What question did this study set out to answer?

To examine the association between Lipid Accumulation Product-defined hepatic steatosis and cardiovascular risk markers, as well as vascular progression, in patients with rheumatoid arthritis.

July 26, 2026Rheumatology InternationalOpen Access

LAP-defined hepatic steatosis and cardiometabolic risk in rheumatoid arthritis: a post-hoc analysis of the FRANCIS randomized trial

Q: What is the clinical evidence from this study?

Study design: RCT. Population: Rheumatoid arthritis without cardiovascular disease or type 2 diabetes (n=236). Intervention: Intensive treat-to-target cardiovascular risk management vs. Standard treatment. Primary outcome: Carotid intima-media thickness (cIMT) progression over 3 years in patients without LAP-defined steatosis (p=0.013).

Q: What does this research mean for the field?

Intensive cardiovascular risk management reduces carotid intima-media thickness progression over 3 years in rheumatoid arthritis patients without LAP-defined hepatic steatosis, but not in those with steatosis. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

Intensive CV risk management halves 3-year cIMT progression vs standard care in RA without steatosis.

P=0.013
n=236

Why the study?

Does intensive cardiovascular risk management reduce cIMT progression in rheumatoid arthritis patients with or without LAP-defined hepatic steatosis?

Population

236 patients with rheumatoid arthritis without cardiovascular disease or type 2 diabetes, mean age 54, 66%…

Comparison

Intensive treat-to-target cardiovascular risk… vs Standard treatment

Design

RCT, Randomized to receive either standard treatment or an intensive…

Follow-up

3 years

Authors

ASAlina SaidiErasmus MC BBBenjamin BurggraafErasmus MC ALA. J. van der LelyErasmus MC

Discussion

Member takes

Implication

Post-hoc analysis examines CV risk markers related to LAP-defined hepatic steatosis in RA patients, indicating implications for treatment.

Key Points

To examine the association between Lipid Accumulation Product-defined hepatic steatosis and cardiovascular risk markers, as well as vascular progression, in patients with rheumatoid arthritis.
Post-hoc analysis of the FRANCIS open-label randomized controlled trial involving 236 patients with rheumatoid arthritis without cardiovascular disease or type 2 diabetes followed for 3 years.
Hepatic steatosis was determined via sex-specific Lipid Accumulation Product (LAP) thresholds to rule in (n=34) or rule out (n=202) severe steatosis.
Carotid intima-media thickness (cIMT) was evaluated at baseline using multivariable linear regression and longitudinally across intensive versus standard cardiovascular risk management strategies.
LAP-defined steatosis trended toward higher baseline cIMT in crude regression (B = 0.036, 95% CI -0.003 to 0.076), but this was abolished after adjusting for age, sex, BMI, and systolic blood pressure (B = -0.016, 95% CI -0.050 to 0.019).
Over 3 years, intensive treatment significantly reduced cIMT progression versus standard care in patients without LAP-defined steatosis (ΔcIMT 0.03 ± 0.07 vs. 0.06 ± 0.12 mm; p = 0.013).
In patients with LAP-defined steatosis, intensive treatment showed no significant effect on cIMT progression compared to standard care (ΔcIMT 0.05 ± 0.05 vs. 0.04 ± 0.05 mm; p = 0.696; treatment-by-steatosis interaction p = 0.192).

Study Design

Type

RCT (n=236)

Blinding

Open-label

Randomization

Randomized to receive either standard treatment or an intensive treat-to-target treatment

Multicenter

Structured PICO

Does intensive cardiovascular risk management reduce cIMT progression in rheumatoid arthritis patients with or without LAP-defined hepatic steatosis?

Population

236 patients with rheumatoid arthritis, free of cardiovascular disease and type 2 diabetes, mean age 54 years, 66% female, followed for 3 years.

Intervention

Intensive treat-to-target cardiovascular risk management (protocol for anti-hypertensive treatment, lipid lowering drugs, metformin, and lifestyle advice)

Comparator

Standard treatment (evaluation and written advice to general physician based on CVD risk guidelines)

Outcome

Carotid intima-media thickness (cIMT) progression over 3 yearssurrogate

Main Result

Absolute Event Rate: 0.03% vs 0.06%

p-value: p=0.013

Limitations

Post-hoc exploratory analysis not powered for steatosis-defined subgroup comparisons
Hepatic steatosis assessed using LAP rather than imaging or histology
Residual confounding by RA-related disease characteristics and treatment exposure
Relatively small number of patients with LAP-defined steatosis
Residual

Cite This Study

Saidi et al. (2026) conducted an RCT in Rheumatoid arthritis without cardiovascular disease or type 2 diabetes (n=236). Intensive treat-to-target cardiovascular risk management vs. Standard treatment was evaluated on Carotid intima-media thickness (cIMT) progression over 3 years in patients without LAP-defined steatosis (p=0.013). Intensive cardiovascular risk management reduced carotid intima-media thickness progression over 3 years compared with standard treatment in rheumatoid arthritis patients without LAP-defined hepatic steatosis, but not in those with steatosis.

synapsesocial.com/papers/6a65a91fd3aea3239cd7918b https://doi.org/10.1007/s00296-026-06254-6

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Implication

Post-hoc analysis examines CV risk markers related to LAP-defined hepatic steatosis in RA patients, indicating implications for treatment.

LAP-defined hepatic steatosis and cardiometabolic risk in rheumatoid arthritis: a post-hoc analysis of the FRANCIS randomized trial

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Main Result

Limitations

Cite This Study

LAP-defined hepatic steatosis and cardiometabolic risk in rheumatoid arthritis: a post-hoc analysis of the FRANCIS randomized trial

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Main Result

Limitations

Cite This Study

Also Consider

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