Endocrine Abstracts

Introduction

Diabetes mellitus (DM) due to cirrhosis is described as hepatogenous diabetes (HD). Despite being frequently described in the literature, it is not recognized as an entity by the ADA/EASD.

Case report

Woman, 70 years old, previous history of autoimmune hepatitis with Child-Turcotte-Pugh A cirrhosis (CTP-A) since 2018, arterial hypertension and overweight (BMI 29.1 kg/m²). No personal or family history of DM. Medicated with bisoprolol 5 mg, candesartan 8 mg, furosemide 20 mg, spironolactone 25 mg. Normal glycemic profile until May 2019, when was admitted in the Emergency Department with polydipsia, polyuria and loss of 10 kg in 2 months. No infectious complications or medication changes were noticed. The patient was diagnosed with hyperosmolar syndrome, with glycemia of 629 mg/dl, ketonemia 0.2 mmol/l, without acidosis (pH 7.43), HbA1c 14.2%. No increase in inflammatory parameters, amylase, lipase and no renal dysfunction was detected. Liver profile was according to the patient’s baseline (AST 79 UI/L; ALT 43 UI/L; ALP 136 UI/L; total bilirubin 0.95 mg/dl). An optimal response to insulin therapy was observed, with discharge after 15 days. During hospitalization, an abdominal CT was performed, which excluded pancreatic lesions or masses. No changes in iron or cortisol metabolism were observed and anti-Langerhans islet antibodies, anti-insulin, anti-GAD studies were negative. During follow-up, after discharge, she maintained an excellent metabolic control (HbA1c 6.2%) medicated with metformin/empagliflozin 850/5 mg twice a day and 34 U/day of glargine insulin.

Discussion

The present case describes a newly diagnosed Diabetes in a patient with cirrhosis, suggesting a HD. The patient had no personal or family history of DM and did not show the progressive worsening usually observed in type 2 Diabetes. Infection, use of hyperglycemic medication, autoimmune and other causes for secondary DM were excluded. Although the prevalence of HD is related to the severity of cirrhosis, this prevalence may reach 20.5% in CTP-A, with an increase of 4.4% just 1 year after diagnosis. Liver dysfunction appears to cause hyperinsulinemia by decreasing insulin clearance and combined with an increase in inflammatory mediators, causes tissues’ insulin resistance and pancreatic islets β cells’ toxicity. These changes lead to a deterioration in glucose metabolism that follows the worsening of cirrhosis. Treatment can be challenging in advanced stages of cirrhosis, due to dysfunctional liver metabolism, which can cause greater susceptibility to hypoglycemia and worse metabolic control.