Serum amyloid A in patients with idiopathic pulmonary fibrosis

Vietri, Lucia; Bennett, David; Cameli, Paolo; Bergantini, Laura; Cillis, Giuseppe; Sestini, Piersante; Bargagli, Elena; Rottoli, Paola

doi:10.1016/j.resinv.2019.03.010

Cited by 28 publications

(35 citation statements)

References 26 publications

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“…Formiga et al reported that inspiratory muscle performance was considerably lower in COPD patients with greater SAA concentration 23 . In addition, SAA was greater in patients with IPF than in healthy controls 22 . Furthermore, serum levels of SAA and CRP together with other in ammatory markers (e.g.…”

Section: Discussionmentioning

confidence: 83%

“…Previous studies showed that SAA is dramatically increased during acute phase of a COPD exacerbation, and that SAA is a sensitive biomarker for exacerbation severity in COPD patients 14 . Other studies showed increased circulating SAA concentration in COPD and other pulmonary diseases such as idiopathic pulmonary brosis (IPF) [22][23][24] . Formiga et al reported that inspiratory muscle performance was considerably lower in COPD patients with greater SAA concentration 23 .…”

Section: Discussionmentioning

confidence: 99%

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Serum Amyloid a in Stable COPD Patients is Associated With the Frequent Exacerbator Phenotype

Zhao

Abbasi

Rossiter

et al. 2020

Preprint

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Background: We sought to determine whether circulating inflammatory biomarkers were associated with the frequent exacerbator phenotypein stable COPD patients i.e. those with two or more exacerbations in the previous year.Methods:88 stable, severe, COPD patients (4 females)were assessed for exacerbation frequency, pulmonary function, fraction of expired nitric oxide (FENO);inflammatory variables were measured in venous blood. Logistic regression assessed associations between the frequent exacerbator phenotype and systemic inflammation.Results:Compared with infrequent exacerbators, frequent exacerbators (n=10; 11.4%)had greater serum concentration(median (25th-75th quartile)) of serum amyloid A (SAA; 134(84-178) vs. 71(38-116) ng/ml; P=0.024), surfactant protein D (SP-D;15.6(9.0-19.3)vs. 8.5(3.6-14.9) ng/ml; P=0.049) and interleukin-4 (IL-4; 0.12(0.08-1.44)vs. 0.03(0.01-0.10) pg/ml;P=0.001). SAA,SP-D and IL-4were not significantly correlated with FEV1 %predicted or FVC %predicted. After adjusting for sex, age, BMI, FEV1/FVC and smoking pack-years, only SAA remained independently associated with the frequent exacerbator phenotype (OR 1.49[1.09-2.04]; P=0.012).The odds of being a frequent exacerbator was 18-times greater in the highest SAA quartile (³124.1ng/ml) than the lowest SAA quartile (£44.1ng/ml) (OR 18.34[1.30-258.81]; P=0.031), and there was a significant positive trend of increasing OR with increasing SAA quartile (P=0.008). For SAA, the area under the receiver operating characteristic curve was 0.721 for identification of frequent exacerbators with an optimal SAA cut-offof 131.7 ng/ml.Conclusion: In stable COPD patients, SAA was independently associated with the frequent exacerbator phenotype, suggesting that SAA maybe a usefulserum biomarker to inform progression or management in COPD.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Serum Amyloid a in Stable COPD Patients is Associated With the Frequent Exacerbator Phenotype

Zhao

Abbasi

Rossiter

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…23 In addition, SAA was greater in patients with IPF than in healthy controls. 22 Furthermore, serum levels of SAA and CRP together with other inflammatory markers (eg, IL-6, IL-8, TNF-a, IP-10) were significantly greater in COPD patients experiencing an exacerbation than during remission and in healthy control subjects. 24 Elevated SAA was reported in patients with cardiovascular disease where COPD was a comorbidity.…”

Section: Discussionmentioning

confidence: 92%

“…14 Other studies showed increased circulating SAA concentration in COPD and other pulmonary diseases such as idiopathic pulmonary fibrosis (IPF). [22][23][24] Formiga et al reported that inspiratory muscle performance was considerably lower in COPD patients with greater SAA concentration. 23 In addition, SAA was greater in patients with IPF than in healthy controls.…”

Section: Discussionmentioning

confidence: 99%

<p>Serum Amyloid A in Stable COPD Patients is Associated with the Frequent Exacerbator Phenotype</p>

