Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 636 episodes of peritonitis occurred in 440 patients who entered our continuous ambulatory peritoneal dialysis (CAPD) program from September 1977 to February 1988. Sixteen patients (8 male and 8 female, aged 37-77 years) died during an episode of peritonitis (fatality rate 2.5%). They had been on CAPD for 3 to 105 (average 39) months. Six of them were diabetics. The peritonitis rate among these 16 patients were 1 episode per 12 patient months, while the corresponding figure for the whole (440) CAPD population was 14 patient months. Risk factors present in the 16 patients were: cardiovascular disease (12), cerebrovascular accident (2) peripheral artery disease (1) and pulmonary fibrosis (1). Fever and leukocytosis were present on admission in 11 patients, while total serum proteins and albumin were significantly lower (p less than 0.001) than the corresponding values before peritonitis (56 +/- 8 vs. 65 +/- 5). Staph. aureus was isolated in 8 patients (50%), multiple organisms in 6, Pseudomonas and Candida albicans in 1 each. An abdominal abscess was found in 4 (25%) patients. The peritoneal catheter was removed between the 5th and 10th day in 6 and after the 10th day in 7 patients. Peritonitis with sepsis was the cause of death in 13 patients. Contributing factors were cardiovascular accident in 9, uremic coma in 2, extensive GI bleeding in 2, GI perforation in 2, intestinal infarction in 1, and pneumonia in 2 patients. We conclude that the risk of peritonitis-related death in CAPD patients is increased with Staph. aureus or multibacterial peritonitis. Contributing factors are concomitant cardiovascular disease and delayed (greater than 5 days) catheter removal.
 ...
PMID:Peritonitis-related deaths in continuous ambulatory peritoneal dialysis (CAPD) patients. 208 82

A study was initiated to determine whether alveolar macrophages from patients with collagen vascular diseases but free of pulmonary symptoms were spontaneously activated and whether they released various mediators related to the pathogenesis of pulmonary fibrosis. Alveolar macrophages obtained by bronchoalveolar lavage from 32 patients with proved collagen vascular disease but no evidence of lung disease were compared with those from 10 patients with collagen vascular disease with interstitial lung disease (CVD-ILD) and from 10 healthy controls. The total number of alveolar macrophages did not differ between patients with collagen vascular disease and controls but were substantially increased in the CVD-ILD group. Alveolar macrophages from 31 of the 32 patients with collagen vascular disease and from all 10 in the CVD-ILD group had at least one criterion of activation. Neutrophil chemotactic activity was detected in supernatants from alveolar macrophage culture in 23 of the 32 patients with collagen vascular disease and from nine of the 10 in the CVD-ILD group; fibronectin secretion by alveolar macrophages was increased in 12 of the 32 patients with collagen vascular disease and in nine of the 10 in the CVD-ILD group. Furthermore, alveolar macrophages from 20 of the 32 patients with collagen vascular disease and four of the 10 CVD-ILD patients spontaneously released increased amounts of superoxide anion. Thus alveolar macrophages were spontaneously activated in a high proportion of patients with collagen vascular disease.
 ...
PMID:Activated alveolar macrophages in subclinical pulmonary inflammation in collagen vascular diseases. 283 61

Idiopathic pulmonary fibrosis (IPF) and pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD) are chronic inflammatory lung disorders which may be characterized in various subgroups of patients by increased numbers of macrophages, neutrophils, lymphocytes, and/or eosinophils. Previous studies have suggested that the cell populations recovered with bronchoalveolar lavage (BAL) may be important in predicting disease progression and response to therapy. We evaluated this hypothesis in 27 patients by determining if the cell populations recovered with BAL differed between patients who improved, remained stable, or worsened in their pulmonary functions (as defined by at least a 15 percent change in forced vital capacity) over a six-month observation period. The findings suggested that BAL eosinophilia may be a marker of progressive lung disease in patients with IPF and PF-CVD.
 ...
PMID:Prognostic role of eosinophils in pulmonary fibrosis. 359 49

To assess the effect of asbestos on the airways, researchers studied 45 shipyard workers who were lifelong nonsmokers and had asbestos-related abnormalities seen on their chest roentgenograms. Patients with interstitial lung disease, bronchial asthma prior to asbestos exposure, recurrent pneumonias, or significant cardiovascular disease were excluded from the study. In addition to chest films, they had spirometry performed before and after bronchodilator inhalation, lung volumes, diffusing capacity, and arterial blood gases. Forced vital capacity and forced expired volume in one second were normal in all patients. Maximum midexpiratory flow rates (MMFR) were abnormal (MMFR less than 75% of predicted) in 13 patients (29%). Therefore, 29% of lifetime nonsmokers with asbestos exposure exhibited evidence of small airways dysfunction. An abnormal MMFR in these workers may be due, in part, to asbestos exposure and could conceivably indicate a population at risk for pulmonary fibrosis and/or obstructive airways disease.
 ...
PMID:Asbestos and airflow limitation. 377 61

