Correlations between serum amyloid A, C‐reactive protein and clinical indices of patients with acutely exacerbated chronic obstructive pulmonary disease

Lin, Tianlai; Chen, Weiwen; Ding, Zhi‐Rong; Wei, Si-can; Huang, Minglian; Li, Cai‐Hui

doi:10.1002/jcla.22831

Cited by 23 publications

(17 citation statements)

References 23 publications

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“…Serum amyloid A is an important acute-phase reactive protein mainly produced by liver, which can eliminate pathogens in the body and facilitate disease recovery. 18,19 And thus, it is a very sensitive marker reflecting an acute inflammatory state. 20 This study combined the regional characteristics of population distribution and eating habits in coastal cities, established strict normative inclusion and exclusion criteria for reference individuals, and finally confirmed 2365 healthy people with physical examinations as the research cohort.…”

Section: Discussionmentioning

confidence: 99%

Distribution of serum amyloid A and establishment of reference intervals in healthy adults

Liu

Yang

et al. 2019

Clinical Laboratory Analysis

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Background: Serum amyloid A (SAA) plays a critical role in acute or chronic and is used in clinical laboratories as an indicator of inflammation. The elevated SAA is closely related to inflammation-mediated diseases, such as liver diseases, autoimmune diseases, metabolism-related diseases, amyloidosis, and tumors. However, there is no unified population reference interval for SAA. This study aimed to investigate the distribution of SAA in healthy Chinese adults 20-79 years of age and to establish its population reference interval.Methods: A total of 2365 healthy subjects met the requirements of this study. The levels of SAA were detected using an AU5821 automatic biochemical analyzer and its original reagents. According to the recommended methods of CLSI C28-A3 and WS/T 402-2012, the population reference interval of SAA was established using the unilateral 95th percentile (P 95 ), and the 90% confidence interval of upper limits was calculated. Results:The distributions of SAA levels were not significantly different between sexes (P> .05) and also did not differ by age (P> .05). Therefore, the population reference interval for SAA was established as an upper limit of 11.0 mg/L (90% confidence interval: 9.3-12.3 mg/L) by using the method of latex immunoturbidimetry. Conclusions:Serum amyloid A is closely related to the occurrence and progression of various diseases. The preliminary establishment of a population reference interval for SAA can fully exert its potential clinical value. K E Y W O R D Sacute-phase reactive protein, reference interval, serum amyloid A

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Section: Discussionmentioning

confidence: 99%

Distribution of serum amyloid A and establishment of reference intervals in healthy adults

Liu

Yang

et al. 2019

Clinical Laboratory Analysis

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“…Furthermore, serum levels of SAA and CRP together with other in ammatory markers (e.g. IL-6,IL-8, TNF-a, IP-10) were signi cantly greater in COPD patients experiencing an exacerbation than during remission and in healthy control subjects 24 .…”

Section: Discussionmentioning

confidence: 92%

“…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%

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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“…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%

“…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. 25 Since half of the deaths in COPD are associated with cardiovascular events, and the incidence of these events increases dramatically after each exacerbation, 26,27 and also because SAA is a good predictor of coronary artery disease as well as future cardiovascular events, SAA might be considered as a potential indicator of frequent exacerbation phenotype as well as an indicator of comorbid cardiovascular disease.…”

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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Correlations between serum amyloid A, C‐reactive protein and clinical indices of patients with acutely exacerbated chronic obstructive pulmonary disease

Cited by 23 publications

References 23 publications

Distribution of serum amyloid A and establishment of reference intervals in healthy adults

Distribution of serum amyloid A and establishment of reference intervals in healthy adults

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>

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