Inflammation markers: hs-CRP

The same protein, measured more carefully

C‑reactive protein is made by the liver and rises when there is inflammation anywhere in the body. The ordinary CRP test was built to detect the large rises of infection — values in the tens or hundreds.

hs‑CRP is the same protein with a more sensitive assay, able to resolve the small differences within the range that used to read as simply "normal". The "hs" is high sensitivity. It is not a different molecule and not a different disease.

That sensitivity is the whole point, because the association with cardiovascular risk lives in those small differences.

What the numbers are taken to mean

The commonly cited stratification, from American Heart Association and CDC guidance, puts low risk below 1 mg/L, average between 1 and 3, and high above 3. Values above 10 mg/L are generally taken to indicate an active inflammatory process or infection rather than background cardiovascular risk, and the usual advice is to find the cause and retest later rather than interpret it as a risk score.

Those bands are population statistics. They describe how groups of people fare, which is not the same as telling an individual what will happen to them.

The reason it is so easily wasted

This is the practical heart of it. hs‑CRP responds to any inflammation at all, and it cannot tell you where that inflammation came from. A head cold, a dental abscess, a flare of arthritis, a recent injury, a hard marathon, a gum infection you have not noticed — any of these will move it, often by more than the cardiovascular signal you were trying to read.

So a raised hs‑CRP in someone who has been unwell in the past fortnight is uninterpretable. It needs repeating when they are well, and ideally twice, a couple of weeks apart, with the lower value used.

It is also raised by obesity, smoking, oral oestrogen and pregnancy, and lowered by statins and by some anti‑inflammatory medicines.

Where the evidence is strong, and where it thins

As a marker, hs‑CRP is consistently associated with cardiovascular events, and the JUPITER trial showed that people with normal LDL but raised hs‑CRP benefited from a statin — which is the strongest clinical use the test has.

What remains contested is whether CRP is a cause of cardiovascular disease or a bystander marking a process driven by something else. Genetic studies have generally not supported a causal role, and lowering CRP for its own sake has not been shown to help.

So it is reasonably read as a thermometer rather than a thing to be treated.

Why it is not in our baseline

It was in the first draft of our panel at ₡18,500 and came out, and the reason was the test we apply to every line: would the result change what we prescribe?

For most people arriving at a metabolic clinic, it would not. The decisions in front of us are driven by glucose, HbA1c, lipids, liver, kidney and thyroid, and an hs‑CRP rarely moves any of them.

Where it does earn its place is the genuinely borderline cardiovascular case — intermediate risk, where a clinician is weighing whether to start a statin and wants one more piece of evidence. That is an addition made for a reason, not a line on a standing panel.

If you have it measured

1. Be well. No infection, no injury, no dental problem, nothing acute in the past two weeks.
2. Not after heavy exercise.
3. Twice, a fortnight apart, and use the lower value.
4. Same laboratory, as with everything you intend to track.
5. Above 10 mg/L, look for a cause rather than reading it as risk.

The boundary

hs‑CRP is one input into an estimate of risk, and risk is not a diagnosis. What yours means depends on your lipids, your blood pressure, your age and your history — and whether it should change anything is a judgement for a physician who has all of them.