PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PULMONARY FIBROSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMed1987

Amiodarone-associated pulmonary fibrosis. Evidence of an immunologically mediated mechanism.

A case of pulmonary fibrosis attributed to amiodarone was studied immunologically and morphologically. A specific antibody of the IgG class was identified in the serum of this patient which reacted with the patient's own lung tissue. The immunoglobulin did not react with normal lung tissue nor was there evidence of reaction with lung tissue from patients with pulmonary fibrosis but without a history of amiodarone therapy. The patient probably developed a humoral antibody response to a lung-amiodarone complex with the amiodarone acting as a hapten which bound in vivo to the lung tissue. The subsequent antibody-antigen reaction stimulated a proliferation of pulmonary fibroblasts and probably enhanced the fibro-collagen deposition in the lung.

Amiodarone↗
PubMed2006

Acute interstitial pneumonia and acute exacerbations of idiopathic pulmonary fibrosis.

Acute interstitial pneumonia (AIP) and acute exacerbations of idiopathic pulmonary fibrosis (AEIPF) are similar respiratory disorders characterized by the rapid development of progressive dyspnea and cough. Both frequently lead to respiratory failure and death. Pathologically, each is characterized by the presence of a diffuse alveolar damage (DAD) pattern; in AIP, DAD is the sole pattern, whereas in AEIPF DAD is superimposed upon a background usual interstitial pneumonia. They differ in that patients with AEIPF have preexisting idiopathic pulmonary fibrosis, whereas patients with AIP have no predisposing disorders to account for their disease. Because both presentations overlap with multiple other causes of acute lung injury, a comprehensive evaluation is necessary to rule out disorders such as overwhelming infection or congestive heart failure. Although a confident diagnosis can be achieved without it, a surgical lung biopsy is necessary to provide a definitive diagnosis. Despite minimal evidence, glucocorticoids are frequently begun once microbiological evaluation confirms the absence of infection. Despite therapy, the case fatality rate ranges up to 70% for both, with most patients dying in the first 2 weeks. Survivors of the acute event can recover to their previous baseline; however, most AIP survivors will stabilize with some functional impairment, whereas in those with AEIPF, progressive fibrosis with functional deterioration is the rule.

Acute Disease↗
PubMed1992

Taurine and niacin offer a novel therapeutic modality in prevention of chemically-induced pulmonary fibrosis in hamsters.

The bleomycin (BL)-hamster model of interstitial pulmonary fibrosis (IPF) is generally associated with increased lung lipid peroxidation, measured as malondialdehyde equivalent (MDAE), calcium and collagen content; and superoxide dismutase (SOD), prolyl hydroxylase (PH) and poly(ADP-ribose) polymerase activities. We found that combined treatment with taurine in drinking water (1%) and niacin IP (250 mg/kg) daily, significantly decreased the BL-induced increases in lung MDAE and calcium content, and SOD, PH and poly(ADP-ribose) polymerase activities. This treatment almost completely ameliorated the BL-induced increases in the lung collagen accumulation as well. Findings of a similar nature were also demonstrated when taurine (2.5%) and niacin (2.5%) were supplemented in the diet of hamsters used in the same BL model of IPF. The diet supplemented with taurine (2.5%), niacin (2.5%), or taurine (2.5%) + niacin (2.5%) also reduced AD-induced increases in lung collagen accumulation, phospholipids, MDAE and SOD activity. It was concluded that diet supplemented with taurine and/or niacin would completely or partially ameliorate chemically-induced pulmonary fibrosis.

Amiodarone↗
PubMedDate not supplied

[Diffusive interstitial pulmonary fibrosis in chronic polyarthritis].

Among 167 in-patients with rheumatoid arthritis, 7 cases (4,2%) of diffuse interstitial pulmonary fibrosis of variable degree were revealed by chest X-ray examination. There was a predominance of the advanced functional classes according to Steinbrocker (where the duration of the disease was approximately the same as in patients without pulmonary fibrosis). There were higher 1-hour erythrocyte sedimentation rates and gamma-globulin valves and lower levels of hemoglobin and hematocrit in the patients with diffuse interstitial pulmonary fibrosis than in those without pulmonary changes. The etiological and pathogenetic aspects of several theories are discussed. The therapeutic possibilities are described and the importance of penicillamine therapy is emphasized.

Adolescent↗
PubMed2002

Differential role of neutrophils and alveolar macrophages in hepatocyte growth factor production in pulmonary fibrosis.

