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C-Reactive Protein (CRP)

CRP is a liver-synthesized positive acute-phase protein. It can support assessment of inflammation, but does not identify its source or diagnose malnutrition. High-sensitivity CRP has a separate role in longer-term cardiovascular risk assessment.[1][2]

Biology and Assays​

CRP binds phosphocholine on microbial or damaged-cell surfaces and participates in complement and innate immune responses. IL-6 is a major driver of hepatic synthesis. Concentrations rise over hours after an inflammatory stimulus, commonly peak around two days, and decline as the stimulus resolves; the plasma half-life is approximately 19 hours.[1][3][4]

Standard CRP and hsCRP measure the same protein. High-sensitivity assays quantify lower concentrations more precisely; detection limits depend on the laboratory platform. Neither an absolute concentration nor a simple range reliably separates bacterial infection from viral disease or sterile postoperative inflammation.[1][5]

For cardiovascular interpretation, hsCRP ≥ 2 mg/L is a risk-enhancing signal. A result obtained during infection, trauma or recovery from surgery should not be treated as the patient's stable cardiovascular baseline; repeat after the acute process resolves when clinically appropriate.[2]

Postoperative Inflammation and Infection​

CRP can help follow a clinical trajectory, but surgery itself raises it. In 51 elective hip-arthroplasty patients, CRP peaked around postoperative day 3. The size and timing of that response should not be applied as a universal normal curve after every pelvic or GU operation.[6]

A persistently elevated or rising value may justify reassessment alongside symptoms, examination, vital signs, wound or drain findings and other tests. It does not mandate CT on a particular postoperative day, and a low value cannot safely exclude an early serious complication.[1][7]

SCCM/IDSA 2023 guidance for new ICU fever permits CRP or procalcitonin as an adjunct when bacterial infection probability is low to intermediate and no focus is apparent, with very low-certainty evidence. In a high-probability presentation, neither should be used to rule out bacterial infection. The guideline excludes severely immunocompromised patients; it does not establish that procalcitonin is unaffected by immunodeficiency.[7]

Nutrition and Visceral Proteins​

Inflammation can raise CRP while lowering albumin, prealbumin and transferrin. This explains part of their prognostic association, but measuring them together does not determine whether nutritional depletion is present.[8]

PatternInterpretation
Low albumin, high CRPInflammation may contribute; assess nutrition and other causes of low albumin independently
Low albumin, normal CRPConsider synthesis, losses, fluid balance and nutrition; this does not prove pure nutritional depletion
Normal albumin, high CRPInflammation may be present; normal albumin does not establish preserved nutritional stores
Both normalNeither result excludes malnutrition or every inflammatory condition

The 2025 GLIM update permits clinical disease burden to establish the inflammatory etiologic criterion. CRP can clarify uncertainty but is not mandatory. A diagnosis still needs an appropriate phenotypic criterion, such as weight loss, low BMI or reduced muscle mass. Albumin and prealbumin are not GLIM diagnostic criteria.[9]

Cardiovascular Prevention​

The 2025 ACC scientific statement supports broad hsCRP screening in primary and secondary cardiovascular prevention.[2] This concerns long-term prevention, rather than proof that adding hsCRP to every preoperative panel improves surgical outcomes or provides a new surgical-clearance threshold.

In JUPITER, 17,802 participants without known cardiovascular disease, with LDL < 130 mg/dL and hsCRP ≥ 2 mg/L, were randomized to rosuvastatin or placebo. The primary composite cardiovascular endpoint was reduced by 44% (HR 0.56, 95% CI 0.46–0.69). The often-quoted 47% reduction concerned the narrower composite of myocardial infarction, stroke or cardiovascular death.[10] The trial did not test perioperative hsCRP screening.

An observational UK Biobank analysis of 448,653 participants without baseline ASCVD found higher subsequent cardiovascular risk with hsCRP > 3 versus < 1 mg/L. This supports prognostic relevance but does not establish that CRP itself is a treatment target in reconstructive surgery.[11]

CRP and Procalcitonin: Practical Differences​

FeatureCRPProcalcitonin
Source during systemic inflammationPredominantly hepatic synthesisExtra-thyroid tissues contribute substantially during systemic bacterial inflammation; thyroid cells alone do not explain the septic response
InterpretationNonspecific inflammatory markerMay support bacterial-infection assessment but is not an independent diagnostic or exclusion test
ConfoundingTissue injury, inflammatory disease, liver dysfunction and timingTissue injury, kidney dysfunction, timing and other noninfectious causes
Cardiovascular usehsCRP has an established risk-assessment roleNo corresponding routine prevention role

Interpret either marker within its clinical setting; do not assume fixed assay turnaround times, universal peaks or immunity to confounding.[1][7][6]

Application to Reconstruction​

  • Use CRP selectively to help follow an inflammatory or postoperative problem; investigate the suspected complication rather than treating the number.
  • Assess malnutrition independently. Routine paired CRP / prealbumin testing is not a validated method to titrate nutrition or schedule flap surgery.
  • Keep cardiovascular prevention assessment separate from immediate surgical evaluation.
  • Remember that an early infection or impaired hepatic response may produce a deceptively low result.[1][7][8]

See Also​

References​

1. Lelubre C, Anselin S, Zouaoui Boudjeltia K, Biston P, Piagnerelli M. "Interpretation of C-Reactive Protein Concentrations in Critically Ill Patients." BioMed Research International. 2013;2013:124021. doi:10.1155/2013/124021

2. Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. "Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement." Journal of the American College of Cardiology. 2025. doi:10.1016/j.jacc.2025.08.047

3. Olson ME, Hornick MG, Stefanski A, et al. "A Biofunctional Review of C-Reactive Protein (CRP) as a Mediator of Inflammatory and Immune Responses." Frontiers in Immunology. 2023;14:1264383. doi:10.3389/fimmu.2023.1264383

4. Zhou HH, Tang YL, Xu TH, Cheng B. "C-Reactive Protein: Structure, Function, Regulation, and Role in Clinical Diseases." Frontiers in Immunology. 2024;15:1425168. doi:10.3389/fimmu.2024.1425168

5. Ridker PM. "A Test in Context: High-Sensitivity C-Reactive Protein." Journal of the American College of Cardiology. 2016;67(6):712–723. doi:10.1016/j.jacc.2015.11.037

6. Battistelli S, Fortina M, Carta S, et al. "Serum C-Reactive Protein and Procalcitonin Kinetics in Patients Undergoing Elective Total Hip Arthroplasty." BioMed Research International. 2014;2014:565080. doi:10.1155/2014/565080

7. O'Grady NP, Alexander E, Alhazzani W, et al. "Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU." Critical Care Medicine. 2023;51(11):1570–1586. doi:10.1097/CCM.0000000000006022

8. Evans DC, Corkins MR, Malone A, et al. "The Use of Visceral Proteins as Nutrition Markers: An ASPEN Position Paper." Nutrition in Clinical Practice. 2021;36(1):22–28. doi:10.1002/ncp.10588

9. Jensen GL, Cederholm T, Correia MITD, et al. GLIM consensus approach to diagnosis of malnutrition: A 5-year update. JPEN J Parenter Enteral Nutr. 2025. doi:10.1002/jpen.2756.

10. Ridker PM, Danielson E, Fonseca FAH, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359:2195–2207. doi:10.1056/NEJMoa0807646.

11. Kurt B, Reugels M, Schneider KM, et al. "C-Reactive Protein and Cardiovascular Risk in the General Population." European Heart Journal. 2025;ehaf937. doi:10.1093/eurheartj/ehaf937