The eosinophil count and concentrations of eosinophil cationic protein (ECP) were measured in bronchoalveolar lavage fluid (BALF) from patients with idiopathic pulmonary fibrosis (IPF), pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD), sarcoidosis, and healthy controls. The patients with IPF and PF-CVD showed significant increased eosinophil count and ECP levels in BALF compared with the controls. When the patients with IPF and PF-CVD were subclassified into chronic stable, progressive, and acute progressive subgroups in accordance with the observed progression of pulmonary dysfunction during the preceding 3- to 6-month period, those in the acute progressive subgroup showed significantly elevated recovered eosinophil count and ECP level, as well as recovered lymphocyte count and total protein, albumin, and type III procollagen aminoterminal peptide-related antigens (pIIIp) in BALF, compared with either of the other two subgroups. Multivariate stepwise logistic regression analysis revealed that, among these variables, only ECP and pIIIp significantly contributed to discrimination among the three subgroups differing in disease activity. These findings suggest that eosinophils are involved in the inflammatory process in pulmonary fibrosis and that the released ECP and other cytotoxic eosinophil products may contribute to the lung injury and development of fibrosis.
 ...
PMID:Eosinophil activation in patients with pulmonary fibrosis. 760 90

Although the pathological patterns of interstitial pneumonia associated with collagen vascular disease (CVD-IP) resemble those of usual interstitial pneumonia in idiopathic interstitial pneumonia (IIP), the clinical features of CVD-IP and IIIP are quite different. We evaluated the differences between these conditions, with regard to the expression of genes in cells obtained by bronchoalveolar lavage. The reverse transcription-polymerase chain reaction was used to measure the levels of mRNA for IL-1 beta, TNF-alpha, IL-8, TGF-beta, PDGF-B, and IGF-1, and no significant differences were found between patients with CVD-IP and those with IIP. However, differential display analysis revealed a fragment that can be considered to have been derived from an unknown gene mRNA, and this was found only in patients with pulmonary fibrosis associated with progressive systemic sclerosis. Expression of specific genes may differentiate CVD-IP from IIP.
 ...
PMID:[Pulmonary manifestation of collagen vascular diseases: role of cytokines in interstitial pneumonia associated with collagen vascular diseases]. 875 19

The aim of this study was to determine whether latent viral infection is associated with idiopathic pulmonary fibrosis (IPF), an interstitial lung disease whose aetiology remains to be elucidated. Cytomegalovirus (CMV) immunoglobulin G (IgG) and complement fixation (CF), Epstein-Barr (EB) viral capsid antigen (VCA) IgG, herpes simplex virus (HSV) IgG, adenovirus CF, and parainfluenza 3 virus haemagglutinin inhibition (HI) titres were measured in the serum from patients with pulmonary diseases. The study included five subject groups: 35 normal controls (aged (mean +/- SD) 38 +/- 17 yrs); 43 IPF (63 +/- 10 yrs), seven collagen vascular disease-related interstitial pneumonitis (CVD-IP) (62 +/- 12 yrs); 22 sarcoidosis (36 +/- 14 yrs); and 17 emphysema (66 +/- 11 yrs). Levels of CMV IgG in IPF (87.6 +/- 51.7) and CVD-IP (101.2 +/- 69.9) were significantly elevated compared to those in the control (30.9 +/- 24.1), sarcoidosis (34.4 +/- 38.3) and emphysema groups (40.3 +/- 24.6), whereas CMV immunoglobulin M (IgM) was generally below the limit of detection. Similarly, CMV CF titres in IPF and CVD-IP were elevated compared to those in other diseases. EB VCA IgG titres in IPF, CVD-IP and emphysema and HSV IgG in IPF were also elevated. In contrast, adenovirus CF and parainfluenza 3 HI titres demonstrated no significant difference among all of the groups investigated. Increases in cytomegalovirus immunoglobulin G and complement fixation titres with negative cytomegalovirus immunoglobulin M suggest that latent cytomegalovirus infection may be more prominent in idiopathic pulmonary fibrosis or collagen vascular disease-related interstitial pneumonitis. Together with the elevation of Epstein-Barr virus viral capsid antigen and herpes simplex virus immunoglobulin G in idiopathic pulmonary fibrosis and/or collagen vascular disease-related interstitial pneumonitis, it is rational to assume that these viruses may be implicated in the development of pulmonary fibrosis. Further study is necessary to investigate the relationship between latent viral infection and pulmonary fibrosis.
 ...
PMID:Elevation of antibodies to cytomegalovirus and other herpes viruses in pulmonary fibrosis. 931 99

