Published online Jun 21, 2020. doi: 10.3748/wjg.v26.i23.3249
Peer-review started: January 31, 2020
First decision: February 27, 2020
Revised: June 6, 2020
Accepted: June 10, 2020
Article in press: June 10, 2020
Published online: June 21, 2020
Processing time: 142 Days and 10.9 Hours
The prevalence of nonalcoholic fatty liver disease (NAFLD) is estimated around 25% of the global population and is expected to increase further in the coming years. Type-2 diabetes mellitus is a major risk factor for NAFLD with significant portion of diabetic patients develop progressive liver disease and a proportion of these patients also develop advanced fibrosis (AF). NAFLD pose significant health care burden and is associated with significant mortality and morbidity.
Patients with diabetes are commonly on multiple medication regimen, of which, some have a positive impact on slowing the progression of NAFLD to AF. For instance, HMG-CoA reductase inhibitors (statins) and Angiotensin converting enzyme inhibitors have been shown previously to be associated with reduction in AF in viral hepatitis patients. There is a paucity of data on the association of these medications on the progression of liver fibrosis in NAFLD patients.
We aimed to understand the association of the different pharmacologic modalities used in the treatment of diabetes mellitus on the progression of liver fibrosis in NAFLD patients with type-2 diabetes.
We identified all adult patients with type-2 diabetes mellitus who underwent liver biopsy for suspected NAFLD at the Cleveland Clinic between January 1, 2000 to December 31, 2015. We retrospectively reviewed a cohort of 1183 patients with type-2 diabetes and biopsy proven NAFLD. We compared demographics, clinical characteristics, and differences in pattern of medication use in patients who had biopsy-proven NAFLD with and without advance fibrosis. A univariate and multivariate analysis was performed to assess the association of different classes of medication with and without the presence of AF.
We found that the patients who were receiving Metformin, Liraglutide, Lisinopril, Hydrochlorothiazide, Atorvastatin and Simvastatin were less likely to have AF on biopsy, while patients who were receiving furosemide and spironolactone were more likely to have AF when they underwent liver biopsy. Diabetic patients with chronic kidney disease were more likely to have AF on liver biopsy.
Our study highlights the protective role of some of the commonly used medications in the treatment of type-2 diabetes mellitus. We propose that Metformin, Liraglutide, Lisinopril, Hydrochlorothiazide, Atorvastatin and Simvastatin may have a beneficial role in slowing down the progression of NAFLD.
Although it is possible that some unknown confounding factors could have impacted our findings, this study lays a solid groundwork for future prospective studies to further investigate the protective role of these medications on the progression of liver fibrosis in diabetic patients with NAFLD.