Neutrophils may participate in the development of lung fibrosis. Hepatocyte growth factor (HGF), a growth factor for type II pneumocytes, is produced by neutrophils. We measured the production of HGF by blood and alveolar neutrophils from patients with either idiopathic pulmonary fibrosis (n = 11) or connective tissue disease-associated pulmonary fibrosis (n = 10) and from control patients (n = 10). HGF secretion by alveolar macrophages and the expression of the HGF receptor by alveolar epithelial cells in pulmonary fibrosis were also evaluated. HGF was not detected in bronchoalveolar lavage fluid from controls. HGF concentration in the epithelial lining fluid from patients was 4-fold higher than in plasma, suggesting a local production within the alveolar space. Alveolar neutrophils secreted HGF in vitro. Basal HGF secretion by alveolar neutrophils positively correlated with HGF in the epithelial lining fluid (p = 0.05, rho = 0.582). HGF secretion by alveolar neutrophils could not be further stimulated with lipopolysaccharide, whereas HGF secretion by blood neutrophils doubled with lipopolysaccharide. Alveolar macrophages did not secrete HGF in vitro. The expression of the HGF receptor was greatly increased in the fibrotic lung, supporting the local function of HGF secreted by neutrophils. We conclude that neutrophils are a source of HGF in patients with pulmonary fibrosis.

Hepatocyte Growth Factor↗
PubMed2000

Role of diminished epithelial GM-CSF in the pathogenesis of bleomycin-induced pulmonary fibrosis.

Evidence derived from human and animal studies strongly supports the notion that dysfunctional alveolar epithelial cells (AECs) play a central role in determining the progression of inflammatory injury to pulmonary fibrosis. We formed the hypothesis that impaired production of the regulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) by injured AECs plays a role in the development of pulmonary fibrosis. To test this hypothesis, we used the well-characterized model of bleomycin-induced pulmonary fibrosis in rats. GM-CSF mRNA is expressed at a constant high level in the lungs of untreated or saline-challenged animals. In contrast, there is a consistent reduction in expression of GM-CSF mRNA in the lung during the first week after bleomycin injury. Bleomycin-treated rats given neutralizing rabbit anti-rat GM-CSF IgG develop increased fibrosis. Type II AECs isolated from rats after bleomycin injury demonstrate diminished expression of GM-CSF mRNA immediately after isolation and in response to stimulation in vitro with endotoxin compared with that in normal type II cells. These data demonstrate a defect in the ability of type II epithelial cells from bleomycin-treated rats to express GM-CSF mRNA and a protective role for GM-CSF in the pathogenesis of bleomycin-induced pulmonary fibrosis.

Animals↗
PubMedDate not supplied

Urinary excretion of protein and non-protein hydroxyproline in patients with sarcoidosis and interstitial pulmonary fibrosis.

The determination of total hydroxyproline (Hyp) with separation into protein and non-protein fractions was carried out in 24-hour urine samples of healthy persons, patients with sarcoidosis and patients with interstitial pulmonary fibrosis (i.p.f.). In the group of sarcoidosis Hyp excretion was evaluated taking into account progression of pulmonary changes and disease activity. It was found that total and non-protein Hyp excretion correlated positively in healthy persons as well as in those with sarcoidosis, and interstitial pulmonary fibrosis. An increased excretion of total and non-protein Hyp occurred in 24% of the patients with sarcoidosis while excretion of protein Hyp remained within the normal range. In 30% of the patients with interstitial pulmonary fibrosis increased excretion of total and non-protein Hyp was demonstrated. The excretion of protein Hyp in these patients did not deviate from normal values. The results of our study indicate that determination of total and nonprotein Hyp in urine may be useful in the evaluation of fibrotic changes in the pulmonary diseases mentioned above. However, these parameters are not usefull in differentiation between sarcoidosis and interstitial pulmonary fibrosis.

Adult↗
PubMed1989

Phenotypic characterization of alveolar capillary endothelial cells, alveolar epithelial cells and alveolar macrophages in patients with pulmonary fibrosis, with special reference to MHC class II antigens.

