fibrosis

Type 2 diabetes mellitus is an important trigger of fibrosis progression. On the other hand, renin-angiotensin-aldosterone system inhibitors may be considered as protective factors to slow fibrosis progression.

 

Obesity and diabetes are important risk factors that also increase the odds of developing liver diseases such as nonalcoholic fatty liver disease (NAFLD). The higher the prevalence of obesity and diabetes, the higher the probability of NAFLD, which in turn, increases the risk for other hepatic disturbances (eg. hepatocellular carcinoma and end-stage liver disease). The progression of fibrosis (the thickening and scarring of connective tissue) is the main determinant of liver disturbances. Nonalcoholic steatohepatitis (NASH), hyperglycemia, weight gain, type 2 diabetes mellitus, and hypertension have been associated with faster fibrosis progression (FPR), while renin-angiotensin-aldosterone system (RAAS) inhibitors may have a protective effect.




A study carried out by Italian researchers and published in the scientific journal PLOS ONE analyzed the determinants of FPR in people living with NAFLD. One-hundred and eighteen people clinically diagnosed with NAFLD were followed up for three years. Decompensated patients and those who use steatosis-inducing drugs were excluded. NASH was defined as the presence of steatosis with both lobular necroinflammation and ballooning. The NAFLD activity score (the sum of the separate scores for steatosis, hepatocellular ballooning, and lobular inflammation) was used to determine disease and fibrosis progression. The AST to platelet ratio index (APRI), which determines the likelihood of hepatic fibrosis and cirrhosis, was also calculated. The use of RAAS inhibitors was controlled.

Fibrosis progression was not necessarily dependent on the presence of NASH at the baseline. However, it was associated with the APRI score, type 2 diabetes mellitus (T2DM), and the length of the observation (i.e., the longer the follow-up, the higher the probability of fibrosis progression). RAAS inhibitors caused slower FPR, and lowered the likelihood of fibrosis progression, suggesting a protective effect. Some limitations are the sample size, demographics characteristics, and other clinical factors related to the management of diabetes and research design.

The study demonstrated that the fibrosis progression is not dependent on the presence of NASH. However, T2DM is an important trigger of fibrosis progression regardless of hepatic inflammation, and most importantly, RAAS inhibitors may be considered as an important strategy to slow the fibrosis progression by treating hypertension or kidney disease in T2DM patients in the presence of NAFLD.

 

Written By: Vagner Raso




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