis, exacerbates the subsequent development of pulmonary fibrosis.

Animals↗

PubMed2004

Adult-onset familial pulmonary fibrosis in Japanese brothers.

Two Japanese brothers were diagnosed in their 20s with familial pulmonary fibrosis, the pathological findings of which were consistent with usual interstitial pneumonia (UIP). However, an atypical characteristic was observed in the lungs of these brothers; 2-mm areas of 'honeycomb' were identified throughout the lungs, which is smaller than the generally observed 5-10 mm honeycombing seen in UIP. Fibroblastic foci were demonstrated in the second eldest brother, but not in the eldest, which indicates that the lungs of the eldest brother was in a more advanced stage of fibrosis. Their youngest brother and parents have no clinical evidence of pulmonary fibrosis. All five family members had low values for the diffusion capacity of the lung for carbon monoxide (DLCO), suggesting the presence of an inheritable disease and the existence of different phenotypes. The genomic DNA of the affected brothers was sequenced for the reported surfactant protein C (SP-C) gene mutations in patients with familial pulmonary fibrosis, but none was documented. It is necessary to clarify the presence of novel gene mutations of SP-C or other genes to explain these particular pathological findings and the low DLCO observed in this family.

Adult↗

PubMedDate not supplied

Effect of endothelin receptor antagonists (BQ-485, Ro 47-0203) on collagen deposition during the development of bleomycin-induced pulmonary fibrosis in rats.

Previous evidence suggests a role for endothelin-1 (ET-1) in the pathogenesis of pulmonary fibrosis. To determine if ET-1 regulates collagen deposition in pulmonary fibrosis, we examined the effect of the non-selective ETA and ETB receptor antagonist bosentan (Ro 47-0203), and a selective ETA receptor antagonist, BQ-485, on collagen deposition during the development of bleomycin-induced pulmonary fibrosis in rats. Lung collagen content, derived from measurements of hydroxyproline and expressed as mg collagen/lung, was increased in the bleomycin-treated animals by day 7 (bleomycin, 22.88+/-1.46; control 18.50+/-0.98; P<0.05), continued to increase up to day 14 (bleomycin, 38.80+/-2.17; control 22.57+/-0.77; P<0.001) and then remained constant to 21 days. Daily treatment by gavage with bosentan (100 mg/kg) did not prevent the increase in collagen deposition induced by instillation of bleomycin at any of the times measured. Continuous administration of BQ-485, by subcutaneously implanted minipump (7.5 mg/day), also failed to prevent the bleomycin-induced collagen deposition at 14 days. These findings suggest that ET-1 does not modulate collagen deposition during the development of bleomycin-induced pulmonary fibrosis. Further studies are required to assess whether endothelin receptor antagonists modulate other components of the fibrotic response or play a role in man.

Animals↗

PubMed1999

[Electron microscopic studies on pathogenesis of idiopathic pulmonary fibrosis].

OBJECTIVE: To observe ultrastructural changes and study the pathogenesis of idiopathic pulmonary fibrosis. METHODS: The clinical manifestations in 9 patients with idiopathic pulmonary fibrosis were selected. Transbronchial lung biopsy materials were obtained for light microscopic and electron microscopic examination. RESULTS: The major morphologic changes were as follows: histologically, alveolar inflammation and interstitial fibrosis were observed. electron microscopic findings were: 1. alveolar type I cells were degenerated, broken-down and desquamated, endothelial cells were swelled, with inter cellular tight junction shortened, alveolar type II cells hyperplastic, basement membrane thinned and deformed; 2. alveolar macrophages and interstitial macrophages were hyperplastic; 3. mast cells were infiltrated and degranulated; 4. electron-dense deposits were present at alveolar wall; 5. myofibroblasts, fibroblasts, collagen and basement membrane like material were hyperplastic. CONCLUSIONS: Electron microscopic observations show that the alveolar epithelial cells, endothelial cells and basement membrane are all injured, interstitial macrophages hyperplasia, mast cells infiltration and degranulation, electron-dense deposits at alveolar wall are present. These morphologic changes provide basis for formation of idiopathic pulmonary fibrosis.

Adult↗