SN6 SHORT NOTE 5M

Write a short note on C-reactive protein and the acute phase reactants.

General Medicine · Final Professional

Definition

The acute phase response is a stereotyped systemic reaction to tissue injury, infection, infarction, trauma or immunological insult. Acute phase reactants are plasma proteins whose concentration changes by at least 25% during this response, driven mainly by IL-6, with IL-1 and TNF-α acting on hepatocytes.

Positive Acute Phase Reactants (rise)	Negative Acute Phase Reactants (fall)
C-reactive protein, serum amyloid A	Albumin
Fibrinogen, haptoglobin	Transferrin
Ferritin, caeruloplasmin	Prealbumin (transthyretin)
Complement C3, C4; alpha-1 antitrypsin	Retinol-binding protein

C-reactive Protein

CRP is a pentraxin synthesised by the liver under IL-6 stimulation. It is named for its ability to precipitate the C-polysaccharide of *Streptococcus pneumoniae*.

Functions: binds phosphocholine on damaged cells and microbial surfaces, activates the classical complement pathway, and opsonises for phagocytosis — a component of innate immunity.

Kinetics — the reason CRP is clinically useful:

Begins to rise within 6 hours of the insult.
Peaks at 48 hours.
Half-life of about 19 hours, constant regardless of the underlying disease, so the level directly reflects ongoing inflammation.
Falls rapidly once the stimulus is removed, making it an excellent monitor of treatment response.

Feature	CRP	ESR
Response to inflammation	Rises within 6 h	Rises after 24–48 h
Return to normal	Within days	Weeks
Affected by anaemia/age/pregnancy	No	Yes
Affected by immunoglobulins/paraproteins	No	Yes (raised in myeloma)
Measures	Protein concentration directly	Rouleaux formation indirectly

CLINICAL PEARL

CRP > 100 mg/L strongly suggests bacterial infection; viral infections usually produce only modest rises. SLE is the classic exception — disease flares raise the ESR but CRP often stays normal. A high CRP in a lupus patient should make you look for infection or serositis, not simply assume a flare.

Clinical Uses of CRP

Distinguishing bacterial from viral infection and supporting antibiotic decisions.
Monitoring response in pneumonia, sepsis, infective endocarditis, septic arthritis and inflammatory bowel disease.
Post-operative surveillance — a secondary rise after day 3 suggests a complication such as anastomotic leak.
Severity scoring — part of assessment in acute pancreatitis (CRP > 150 mg/L at 48 hours indicates severe disease).
hs-CRP (high-sensitivity CRP) for cardiovascular risk stratification: < 1 mg/L low risk, 1–3 mg/L intermediate, > 3 mg/L high risk.

Other Markers

Procalcitonin — rises more specifically in bacterial infection and sepsis, within 3–4 hours; used to guide starting and, importantly, stopping antibiotics.
Ferritin — an acute phase reactant, so a normal ferritin does not exclude iron deficiency in the presence of inflammation. Very high ferritin (> 10 000 ng/mL) suggests HLH, adult Still's disease or haemochromatosis.
Serum amyloid A — persistent elevation leads to secondary (AA) amyloidosis in chronic inflammatory disease.

Limitations

CRP is sensitive but not specific — it rises in infection, infarction, malignancy, trauma, surgery and autoimmune disease alike. It cannot localise disease, may be normal in early infection or in liver failure (impaired synthesis), and should always be interpreted with the clinical picture rather than in isolation.

NEEDS VERIFICATION

hs-CRP cardiovascular risk cut-offs and the pancreatitis CRP threshold — confirm against current cardiology and pancreatitis guidance.

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