Major histocompatibility complex (MHC) class II antigens are essential in the presentation of antigens to T lymphocytes, and cells expressing MHC class II antigens are known to play a role as antigen presenting cells (APC). We investigated the distribution of MHC class II antigens and the reactivity of monoclonal antibodies OKM1 and OKM5 in normal and fibrotic lungs immunohistochemically. The results showed that alveolar capillary endothelial cells (ACEnd) expressed MHC class II antigens and were reactive with OKM5 in both normal lungs and the non-thickened parts of alveolar septa of pulmonary fibrosis. However, ACEnd did not express MHC class II antigens and were not reactive with OKM5 in thickened alveolar septa of pulmonary fibrosis. Type II alveolar epithelial cells (AEp) proliferating and replacing type I AEp in pulmonary fibrosis expressed MHC class II antigens strongly. Alveolar macrophages expressed MHC class II antigens strongly and reacted with OKM1 in pulmonary fibrosis, especially in alveolar spaces. These findings suggest that the phenotypic changes of ACEnd may be involved in the process of pulmonary fibrosis, and type II AEp and alveolar macrophages in the parts of thickened alveolar septa may play a role as APC.

Antibodies, Monoclonal↗
PubMed1985

[Dermatopolymyositis and pulmonary fibrosis associated with Gougerot-Sjogren syndrome. Study of 3 cases].

3 new cases of dermatomyositis associated with diffuse interstitial pulmonary fibrosis and, more exceptionally, with Sjögren's syndrome are reported. The pulmonary fibrosis observed in patients with dermatomyositis differs from that found in other connective tissue diseases in that it follows a more acute course and may respond to corticosteroids. Thus, in 2 of these patients treated with corticosteroids (combined in 1 case with cyclophosphamide) the high percentage of lymphocytes and polymorphonuclears in the broncho-alveolar lavage fluid, which reflects alveolitis activity, was reduced and the pulmonary fibrosis was cured in one patient and stabilized in the other.

Cyclophosphamide↗
PubMed1986

Role of inflammation in the lung disease of systemic sclerosis: comparison with idiopathic pulmonary fibrosis.

Alveolar inflammation is thought to underlie the development of pulmonary fibrosis in several forms of diffuse lung disease including the connective tissue diseases. The relationship between inflammation and the clinical manifestations of systemic sclerosis (scleroderma), such as skin and lung involvement, is less clear. We therefore evaluated 14 never-smoking patients with systemic sclerosis with pulmonary involvement by bronchoalveolar lavage (BAL) and compared the results with those found in eight nonsmoking patients with idiopathic pulmonary fibrosis (IPF) and eight normal subjects. The patients with scleroderma also underwent gallium citrate Ga 67 scanning. We found that patients with scleroderma and pulmonary involvement have alveolitis that appears to wane with time. In addition, patients with systemic sclerosis have a cellular profile in lavage fluid that appears to differ from that of patients with IPF. Finally, we found a significant correlation between BAL cellular recovery and the single-breath carbon monoxide diffusing capacity in patients with systemic sclerosis but not in patients with IPF. We conclude that inflammation may play an important role in the pathogenesis of the pulmonary disease of scleroderma and that different mechanisms may lead to fibrosis in IPF and scleroderma.

Adult↗
PubMed2001

[Unilateral pulmonary fibrosis following ipsilateral single-lung ventilation and anesthesia].

We experienced a rare case of unilateral pulmonary fibrosis following ipsilateral single-lung ventilation and anesthesia. A 75-year-old man with a 1-pack a day smoking history for 50 years was scheduled for right upper and middle lobectomy for lung cancer. The trachea and left bronchus were intubated with a 37-Fr double-lumen endobronchial tube, and anesthesia was maintained with oxygen, nitrous oxide, isoflurane, and epidural lidocaine. Left single-lung ventilation was maintained for 3.5 hours with FIO2 at 0.8-1.0, vital capacity at 10 ml.kg-1, and peak inspiratory pressure at 25 cmH2O. On postoperative day 55, reticular nodular density in chest roentogenography appeared only in the left lung while right lung showed pleural fluid and pneumonia. On postoperative day 105, a high-resolution computed tomographic scan revealed honeycomb pattern in the left lung and organized pneumonia in the right lung. The patient died from respiratory failure on postoperative day 155, and autopsy was not performed. Although the causative mechanisms of unilateral pulmonary fibrosis in this case was unclear, the patient had not been exposed to any drugs and inhalation agents known to induce pulmonary fibrosis. We speculate that high oxygen concentration, high peak inspiratory pressure, and overdistension of the left lung during the left single-lung ventilation and anesthesia were likely major initiating and contributing factors.

Aged↗
PubMed1992

[Cardiopulmonary function disorders in pulmonary fibrosis of various etiology].

