This cross-sectional study aimed to investigate the association between non-alcoholic fatty liver disease (NAFLD) and atherosclerotic cardiovascular disease (ASCVD), a global public health concern. A total of 9044 out of 10,104 adults from Guangzhou, China, were included in the analysis. We utilized the fatty liver index (FLI), a noninvasive indicator of NAFLD, and the pooled cohort equations (PCE) based on the 2013 ACC/AHA Guideline, the China-PAR model, and the Framingham Risk Score to assess the 10-year ASCVD risk. The results demonstrated a significant association between FLI and 10-year ASCVD risk (p < 0.001). Adjusted for age, individuals with high FLI (≥60) had an odds ratio of 3.91 (95% CI 2.52–6.08) compared to those with low FLI (<30). These findings persisted after adjusting for metabolic indicators. Notably, this association was consistently observed across all three risk prediction models: the PCE model, the China-PAR model, and the Framingham Risk Score. In conclusion, our study provides evidence supporting FLI as a reliable indicator of increased 10-year ASCVD risk in Chinese NAFLD patients. FLI serves as a valuable marker for early detection of ASCVD, highlighting its potential in clinical practice for risk assessment and prevention strategies.

Background: Trisomy is a common chromosomal aberration, which usually presents with similar phenotypic abnormalities and developmental delay. Although defined as chromosome abnormalities with recognized symptoms including growth retardation, trisomy 9p and trisomy 14q have been rarely reported to occur at the same time. Case presentation: Here, we describe a 16-year-old adolescent female affected by developmental delay and mild intellectual disability. She was confirmed to have both partial trisomy 9p (p24.3-p23) and 14q11.2 microduplication by chromosome microarray analysis (CMA). It is speculated that the extra chromosome in the patient may be a derivative 14 chromosome inherited from the parent after 3:1 disjunction during meiosis. The extra 9p segment proves to be pathogenic while the duplicated 14q11.2 remains indefinite. Conclusions: Further studies are needed to assign the genes responsible for the developmental delay and craniofacial dysmorphisms and appoint dosage-sensitive genes of chromosome 9p.