Novel biomarkers for acute phase reactants

Article information

Clin Exp Emerg Med. 2025;12(1):1-3
Publication date (electronic) : 2024 December 11
doi : https://doi.org/10.15441/ceem.24.336
Department of Laboratory Medicine, Kyung Hee University Hospital, Kyung Hee University College of Medicine, Seoul, Korea
Correspondence to: Sun Young Cho Department of Laboratory Medicine, Kyung Hee University Hospital, Kyung Hee University College of Medicine, 23 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea Email: untoyou@hanmail.net
Received 2024 October 11; Accepted 2024 October 21.

Acute phase reactants (APRs) are defined by plasma concentrations that increase (positive APR) or decrease (negative APR) by at least 25% during inflammatory disorders [1]. C-reactive protein (CRP) is an APR synthesized by the liver in response to interleukin 6 (IL-6) and the most frequently studied conventional biomarker of inflammation [2]. Recently, novel biomarkers for acute inflammation such as serum amyloid A (SAA), procalcitonin, presepsin, and calprotectin have been introduced in clinical laboratories. In this brief review, we outline the characteristics and advantages of these biomarkers.

SERUM AMYLOID A

SAA was discovered a quarter of a century ago as a plasma component that shares antigenicity with amyloid AA, a fibrillogenic precursor in amyloidosis [3]. This component can increase by 100- to 1,000-fold over the baseline level of approximately 1 μg/mL during acute phase reactions [3]. CRP has become the gold standard in the management of inflammatory diseases, but SAA has major advantages over CRP tests. First, the amplitude of the increase of SAA is greater than that of CRP [4], especially in viral infections such as measles, adenovirus, mumps, rubella, varicella and influenza, in which SAA levels are often elevated even when CRP is below the detection level [5]. Second, SAA more accurately predicts poor prognosis of elderly inpatients than does CRP [4]. SAA can also detect some events such as minor infection which may occur in the elderly and patients with chronic disorders such as diabetes [6]. Third, discrepancies between SAA and CRP have been observed in patients with kidney transplantations [4]. During transplant rejection, SAA is markedly elevated along with serum creatinine and the changes are dramatic enough to be recognized easily [7]. In contrast, CRP response is poor during rejections, not only in the early phases but throughout subsequent days [7]. Therefore, SAA tests can be recommended in clinical conditions in which CRP does not show a useful response. Finally, SAA is a sensitive biomarker with potential to assess disease severity and survival outcomes in COVID-19 patients and a better choice than CRP for predicting the prognosis of patients with COVID-19 [8].

PROCALCITONIN AND PRESEPSIN

Sepsis is a life-threatening condition characterized by organ failure and is a result of a dysregulated host response to infection [9]. Serum procalcitonin (PCT) levels increase to very high values in patients with severe invasive bacterial infections compared to patients with mild local bacterial infections or viral infections [10]. PCT is a biomarker that can be used to differentiate sepsis from noninfectious triggers of systemic inflammatory response syndrome in critically ill patients [10]. However, PCT can be increased in some disorders, especially following trauma without the presence of infection [9,11]. Compared with other markers, presepsin may have better sensitivity and specificity for the diagnosis of sepsis [12]. The sensitivity of presepsin for the diagnosis of sepsis was 91.9%, PCT 89.9%, IL-6 88.9%, and blood culture 35.4%, suggesting that presepsin has good performance for the diagnosis of sepsis, and that PCT has nearly equal performance compared to presepsin for detecting sepsis [12,13]. However, presepsin increases earlier and faster in patients with sepsis 2 hours after infection, peaks at 3 hours, and declines at 4 to 8 hours [12]. Compared with presepsin, PCT increases within 4 hours after infection, reaches a plateau at 8 to 24 hours, and peaks 24 hours after infection [12]. In the emergency department, presepsin is most useful because it increases in plasma earlier than other biomarkers [9].

CALPROTECTIN

Calprotectin (CLP) is a stable heteromorphic dimer of S100A8 and S100A9 [14]. CLP plays an important role in the inflammatory cascade and has a wide range of proinflammatory functions such as cytokine promotion, chemokine production, and leukocyte aggregation, adhesion, and migration [15]. According to a previous report, serum CLP levels increase in close correlation with traditional markers of oxidative stress and inflammation [16]. Increased plasma calprotectin levels have been found in inflammatory chronic diseases such as inflammatory bowel diseases, rheumatoid arthritis, systemic lupus erythematosus, juvenile idiopathic arthritis, multiple sclerosis, and cystic fibrosis [17]. Moreover, it was independently associated with mortality, functional dependence, and hemorrhagic transformation in acute ischemic stroke [18]. In patients with aneurysmal subarachnoid hemorrhage, serum CLP levels show significant correlations with severity and the poor prognosis [18]. Serum CLP has also recently been suggested as a novel biomarker for acute brain injury, as its levels are closely related to inflammatory reaction after severe traumatic brain injury [18].