Zhao¹,

Abbasi²,

Rossiter³

et al. 2020

COPD

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Background: We sought to determine whether circulating inflammatory biomarkers were associated with the frequent exacerbator phenotype in stable COPD patients ie, those with two or more exacerbations in the previous year. Methods: Eighty-eight stable, severe, COPD patients (4 females) were assessed for exacerbation frequency, pulmonary function, fraction of expired nitric oxide (F E NO); inflammatory variables were measured in venous blood. Logistic regression assessed associations between the frequent exacerbator phenotype and systemic inflammation. Results: Compared with infrequent exacerbators, frequent exacerbators (n=10; 11.4%) had greater serum concentration (median (25th-75th quartile)) of serum amyloid A (SAA; 134 (84-178) vs 71 (38-116) ng/mL; P=0.024), surfactant protein D (SP-D; 15.6 (9.0-19.3) vs 8.5 (3.6-14.9) ng/mL; P=0.049) and interleukin-4 (IL-4; 0.12 (0.08-1.44) vs 0.03 (0.01-0.10) pg/mL; P=0.001). SAA, SP-D and IL-4 were not significantly correlated with FEV 1 % predicted or FVC %predicted. After adjusting for sex, age, BMI, FEV 1 /FVC and smoking pack-years, only SAA remained independently associated with the frequent exacerbator phenotype (OR 1.49[1.09-2.04]; P=0.012). The odds of being a frequent exacerbator was 18times greater in the highest SAA quartile (≥124.1 ng/mL) than the lowest SAA quartile (≤44.1 ng/mL) (OR 18.34[1.30-258.81]; P=0.031), and there was a significant positive trend of increasing OR with increasing SAA quartile (P=0.008). For SAA, the area under the receiver operating characteristic curve was 0.721 for identification of frequent exacerbators; an SAA cutoff of 87.0 ng/mL yielded an 80% sensitivity and 61.5% specificity. Conclusion: In stable COPD patients, SAA was independently associated with the frequent exacerbator phenotype, suggesting that SAA may be a useful serum biomarker to inform progression or management in COPD.

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“…Diverse functions of SAA have been proved in cardiovascular diseases (CVD), including regulating matrix metalloproteinase-2 activity in aorta (13), modifying the vascular functionality of HDL-C (14), and regulation of systemic inflammatory reaction (15). Recent research efforts have focused on the potential role of SAA as a biomarker in clinical disorders (16,17).…”

Section: Introductionmentioning

confidence: 99%

Serum Amyloid A Protein as a Potential Biomarker in predicting acute onset and association with in-hospital death in acute aortic dissection

Xing³

et al. 2019

Preprint

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Background: Acute aortic dissection (AAD) is a life-threatening disorder in vascular surgery with a high early mortality. Serum amyloid A (SAA) is a kind of acute-phase protein with a rapid diagnostic value in other diseases. However, the researches on the performance of SAA for the diagnosis of AAD is still lacking. This retrospective study aimed to evaluate the SAA levels and further explore its potential diagnostic role in AAD patients. Methods: SAA levels were measured by enzyme-linked immunosorbent assay (ELISA) in 63 controls and 87 AAD patients. Laboratory examinations were also performed. And relative clinical information was collected from participants included in this study.Results: SAA levels were significantly higher in AAD patients than those in healthy controls. SAA levels were independently associated with the risk of AAD. There was a positive significant correlation between SAA and C reactive protein (R=0.442, and P=0.001). Based on receiver-operating characteristic (ROC) analysis, the area under the curve (AUC) of SAA for the diagnosis of AAD were 0.942 with optimal cut-off points of 0.427mg/L. For in-hospital mortality, the AUC of SAA were 0.732 with optimal cut-off points of 0.500mg/L. According to logistic regression analysis, higher SAA levels represent a higher risk of in-hospital mortality (OR=1.25; 95%CI: 1.07-1.47; P=0.005). Conclusion:Our findings demonstrated that SAA levels were significantly enhanced in AAD. SAA was closely correlated with inflammatory parameters and coagulation-related parameters in AAD. Furthermore, SAA could be a potential bio-marker for identifying AAD in the early diagnosis. Finally, SAA >5.0 mg/L are independently related to AAD in-hospital mortality. BackgroundAcute aortic dissection (AAD) is a life-threatening disorder in vascular surgery defined as the separation of aortic wall layer (1, 2). In line with the Stanford classification, AAD is commonly divided into type A aortic dissection (TAAD) (involving ascending aorta) as well as type B aortic dissection (TBAD) (ascending aorta not affected) by considering both dissection extent and lesion site (3,4). AAD is characterized by acute onset, rapid progression as well as high morbidity and mortality in early stage. It has been previously reported that approximately 48.6% of untreated AAD patients die pre-hospitally (5). Meanwhile, both TAAD and TBAD have high short-term in-hospital mortality. outcomes, which would definitely contribute to the prognostic evaluation of AAD. Abbreviations

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Serum amyloid A in patients with idiopathic pulmonary fibrosis

Cited by 28 publications

References 26 publications

Serum Amyloid a in Stable COPD Patients is Associated With the Frequent Exacerbator Phenotype

Serum Amyloid a in Stable COPD Patients is Associated With the Frequent Exacerbator Phenotype

<p>Serum Amyloid A in Stable COPD Patients is Associated with the Frequent Exacerbator Phenotype</p>

Serum Amyloid A Protein as a Potential Biomarker in predicting acute onset and association with in-hospital death in acute aortic dissection

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