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At least 1,153 records · Page 64Linked to original sources
PubMed2005

High-resolution computed tomography in idiopathic pulmonary fibrosis: diagnosis and prognosis.

RATIONALE: High-resolution computed tomography (HRCT) is an integral aspect of the evaluation of patients with suspected idiopathic pulmonary fibrosis (IPF). However, few studies have evaluated its use in a large cohort. OBJECTIVES: To describe HRCT features in patients with mild to moderate IPF, compare diagnostic evaluations by a radiology core (three thoracic radiologists) with those by study-site radiologists, correlate baseline clinical and physiologic variables with HRCT findings, and evaluate their association with mortality. METHODS: We assessed HRCT scans from patients with IPF (n = 315) enrolled in a randomized controlled study evaluating IFN-gamma1b. MEASUREMENTS AND MAIN RESULTS: There was concordance between study-site and core radiologists regarding the diagnosis of IPF in 86% of cases. Diffusing capacity of carbon monoxide (DLCO) was the physiologic characteristic most highly correlated with HRCT findings. Multivariate analysis identified three independent predictors of mortality: a higher extent of fibrosis score increased the risk of death (p < 0.0001), whereas a higher percent-predicted DLCO (p = 0.004) and treatment assignment to IFN-gamma1b rather than placebo (p = 0.04) reduced the risk of death. CONCLUSIONS: A study-site diagnosis of IPF on HRCT was regularly confirmed by core radiologists. Extent of reticulation and honeycombing on HRCT is an important independent predictor of mortality in patients with IPF.

Female↗
PubMed1990

A dental technician with pulmonary fibrosis: a case of chromium-cobalt alloy pneumoconiosis?

A 45 yr old male developed pulmonary fibrosis after 29 yrs of employment as a dental technician. He subsequently developed adenocarcinoma of the lung. Diffuse interstitial fibrosis was seen using light microscopy. Neutron activation analysis of non-neoplastic lung tissue demonstrated high levels of chromium and cobalt suggesting the possibility of a chromium-cobalt alloy pneumoconiosis.

Biopsy↗
PubMed2006

The presence of emphysema further impairs physiologic function in patients with idiopathic pulmonary fibrosis.

BACKGROUND: Emphysema, especially in the upper lobes, is frequently observed in association with idiopathic pulmonary fibrosis (IPF). However, the combination of emphysema plus IPF has received little attention. OBJECTIVE: To investigate the additional functional impairment from emphysema in IPF patients. METHODS: Twenty-one patients (mean age 66 y, 20 men) (Group I) who had both IPF (mean 35% of total lung volume) and emphysema (mean 14% of total lung volume) were compared to a group of 21 subjects who had IPF but no emphysema (Group II). The groups were matched for (among other criteria) the total extent of disease. Pulmonary function tests, Medical Research Council dyspnea score, 6-min walk test, and radiographic extents of both IPF and emphysema were obtained for each patient. The Composite Physiologic Index was calculated. In the total population (n = 42), the independent contributions of IPF and emphysema to several physiologic variables were investigated by using stepwise multiple regression analysis. RESULTS: Despite the limited extent of emphysema, Groups I and II had similar physiologic impairment. Only residual volume and total lung capacity were significantly higher in Group I. According to stepwise multiple regression analysis, the extent of IPF and either the presence or the extent of emphysema in the total population were independent and significant predictors of dyspnea score, 6-min walk test, P(aO2), forced expiratory volume in the first second (FEV(1)), forced vital capacity (FVC), FEV1/FVC, the diffusing capacity of the lung for carbon monoxide, carbon monoxide diffusing capacity adjusted for alveolar volume (gas-transfer coefficient), and residual volume. The Composite Physiologic Index was closely related to the extent of IPF (r = 0.65, p < 0.0001) and to the dyspnea score (rho = 0.59, p < 0.0001). CONCLUSIONS: In former smokers with IPF, the presence and the extent of emphysema have a profound influence on physiologic function in terms of both further impairment and confounding effects.

Adult↗
PubMed1972

Pulmonary fibrosis following therapy with Melphalan for multiple myeloma.

A patient suffering from multiple myeloma developed pulmonary fibrosis, of a type known to be associated wtih busulphan, whilst being treated with Melphalan. The possible role of Melphalan as the causative agent is discussed. Reference is made to other possible aetiological agents and the reasons for their exclusion are discussed.

Autopsy↗
PubMed1977

[Extensive apical pulmonary fibrosis complicating ankylosing spondylitis. 2 cases (author's transl)].

The authors describe two cases of pulmonary fibrosis in patients suffering from ankylosing spondylitis. The diagnosis of tuberculosis was rejected on the basis of negative studies for tubercle bacilli and the total ineffectiveness of specific therapy. No evidence of microbial or parasitic infection was found. This fibrosis was associated with a considerable worsening in general condition. Nevertheless, the first patient remains alive 15 years after the onset of this pathological manifestation. The second patient died but autopsy was not possible. A wide review of the literature is undertaken in the light of these two cases.