CONCLUSION

Emerging studies present a broad spectrum of novel biomarkers in inflammation and infection. Novel biomarkers, such as various APRs, can greatly aid in the differential diagnosis and prognosis of inflammatory and infectious disease. In addition, clinicians will benefit from earlier availability of blood test results, with many new inflammatory biomarkers showing rapid diagnosis of disease and prompt reflection of changes in patient status.

Notes

Conflicts of interest

The author has no conflicts of interest to declare.

Funding

The author received no financial support for this study.

Data availability

Data sharing is not applicable as no new data were created or analyzed in this study.

References

1. Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation. N Engl J Med 1999;340:448–54. 10.1056/nejm199902113400607. 9971870.
2. Del Giudice M, Gangestad SW. Rethinking IL-6 and CRP: why they are more than inflammatory biomarkers, and why it matters. Brain Behav Immun 2018;70:61–75. 10.1016/j.bbi.2018.02.013. 29499302.
3. Zhang Y, Zhang J, Sheng H, Li H, Wang R. Acute phase reactant serum amyloid A in inflammation and other diseases. Adv Clin Chem 2019;90:25–80. 10.1016/bs.acc.2019.01.002. 31122611.
4. Yamada T. Serum amyloid A (SAA): a concise review of biology, assay methods and clinical usefulness. Clin Chem Lab Med 1999;37:381–8. 10.1515/cclm.1999.063. 10369107.
5. Miwata H, Yamada T, Okada M, Kudo T, Kimura H, Morishima T. Serum amyloid A protein in acute viral infections. Arch Dis Child 1993;68:210–4. 10.1136/adc.68.2.210. 8481043.
6. Lozanski G, Jiang SL, Samols D, Kushner I. C-reactive protein and serum amyloid A mRNA stability following induction by cytokines. Cytokine 1996;8:534–40. 10.1006/cyto.1996.0072. 8891434.
7. Maury CP, Teppo A, Eklund B, Ahonen J. Serum amyloid A protein: a sensitive indicator of renal allograft rejection in humans. Transplantation 1983;36:501–4. 10.1097/00007890-198311000-00006. 6356513.
8. Abbas AA, Alghamdi A, Mezghani S, et al. Role of serum amyloid A as a biomarker for predicting the severity and prognosis of COVID-19. J Immunol Res 2022;2022:6336556. 10.1155/2022/6336556. 36465717.
9. Paraskevas T, Chourpiliadi C, Demiri S, et al. Presepsin in the diagnosis of sepsis. Clin Chim Acta 2023;550:117588. 10.1016/j.cca.2023.117588. 37813329.
10. Samsudin I, Vasikaran SD. Clinical utility and measurement of procalcitonin. Clin Biochem Rev 2017;38:59–68. 29332972.
11. Parli SE, Trivedi G, Woodworth A, Chang PK. Procalcitonin: usefulness in acute care surgery and trauma. Surg Infect (Larchmt) 2018;19:131–6. 10.1089/sur.2017.307. 29356604.
12. Zou Q, Wen W, Zhang XC. Presepsin as a novel sepsis biomarker. World J Emerg Med 2014;5:16–9. 10.5847/wjem.j.issn.1920-8642.2014.01.002. 25215141.
13. Turgman O, Schinkel M, Wiersinga WJ. Host response biomarkers for sepsis in the emergency room. Crit Care 2023;27:97. 10.1186/s13054-023-04367-z. 36941681.
14. Ehrchen JM, Sunderkotter C, Foell D, Vogl T, Roth J. The endogenous Toll-like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancer. J Leukoc Biol 2009;86:557–66. 10.1189/jlb.1008647. 19451397.
15. Ryckman C, Vandal K, Rouleau P, Talbot M, Tessier PA. Proinflammatory activities of S100: proteins S100A8, S100A9, and S100A8/A9 induce neutrophil chemotaxis and adhesion. J Immunol 2003;170:3233–42. 10.4049/jimmunol.170.6.3233. 12626582.
16. Guo D, Zhu Z, Xu T, et al. Plasma S100A8/A9 concentrations and clinical outcomes of ischemic stroke in 2 independent multicenter cohorts. Clin Chem 2020;66:706–17. 10.1093/clinchem/hvaa069. 32285094.
17. Mariani A, Marsili M, Nozzi M, Faricelli R, Chiarelli F, Breda L. Serum calprotectin: review of its usefulness and validity in paediatric rheumatic diseases. Clin Exp Rheumatol 2015;33:109–14. 25535818.
18. Yang Y, Shen L, Xu M, Chen L, Lu W, Wang W. Serum calprotectin as a prognostic predictor in severe traumatic brain injury. Clin Chim Acta 2021;520:101–7. 10.1016/j.cca.2021.06.009. 34102135.

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