RESUMO
BACKGROUND AND OBJECTIVES: It is well known that lipid abnormalities exist in the context of non-alcoholic fatty liver disease (NAFLD). The association between lipoprotein(a) [Lp(a)] levels and NAFLD is poorly understood. The main objective of the present study was to assess the association between Lp(a) levels and NAFLD. METHODS: This systematic review was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (PROSPERO CRD42023392526). A literature search was performed to detect studies that evaluated the association between Lp(a) levels, NAFLD and steatohepatitis (NASH). RESULTS: Ten observational studies, including 40,045 patients, were identified and considered eligible for this systematic review. There were 9266 subjects in the NAFLD groups and 30,779 individuals in the respective control groups. Five studies evaluated patients with NAFLD (hepatic steatosis was associated with lower Lp(a) levels in four studies, while the remaining showed opposite results). Two studies evaluating NASH patients showed that Lp(a) levels were not different compared to controls. However, the increment of Lp(a) levels was correlated with liver fibrosis in one of them. In addition, one study analyzed simultaneously patients with NAFLD and NASH, showing a neutral result in NAFLD patients and a positive relationship in NASH patients. Two studies that included patients with the new definition of metabolic-associated fatty liver disease (MAFLD) also showed neutral results. CONCLUSION: Although there could be an association between Lp(a) levels and hepatic steatosis, the results of the studies published to date are contradictory and not definitive.
RESUMO
Accumulation of epicardial adipose tissue (EAT) and Subclinical hypothyroidism (SH) are associated with increased cardio-metabolic risk. The objective of this study was to quantitatively compare EAT thickening between patients with SH and healthy controls. Therefore, after searching the PubMed/MEDLINE, Embase, Science Direct, Scopus, Google Scholar, and Cochrane databases; we analyzed a group of observational studies who compare the EAT changes between SH vs control groups. A total of 9 studies were included in the final analysis, for a total of 424 patients with SH and 330 controls. Random or fixed effects models were used. Pooled analysis revealed that HS increased EAT (MD: 1.0 mm [0.40; 1.50]; P < 0.01). This meta-analysis suggests that the amount of EAT is significantly increased in SH patients. EAT might be a marker of cardiovascular risk in patients with SH.