Aged↗
PubMed1986

Bleomycin-induced nodular pulmonary fibrosis masquerading as metastatic testicular cancer.

Bleomycin has become an important component of combination chemotherapy, particularly in the treatment of metastatic testis carcinoma. Pulmonary toxicity is a major risk and irreversible pulmonary fibrosis or even death may result from its use. Rarely diffuse fibrosis may lead to discrete nodularity mimicking pulmonary metastasis. We report such a case, and discuss the various clinical, radiographic and histopathological forms of bleomycin-induced pulmonary toxicity.

Adult↗
PubMed1988

CREST syndrome: a variant of progressive systemic sclerosis, associated with interstitial pulmonary fibrosis and malignancy.

We have described a patient who had a clinical picture of CREST syndrome and pulmonary interstitial fibrosis, and in whom adenocarcinoma of the lung developed over a four-year period. Despite absence in the literature of the association of lung carcinoma in patients with CREST syndrome, our case is an example of pulmonary fibrosis complicated by lung cancer without any evidence of other risk factors. We believe this to be the first report of such an association. Clinicians, therefore, must be aware that pulmonary interstitial fibrosis in patients with the CREST syndrome may represent a risk for lung cancer.

Adenocarcinoma↗
PubMed2006

Targeting genes for treatment in idiopathic pulmonary fibrosis: challenges and opportunities, promises and pitfalls.

The currently accepted approach to treatment of idiopathic pulmonary fibrosis (IPF) is based on the assumption that it is a chronic inflammatory disease, and most available antiinflammatory drugs target numerous biological processes involving multiple genes, but are not often beneficial. More novel therapeutic strategies take recent findings about the underlying molecular mechanisms of fibrogenesis into account, and ongoing and as yet unpublished clinical trials in IPF aim to block single gene targets believed to play major roles in disease progression. Characterization of the mechanisms involved in the pathogenesis of IPF has largely come from the use of animal disease models in rodents. Most data suggest, from among the different factors, a prominent role for the transforming growth factor (TGF)-beta1 and platelet-derived growth factor pathways. Inflammation is a critical element of the initiation of fibrosis and data indicate that the Smad pathway is a necessary link to fibrosis through TGF-beta and Smad3 signaling, which introduces matrix regulation as a new target for therapeutic intervention. Regardless, gene targeted therapy has numerous pitfalls that have to be addressed before we see a real therapeutic advance.

Clinical Trials as Topic↗
PubMed1981

Epithelial-mesenchymal associations of cells in human pulmonary fibrosis and in BHT-oxygen-induced fibrosis in mice.

It was reported earlier that in the lungs of individuals with idiopathic pulmonary fibrosis, many cells lining small air spaces have intimate associations with underlying interstitial cells. The present study confirms and extends these previous observations by describing changes seen in a different patient group. Light microscopy of lung biopsy tissue showed thickened alveolar walls with infiltrates of mixed inflammatory cells. There were undefined associations between interstitial cells and cuboidal and attenuated epithelial cells lining smaller air spaces. Electron microscopy demonstrated that cytoplasmic processes from the lining cells protruded through discontinuities in underlying basement membranes, and that intimate connections between lining cells and interstitial cells frequently were present. In addition, some of the cells lining air spaces had few microvilli, rare pinocytotic vesicles, and did not lie on basement membranes. These cells were mesenchymal-like in appearance and were clearly associated with interstitial cells and connective tissue. Similar pulmonary lesions were observed in mice that received a single intraperitoneal injection of butylated hydroxytoluene and were exposed subsequently to 70% oxygen for 6 days. Our findings suggest that communication between a regenerating epithelium and the underlying mesenchyme is an integral step for ongoing alveolar repair.

Animals↗
PubMed1980

[Respiratory function impairment in idiopathic pulmonary fibrosis: with special emphasis on the apparently obstructive signs of small airways (author's transl)].

1) Respiratory function tests were performed in 6 cases with idiopathic pulmonary fibrosis (IPF) and 10 cases with pulmonary fibross associated with collagen disease. Obtained results were as follows: 2) In IPF, maximum mid-expiratory flow rate (MMF), maximal expiratory flows at 50 per cent (V50) and at 25 per cent (V25) of vital capacity significantly decreased, but no abnormal values was obtained in dynamic compliance test and multibreath N2 washout test. 3) The single model analysis of the lung functions suggested that the decrease of MMF, V50 or V25 in IPF was possibly resulted from the decrease of vital capacity. 4) These results suggest that the decrease of MMF, V50 or V25 observed in IPF is not the sign of the obstructive abnormalities in small airways, but the secondary sign caused by limitation of the lung volume.

Adult↗
PubMed1987

Diffuse interstitial pulmonary fibrosis and lung cancer.

