NONALCOHOLIC FATTY LIVER DISEASE IN SYSTEMIC LUPUS ERYTHEMATOSUS: ASSOCIATIONS WITH CARDIOVASCULAR RISK FACTOR GOAL ACHIEVEMENT AND ATHEROSCLEROTIC PLAQUE PROGRESSION OVER THE PAST 10 YEARS
Bibliographic record
Abstract
PV057 / #707 Poster Topic: AS06 - Comorbidities Background/Purpose Nonalcoholic fatty liver disease (NAFLD) is a broad term including different stages of liver steatosis and fibrosis, and is the most common liver disease worldwide. It has been identified as an independent predictor of cardiovascular disease in the general population,[1] and has been associated with multiple cardiovascular risk factors (CVRFs) and atherosclerosis. However, evidence on the prevalence and predictors of NAFLD in Systemic Lupus Erythematosus (SLE) is limited. We compared the prevalence of NAFLD in patients with SLE vs healthy controls (HCs) and examined associations with sustained CVRF goal achievement, progression of atherosclerotic plaques over the past 10 years, and potential disease-related CVRFs. Methods Patients with SLE and age and sex-matched HCs who had a 10-year carotid and femoral ultrasound follow-up examination in our department were contacted to participate in the study. Liver transient elastography was performed to assess liver steatosis and fibrosis presence in 77 patients with SLE and 45 age- and sex-matched HCs. Liver steatosis was graded based on Control Attenuation Parameter (CAP) values, as follows: S0 (absent): 100–238 decibels/meter (dB/m), S1 (mild): 238–260 dB/m, S2 (moderate): 260–290 dB/m, and S3 (severe): > 290 dB/m. Liver steatosis presence was defined as grade ≥ S1. Liver stiffness was graded as F0–F1: 2–7 kilopascals (kPa), F2: 7–10 kPa, F3: 10–14 kPa, and F4: > 14 kPa. Liver fibrosis was defined as grade ≥ F2. Logistic regression analysis assessed potential predictors of NAFLD in patients with SLE, including alcohol consumption defined as drinks per week, Mediterranean Diet score (tool for the assessment of mediterranean diet adherence), CVRFs (blood pressure, total cholesterol, Low-Density Lipoprotein, High-Density Lipoprotein, triglycerides, smoking status, physical activity, BMI, waist circumference, family history of coronary artery disease), Systemic Coronary Risk Evaluation (SCORE) prediction score, sustained CVRF target attainment for blood pressure, lipids, smoking, physical activity, and body weight, as defined by the 2016 European Society of Cardiology guidelines, and atherosclerotic carotid and femoral plaque progression. Among disease-related potential predictors, we examined the persistent achievement of Lupus Low Disease Activity State (LLDAS) and Definition of Remission in SLE (DORIS) clinical remission, and persistent antiphospholipid antibody positivity during the 10-year follow-up period. Cardiovascular disease-related (antihypertensives, lipid-lowering agents and antiplatelets) and SLE-related medications (cumulative glucocorticoid exposure, consistent hydroxychloroquine use during the 10-year follow-up, immunosuppressives) were also assessed. Results Liver steatosis presence did not differ significantly between SLE and HC individuals (40,25% vs 44,44% respectively, p = 0.651). No liver fibrosis was detected in either group. In the SLE group, multivariate analysis showed that atherosclerotic femoral plaque progression over the past 10 years was associated with a 3.6-fold higher risk for NAFLD (Odds Ratio [OR]: 3.62, 95% CI 1.018-12.93, p = 0.021). NAFLD was also independently associated with persistent positivity of IgG anti-beta2 glycoprotein I antibodies (OR: 6.58, 95% CI 1.33-32.566, p = 0.021) during the 10-year follow-up. Each cardiovascular risk factor (including blood pressure, lipids, smoking, physical activity, and body weight) persistently on target during the 10-year follow-up period reduced NAFLD risk by 55% (OR: 0.45, 95% CI 0.231-0.889, p = 0.021). Conclusions Atherosclerotic femoral plaque progression and persistent IgG anti-beta2 glycoprotein I antibodies positivity were independent predictors of liver steatosis in patients with SLE, which can be drastically mitigated by sustained CVRF goal achievement. References: [1.] Stahl EP. J Am Coll Cardiol 2019;73:948-63.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.003 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".