A large number of different pulmonary diseases eventually result in producing the final morphological pattern of pulmonary fibrosis. Basing on essential cardiopulmonary functional parameters, four relatively frequently encountered fibrotic pulmonary diseases are compared with each other. Patients suffering from bird breeder's lung show typical obstructive disturbances of ventilation that are even more marked in collagenoses with lung involvement. Patients suffering from electric welder's lung are notable for enhanced respiratory tract obstructions and increased residual volumes. In patients with sarcoidosis it is recommended to determine, above all, the lung compliance besides measuring the diffusion capacity. The specific compliance should be chosen as criterion to assess the compliance, so that the preliminary extension of the lung by emphysema is taken into consideration. Welder's lungs, bird breeder's lungs and collagenoses show a load-conditioned respiratory partial insufficiency and a latent pulmonary hypertonia. The examined groups of patients showed similar functional patterns, but individual parameters were disease-specifically considerably different from standard values.

Adult↗
PubMed2002

Effects of intercellular adhesion molecule 1 (ICAM-1) null mutation on radiation-induced pulmonary fibrosis and respiratory insufficiency in mice.

BACKGROUND: Therapy-induced inflammation and progressive fibrosis limit the efficacy of thoracic radiotherapy for lung neoplasms. However, mice bearing a null mutation of intercellular adhesion molecule 1 (ICAM-1) have previously been found to display no inflammatory cell infiltration into the lung following thoracic irradiation. We investigated the role of ICAM-1-mediated inflammation in the pathogenesis of radiation-induced pulmonary fibrosis in mice with a homozygous null mutation in the ICAM-1 gene (ICAM-1(-/-)) and in wild-type mice (ICAM-1(+/+)). METHODS: Groups of 10 mice were each irradiated with total doses of 12.5, 14, 16, 17, or 18 Gy to the thorax or were mock irradiated. Inflammatory cell infiltration was measured by immunohistochemical staining of lung sections for leukocyte-common antigen (LCA). Dynamic pulmonary compliance was determined by plethysmography. Pulmonary fibrosis was evaluated by measuring alveolar septal wall thickness and the hydroxyproline content of lungs by immunohistochemical staining of lung sections for collagen III and by Masson's trichrome staining of lung sections. All statistical tests were two-sided. RESULTS: Lungs of irradiated ICAM-1(-/-) mice had statistically significantly fewer LCA-positive cells than the lungs of irradiated ICAM-1(+/+) mice at all radiation doses (P<.001). ICAM-1(-/-) mice had a higher mean dynamic pulmonary compliance than ICAM-1(+/+) mice following irradiation. The incidence of respiratory insufficiency 18 months after thoracic irradiation was statistically significantly lower in ICAM-1(-/-) mice than in ICAM-1(+/+) mice (odds ratio = 0.19 [95% confidence interval = 0.06 to 0.58], overall P =.0036). ICAM-1(-/-) mice had less pulmonary fibrosis and reduced thickening of the alveolar septum following thoracic irradiation than did ICAM-1(+/+) mice. The lungs of irradiated ICAM-1(-/-) mice had less hydroxyproline than did the lungs of irradiated ICAM-1(+/+) mice (P =.04). CONCLUSIONS: ICAM-1 and inflammation contribute to pulmonary fibrosis and impaired pulmonary compliance following thoracic irradiation. Agents that block ICAM-1 function or expression should be studied for their effects on the prevention of radiation-induced pulmonary fibrosis.

Animals↗
PubMed1980

[The association of diffuse pulmonary fibrosis and hiatal hernia: a simple coincidence? (author's transl)].

Gastroesophageal diseases with reflux can cause numerous pulmonary complications (bronchospasm crisis, bronchitis, pneumonias, lung abscesses). These manifestations are very frequent in the hiatal hernias and in some series have reached up to 46 percent of the cases studied. Recently it has been suggested that microaspirations, repeated over a long period of time, may cause an alteration of the pulmonary interstitium and the consecutive development of a clinical and roentgenologic picture similar to pulmonary fibrosis. The aspirations are produced more frequently at night, favoured by the lying down position and because of it the patients present attacks of nocturnal cough. In this paper, two patients who presented the association of pulmonary fibrosis and hiatal hernia with esophageal relux are described. The first case was diagnosed early; he had minimal radiographic anomalies and the disappearance of the respiratory symptomatology was achieved by means of the medical treatment of the esophageal reflux. The second case was in a very advanced stage with severe respiratory insufficiency and gastrointestinal manifestations of many years' evolution. Both patients had been diagnosed as having idiopathic pulmonary fibrosis. Although there is no experimental proof of the "reflux-fibrosis" theory, we think that this possibility should be kept in mind before diagnosing the interstitial pulmonary pattern as idiopathic, especially in the cases of only slight radiographic and functional involvement susceptible to improvement with correction of the esophageal reflux.

