Author information

¹SC- Medicina-Indirizzo Metabolico, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico di Milano, Milan, Italy; Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy. Electronic address: rosa.lombardi@unimi.it.

²Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, University and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, Italy.

³SC- Medicina-Indirizzo Metabolico, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico di Milano, Milan, Italy; Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.

⁴UO di Medicina, Azienda Ospedaliera "Card. G. Panico" di Tricase, Italy.

⁵Pediatric Diabetes and Metabolic Disorders Unit, Department of Surgical Sciences, Dentistry, and Pediatrics, and Gynaecology, University Hospital of Verona, Verona, Italy.

⁶Gastroenterology Unit, Department of Medical Specialities, University Hospital of Modena, University of Modena & Reggio Emilia, Modena, Italy.

⁷Gastroenterology Unit, University and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, Italy.

⁸Centro C.U.R.E, Dept. of Medical and Surgical Sciences, University of Foggia, Italy.

⁹Department of Medical Science, Endocrinology and Diabetes Unit, Ca' Granda IRCCS Foundation, Policlinico Hospital, University of Milan Italy.

¹⁰SC- Medicina-Indirizzo Metabolico, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico di Milano, Milan, Italy.

¹¹Department of Medicine, University of Verona, Verona, Italy; Metabolic Diseases Research Unit, IRCCS Sacro Cuore Don Calabria Hospital, Negrar di Valpolicella, Italy.

¹²Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.

Abstract

Background and aims: Patients with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) are at high risk of hepatic fibrosis. To prospectively evaluate changes in fibrosis in diabetic patients with NAFLD, predisposing factors and sodium glucose cotransporter 2 inhibitors (SGLT2i) influence.

Methods: 237 T2DM outpatients (mean age 67 ± 9 years, 54% male) were enrolled and re-evaluated after 52 ± 10 months. At baseline and follow-up NAFLD and liver fibrosis (LSM) were detected by ultrasonography and Fibroscan®.

Results: During follow-up an increase in LSM (6.0 ± 2.8 vs 5.8 ± 2.7 kPa, p = 0.02) and in the prescription of SGLT2i (20% vs 6%, p<0.001) was registered, despite stability of diabetic control. LSM worsened in 133(56%) subjects, 92 (39%) with worsening >10% from baseline. Patients with worsening versus non worsening of LSM had higher prevalence of increase in BMI during follow-up (45% vs 32%, p = 0.06) and lower SGLT2i prescription (15% vs 27%, p = 0.034). In multivariate analysis use of SGLT2-inhibitors at follow-up reduced the risk of LSM worsening (HR 0.34, 95% CI 0.13-0.88), even when considered>10% from baseline.

Conclusions: A high prevalence of fibrosis progression was observed in diabetic subjects with NAFLD over a nearly 5-years follow up and SGLT2-inhibitors seem to reduce the risk of worsening of liver stiffness.