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Is LDL-C worth drawing at baseline before starting cagrilintide?

Asked 14 Oct 2024Modified 19 months agoViewed 19k times
This question was marked as a duplicate of Is ALT worth drawing at baseline before starting mazdutide?Closed 21 Nov 2024. It remains here because the answers below are specific to how it was asked.
38

What I am working with: LDL-C · cagrilintide.

I would like to set this up properly once, rather than adjust it repeatedly.

My budget is real but not tight, and my tolerance for uncertainty is low.

How would you structure this, and what thresholds would you set in advance?

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askedbufferline4249k13814 Oct 2024
Does this hold at lower concentrations, or does adsorption dominate? – dermot_kiely 7 months ago
Worth flagging that this changed in 2025, so older answers on the site are out of date. – Dr_Priya_Raghunathan 5 months ago
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5 Answers

Accepted answer first, then by votes
54

Accepted answer

Stated carefully, start with the population. The inclusion criteria of the trial determine what its result can be extrapolated to, and the extrapolation people want is usually to a population the trial excluded.

The rodent thyroid C-cell findings that generated the labelled warning appear to be species-specific: rodent C-cells express GLP-1 receptors at high density, human C-cells at very low density, and human calcitonin data across large trial populations has not reproduced the signal. A family history of medullary thyroid carcinoma or MEN2 is nonetheless a genuine contraindication rather than a theoretical one.

Headline results, principal programmes

TrialAgentnDurationPrimary result
STEP 1Semaglutide 2.4 mg1,96168 wk−14.9 % vs −2.4 % weight
STEP 2Semaglutide 2.4 mg, T2DM1,21068 wk−9.6 % vs −3.4 % weight
SURMOUNT-1Tirzepatide 5/10/15 mg2,53972 wk−15 / −19 / −21 % weight
SURMOUNT-4Tirzepatide, withdrawal67088 wkContinued loss vs substantial regain
SELECTSemaglutide 2.4 mg17,604~40 moMACE HR 0.80 (0.72–0.90)
FLOWSemaglutide 1.0 mg, CKD3,533~3.4 yrRenal composite reduced; stopped early
SURMOUNT-OSATirzepatide, OSA46952 wkAHI reduced with and without PAP

Absolute risk reduction, worked: if the control-arm event rate is 8.0 per cent over the follow-up period and the hazard ratio is 0.80, the treated rate is approximately 6.4 per cent, the absolute risk reduction is 1.6 percentage points, and the number needed to treat is 1 ÷ 0.016 ≈ 63 over that period. A 20 per cent relative reduction and a number needed to treat of 63 are the same finding stated two ways, and only one of them sounds impressive.

FLOW tested a composite renal endpoint — kidney failure, sustained 50 per cent eGFR decline, or renal or cardiovascular death — in type 2 diabetes with chronic kidney disease, and was stopped early for efficacy[1].

One qualification: a trial that demonstrates an endpoint at a given dose has demonstrated it at that dose. Extrapolating the endpoint down the dose ladder is an assumption, not a finding.

If the trend across three draws is flat, the difference between draws one and two was noise. Most of what people react to is noise.

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answered · acceptedpetra_hovland42k3828 Nov 2024
Is there a reason to prefer the second method over the first, other than cost? – Dr_Elias_Weiss 4 months ago
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49

Worth being precise here: this is a question about what the trial was designed to answer, and the honest response is that it was not designed to answer this.

The early fall in estimated glomerular filtration rate on treatment is haemodynamic rather than structural. Reduced intraglomerular pressure lowers the filtration rate acutely and preserves the glomerulus chronically — the same pattern seen with renin-angiotensin blockade and with SGLT2 inhibition. A dip of a few millilitres per minute in the first weeks, followed by a shallower long-term slope, is the desired trajectory, not a warning sign.

On the detail: liver enzymes are a poor surrogate for hepatic histology in both directions: substantial steatohepatitis with normal transaminases is common, and modest enzyme elevation with minimal fibrosis is common. If the question is fibrosis, the answer comes from a non-invasive score such as FIB-4 or a stiffness measurement, not from ALT.

The caveat is the population. Trial participants were screened, monitored and supported; the effect size in an unmonitored setting is not the trial effect size, and it is not obvious in which direction the difference runs.

The papers are readable. Read the paper rather than the summary of the paper, especially where the summary is enthusiastic.

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SK
answereds_kalniete47k3817 Nov 2024
26

The hazard ratio is the relative effect. What changes decisions is the absolute effect, and converting between them requires the event rate in the control arm, which is usually in the same table and rarely in the abstract.

A fasting lipid panel drawn during rapid weight loss reads oddly for a mechanical reason: mobilised adipose tissue delivers free fatty acids to the liver, and hepatic triglyceride export rises. Triglycerides can transiently increase while the person is doing exactly the right thing. Draw the panel when weight has been stable for a few weeks if you want an interpretable number.

Put another way, a network meta-analysis can rank agents that were never compared directly, but only under a transitivity assumption — that the trials being linked are similar enough in population, duration and endpoint definition for the indirect comparison to hold. In this field that assumption is often visibly violated, which is why indirect rankings should be read as hypotheses.

SURMOUNT-4 randomised participants after an open-label lead-in to continued tirzepatide or placebo, and the withdrawal arm regained a substantial proportion of the lost weight over the following year[1].

None of this replaces a clinician who can see the whole picture, and the whole picture is usually where the answer is.

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answeredlipid_panel_q44k1389 Dec 2024
4This should probably be in the site help pages rather than buried in an answer. – lyoph_cake 9 months ago
3Good answer, but the confidence interval in the cited trial is wider than implied. – rota_site 8 months ago
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20

Read the estimand before the effect size. Almost every apparent contradiction between two published figures from the same trial resolves once you notice that one is a trial-product estimand and the other is a treatment-policy estimand.

HbA1c is a weighted average, not a flat one: roughly half the signal comes from the most recent month. That is why a value drawn six weeks after a change already reflects most of the effect, and why a value drawn during rapid haematological turnover reflects something other than glycaemia.

Read the confidence interval, read the estimand, and compute the absolute effect yourself. It takes two minutes and it changes how the result feels.

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answeredh_pergande86k25821 Dec 2024
5Worth flagging that this changed in 2025, so older answers on the site are out of date. – label_claim 4 months ago
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14

The confidence interval is the informative part. A point estimate with an interval spanning no effect is a different object from the same point estimate with a tight interval, and the abstract presents them identically.

ApoB and LDL-C disagree because they measure different things: LDL-C is the cholesterol mass carried in the LDL fraction, ApoB is a count of atherogenic particles. Small dense particles carry less cholesterol each, so a person with many small particles has a concordantly higher ApoB than their LDL-C suggests. When they disagree, ApoB is the better risk marker.

Convert everything to an absolute effect before you compare two interventions. Relative effects are not comparable across different baseline risks.

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answeredsian_llewellyn85k2481 Jan 2025

Your answer

Ask PeptideStack is a static archive. Posting is closed, but the norms are worth stating: answer the question that was asked, show your working, cite the trial or the certificate, and say plainly where the evidence runs out.

Not medical advice. Research-use-only compounds are not approved for human use.