Forty-two cases of lung cancer complicated with diffuse interstitial pulmonary fibrosis (DIPF) were selected from 13,056 autopsy cases. They were divided into primary (Group I and II) and secondary (Group III) DIPF, and histopathologic and clinicopathologic studies were made. The prevalence of lung cancer with primary DIPF was 17% (8/47) which was significantly (p less than 0.01) higher than that without DIPF (7% or 886/13,009). All eight cases of lung cancer in Group I and II were male, and 7 had cigarette-smoking history. The anatomical sites of lung cancer and DIPF were all peripheral in origin, and in 7 cases located primarily in the lower lobes (left:right = 6:1). Adenocarcinoma was the most common type. The study suggests that male DIPF patients with long clinical history should be followed thoroughly for lung cancer.

Adenocarcinoma↗
PubMed2001

Epstein-Barr virus and wild p53 in idiopathic pulmonary fibrosis.

Both Epstein-Barr virus (EBV) and p53 have independently been associated with idiopathic pulmonary fibrosis (IPF). This study explores further whether a relationship potentially exists between EBV and p53 in IPF, thereby providing a possible mechanism for the role of EBV in the disease progression of IPF. Lung tissue from open lung biopsies of 14 IPF patients was compared with a control group of 19 patients. EBV status was determined using both immunohistochemistry and PCR, while p53 expression was assessed with immunohistochemistry Seven of 14 IPF patients expressed p53 compared to one of 19 control subjects (P = 0.011). Eight IPF patients and no controls were positive for EBV (P < 0.01). Four IPF patients demonstrated both EBVand p53 expression compared with no controls, (P = 0.05). This study suggests that a relationship between EBV and p53 may exist in patients with IPF.

Case-Control Studies↗
PubMed2005

[Clinicopathologic study of 50 autopsy cases of idiopathic pulmonary fibrosis and non-diffuse usual interstitial pneumonia].

We investigated 50 autopsy cases of idiopathic pulmonary fibrosis (IPF) and non-diffuse usual interstitial pneumonia (UIP), and subgrouped them into three subtypes based on morphologic differences in the fibrosis (honeycomb): typical thick-walled honeycomb type (16 cases), atypical thin-walled honeycomb type (27 cases) and atelectatic indurated type (6 cases), with one undetermined case. In the thin-walled type, the percentage of males (93%), the percentage of smokers (89%), and the percentage of lung cancer cases (52%) were significantly higher than in the other two subtypes (p < 0.02, p < 0.001 and p < 0.05, respectively). However, in the thick-walled and indurated types there were significantly higher percentages of DAD (38% and 67%, respectively) than in the thin-walled type (15%) (P < 0.05). Accordingly, each subtype was thought to be closely related to its IPF clinical features, and showed differences in the development of acute exacerbation and lung cancer. This study proposes the existence of a UIP subset and suggests that this subgrouping can help in the management of the disease.

Aged↗
PubMed2002

Role of extracellular superoxide dismutase in bleomycin-induced pulmonary fibrosis.

Bleomycin administration results in well-described intracellular oxidative stress that can lead to pulmonary fibrosis. The role of alveolar interstitial antioxidants in this model is unknown. Extracellular superoxide dismutase (EC-SOD) is the primary endogenous extracellular antioxidant enzyme and is abundant in the lung. We hypothesized that EC-SOD plays an important role in attenuating bleomycin-induced lung injury. Two weeks after intratracheal bleomycin administration, we found that wild-type mice induced a 106 +/- 25% increase in lung EC-SOD. Immunohistochemical staining revealed that a large increase in EC-SOD occurred in injured lung. Using mice that overexpress EC-SOD specifically in the lung, we found a 53 +/- 14% reduction in bleomycin-induced lung injury assessed histologically and a 17 +/- 6% reduction in lung collagen content 2 wk after bleomycin administration. We conclude that EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration.

Animals↗
PubMed1987

Aluminum-induced pulmonary fibrosis: do fibers play a role?

A 50-yr-old man with a history of 19 yr of work in the aluminum smelting industry, including 14 years in the potrooms, was found to have diffuse interstitial fibrosis, slightly more severe in the upper zones. He died of respiratory insufficiency 5 yr after initial presentation. Analysis of lung by electron optical techniques revealed 15,000,000,000 nonfibrous particles and 1,300,000,000 fibrous particles of aluminum oxide/g dry lung, values representing approximately a 1,000-fold increase over background exposure. The nonfibrous particles had a geometric mean diameter of 0.4 mu, and the fibers had a geometric mean length of 1.0 mu, a width of 0.06 mu, and an aspect ratio of 16. X-ray diffraction demonstrated alpha but not gamma aluminum oxide. These studies indicate that previous suggestions relating aluminum-induced fibrosis to the presence of gamma aluminum oxide are not correct. Although pulmonary fibrosis in this case may be a response to a very high total aluminum particle burden, the presence of large numbers of fibers raises the possibility that fibers play a role in aluminum fibrosis.

Aluminum↗