Aged↗
PubMed1998

[Expression of surfactant protein SP-A, SP-B, and SP-C mRNA in lungs of rats with bleomycin-induced pulmonary fibrosis].

OBJECTIVE: The expressions of surfactant protein (SP)SP-A, SP-B, and SP-CmRNA in lungs of rats with bleomycin-induced pulmonary fibrosis were studied. METHOD: A single dose of bleomycin(BLM) was intratracheal injected to induce pulmonary fibrosis of rats. Animals were killed at day 3, 7, 14 and 28 after BLM administration. The total RNA was extracted from the lung tissue. The expressions of SPsmRNA were analyzed with Northern blot. RESULT: The number of alveolar type II epithelial cells increased in BLM-administered rats. The expressions of SP-A, SP-B and SP-CmRNA decreased at day 3 after BLM administration and decreased maximally at day 7, and then began to increase at day 14 and significantly increased at day 28, though they were still below the control levels. CONCLUSION: The results show that the changes of expressions of SP-A, SP-B and SP-CmRNA occur during the development of bleomycin-induced pulmonary fibrosis in rats and they may play a role in the pathogenesis of lung fibrosis.

Animals↗
PubMed2001

Bleomycin-induced chronic lung damage does not resemble human idiopathic pulmonary fibrosis.

Administration of bleomycin into the lungs of experimental animals has been utilized as a model to understand human pulmonary fibrosis. Most of the studies, however, have focused on early stages of the lung reaction. We hypothesized that chronic stages of the model may not mimic idiopathic pulmonary fibrosis, since in preliminary studies, lung volume and compliance were not decreased. Eight male Sprague-Dawley rats receiving intratracheal bleomycin (0.5 U/100 g body weight) underwent measurement of FRC, inspiratory capacity, and lung compliance 120 d later. Lung histologic changes were evaluated using light microscopy. Eight rats without intervention served as controls. Results show that our model, in early stages, has histologic changes no different from those previously described elsewhere. In chronic stages, however, the model does not behave as a restrictive syndrome: FRC is normal or increased, whereas lung compliance is normal. Focal peribronchiolar inflammation and fibrosis associated with paracicatricial emphysematous changes are the main histologic features of long-term lung remodeling after bleomycin. We conclude that while the chronic stages of the model may be informative in understanding mechanisms of fibrosis, care should be taken not to extrapolate to human idiopathic pulmonary fibrosis. We speculate that the model might resemble a particular subgroup of human interstitial lung disease, namely, those involving peribronchiolar structures.

Animals↗
PubMed1990

Effect of lung T lymphocytes on fibroblasts in idiopathic pulmonary fibrosis and extrinsic allergic alveolitis.

Increased fibroblast replication and interstitial collagen accumulation occur commonly in the interstitial lung disease that progress to fibrosis. The processes controlling lung fibrogenesis are not completely understood, however. This study was designed to analyse the influence of T lymphocytes from lung tissue obtained at open lung biopsy from four patients with idiopathic pulmonary fibrosis and four patients with extrinsic allergic alveolitis on fibroblast proliferation and collagen synthesis in vitro. Lung T cell supernatants from patients with both diseases induced a moderate but significant inhibition of human lung fibroblast cell line growth. In contrast, there was a clear difference in the effect of T cells from the two groups of patients in relation to collagen production. Lung T lymphocytes from all four patients with idiopathic pulmonary fibrosis produced a substantial increase in collagen synthesis (from 371% to 514% of control values), whereas T cells from three of the four patients with extrinsic allergic alveolitis induced a significant decrease in collagen production (to 35%, 36%, and 43% of control values); in the fourth case there was an increase in collagen synthesis but this was lower than that seen with T cells from any of the patients with idiopathic pulmonary fibrosis. Peripheral T cells from six patients and control subjects caused a small increase in fibroblast proliferation and no change in collagen synthesis. The findings suggest that at least two types of interaction occur between lung T cells and fibroblasts in these disorders. A variable degree of inhibition of cell proliferation is observed in response to lung T cell supernatants from patients with both idiopathic pulmonary fibrosis and extrinsic allergic alveolitis; a substantial increase in collagen synthesis is triggered by lymphokines from patients with idiopathic pulmonary fibrosis.

Adult↗