Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q99581 (FEV)
 3,296 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute phase reactants have been implicated for their involvement as proinflammatory molecules in various inflammatory diseases. However, little is known regarding their role in the allergic airway disease. The aim of the present study was to examine the blood concentrations of three acute-phase proteins, namely C-reactive protein (CRP), serum amyloid A (SAA) and fibrinogen in patients with allergic rhinitis and asthma. Three study groups include: non-smoker allergic rhinitis (n = 50), non-smoker asthma (n = 20), and non-allergic, non-smoker healthy control subjects (n = 20). Patients who have had recent upper or lower respiratory tract infection and trauma, any rheumatological illnesses, malignancy or obesity were excluded. Blood samples were obtained from all the patients and control subjects and were analyzed for serum CRP, SAA and plasma fibrinogen. The mean CRP and fibrinogen values in the rhinitis and asthma groups were not significantly different when compared to the control group. However, the mean SAA levels of both groups were found to be significantly higher than those of the control group (p = 0.002 for rhinitis, p = 0.02 for asthma). There was no significant correlation between the FEV(1) values and the levels of the serum markers. This study demonstrates that acute phase reactant SAA rises in patients with allergic rhinitis and patients with asthma. We therefore suggest that SAA may have a role in the inflammatory airway disease.
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PMID:Acute phase reactants in allergic airway disease. 1550 20

The soluble receptor for advanced glycation end-products (sRAGE) has anti-inflammatory properties, and deficiency of circulating sRAGE is associated with various human diseases. Whether sRAGE concentrations are reduced in chronic obstructive pulmonary disease (COPD) has not been determined. The aim of this study was to determine plasma levels of sRAGE in COPD patients and establish whether sRAGE varies in relation to forced expiratory volume in 1 s (FEV(1)) and other inflammatory markers. 61 COPD patients and 42 healthy controls were recruited. Plasma sRAGE, C-reactive protein (CRP) and serum amyloid A (SAA) were measured in patients with stable COPD. A subgroup had measurements during acute exacerbations of COPD (AECOPD). sRAGE was significantly lower in stable COPD than in healthy controls (p<0.001), while CRP (p<0.001) and SAA (p = 0.015) were higher in stable COPD than in healthy controls. Multiple linear regression confirmed that COPD was negatively associated with sRAGE (p<0.001). Plasma sRAGE was positively correlated with FEV(1) (r(2) = 0.530, p<0.001), while CRP and SAA were inversely proportional to FEV(1). Multiple linear regression analysis showed that only sRAGE was a strong predictor of FEV(1). AECOPD were associated with even lower sRAGE levels that increased with convalescence. Circulating sRAGE is lower in COPD and shows a strong correlation to the degree of airflow limitation.
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PMID:Reduced soluble receptor for advanced glycation end-products in COPD. 2188 23

A crucial pathogenetic role of serum amyloid A (SAA) in granulomatous inflammation of sarcoidosis has recently been reported. In this study we analyzed SAA expression in detail, starting from proteomic analysis of serum of sarcoidosis patients. We also used the faster ELISA method that enabled us to examine a greater number of samples. Serum concentrations of SAA were significantly higher in sarcoidosis patients than controls (p<0.001), inversely correlated with FEV(1) and significantly higher in patients with subacute onset requiring prolonged and multiple steroid treatments (class 6 SCAC) than in patients with subacute onset not requiring therapy (class 4 SCAC) (p<0.001). Our results suggest that serum amyloid A could be a suitable marker of sarcoidosis: its serum concentrations are significantly higher in sarcoidosis patients than controls, the protein is only expressed in gels of sarcoidosis patients and not in healthy subjects, and the SAA1 isoforms could match the unidentified biomarker of sarcoidosis reported in a previous proteomic study by another group. The effectiveness of SAA as a clinical biomarker of sarcoidosis should now be investigated in a large prospective study.
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PMID:Analysis of serum amyloid A in sarcoidosis patients. 2121 7