Emphasis has recently been placed on the roles of chemotactic cytokines called chemokines to explain the accumulation of inflammatory cells in the lung that may precede or accompany pulmonary fibrosis in interstitial lung diseases. We hypothesized that RANTES, a member of the C-C chemokines, is one such chemokine. Bronchoalveolar lavage was done in 20 patients with sarcoidosis, 10 patients with interstitial pneumonia associated with collagen vascular disease (CVD-IP), 10 patients with idiopathic pulmonary fibrosis (IPF), and eight healthy volunteers (HV), all of whom were never-smokers. We semiquantitated the spontaneous RANTES mRNA expression by a competitive reverse transcription-polymerase chain reaction (RT-PCR) technique, and measured the levels of RANTES protein by enzyme-linked immunosorbent assay. In all disease groups the expression of RANTES mRNA by bronchoalveolar lavage fluid (BALF) cells and the levels of RANTES protein in BALF were significantly increased compared with those in HV. Patients with sarcoidosis and CVD-IP had a significant positive correlation between the expression of RANTES mRNA by BALF cells and BALF lymphocytosis. The amounts of RANTES mRNA expressed by peripheral blood mononuclear cells and the levels of RANTES protein in serum did not differ among all study groups. Our study demonstrates the adaptability of a semiquantitative RT-PCR method for determining cytokine mRNA expression in vivo. Our results suggest that RANTES may be one of the chemokines that are involved in the mechanism for the accumulation of inflammatory cells in the lung of some distinct interstitial lung diseases.
 ...
PMID:Expression of RANTES by bronchoalveolar lavage cells in nonsmoking patients with interstitial lung diseases. 953 40

The present study evaluated the clinical significance of hepatocyte growth factor (HGF) in patients with pulmonary fibrosis. Twenty-one patients with a diagnosis of pulmonary fibrosis [14 with idiopathic pulmonary fibrosis (IPF) and seven with pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD]) and 21 normal subjects as control were studied. HGF levels in sera of patients with pulmonary fibrosis (0.34 +/- 0.02 ng ml-1) were elevated significantly as compared with normal subjects (0.21 +/- 0.01 ng ml-1) (P < 0.0001). HGF/albumin levels in broncho-alveolar lavage fluid (BALF) of patients with pulmonary fibrosis (72 +/- 17 ng g-1 albumin) were also significantly elevated as compared with normal subjects (under the detection limit) (P < 0.01). HGF levels in sera correlated significantly with elastase levels in sera and C-reactive protein, and correlated negatively with PaO2. HGF levels in sera were significantly higher in smokers with pulmonary fibrosis (0.42 +/- 0.03 ng ml-1) as compared with non-smokers with pulmonary fibrosis (0.29 +/- 0.03 ng ml-1) (P < 0.005). HGF/albumin levels in BALF correlated significantly with elastase/albumin levels in BALF, lactate dehydrogenase/albumin in BALF, Immunoglobulin A/albumin in BALF, total cell count/albumin in BALF, total number of alveolar macrophage/albumin in BALF, total number of neutrophil/albumin in BALF, CEA/albumin in BALF, CA19-9/albumin in BALF, and SCC/albumin in BALF. These results suggest that following lung injury, HGF may be a mediator involved in the repair which leads to pulmonary fibrosis.
 ...
PMID:Measurement of hepatocyte growth factor in serum and bronchoalveolar lavage fluid in patients with pulmonary fibrosis. 961 25

Fas is expressed in various cells and transduces the cell death signal. p21 is a mediator of p53-dependent G1 arrest associated with deoxyribonucleic acid (DNA) damage. The upregulation of p53 and p21 associated with DNA damage in idiopathic pulmonary fibrosis has been described previously. In this study, p53, p21, and Fas expression and DNA damage were examined in interstitial pneumonia associated with collagen vascular diseases (CVD-IP). DNA damage was assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end-labelling (TUNEL) and p53, p21 and Fas proteins were detected by immunohistochemistry in 13 cases of CVD-IP, 13 of sarcoidosis, seven of hypersensitivity pneumonitis (HP) and eight control patients with normal lung parenchyma. TUNEL-positive signals were found in bronchiolar or alveolar epithelial cells in 11 of 13 (85%) specimens of CVD-IP, but not in sarcoidosis, HP or controls, except for a case of chronic HP with pulmonary fibrosis. p53, p21 and Fas were detected in bronchiolar or alveolar epithelial cells in nine (69%), 10 (77%) and 12 (92%) of 13 specimens of CVD-IP, respectively, but not in sarcoidosis, HP or controls, except for a case of chronic HP. These results suggest that the upregulation of p53, p21 and Fas in bronchiolar and alveolar epithelial cells associated with deoxyribonucleic acid damage may participate in the process of pulmonary fibrosis in interstitial pneumonia associated with collagen vascular diseases and chronic hypersensitivity pneumonitis.
 ...
PMID:Expression of p53, p21 (Waf1/Cip1/Sdi1) and Fas antigen in collagen vascular and granulomatous lung diseases. 981 69


1 2 3 4 Next >>