Intraperitoneal insulin infusion (IPII) using implantable devices is used in treatment of hypoglycemia-prone diabetes. A 35-year-old type 1 diabetic woman had been treated with IPII for 3 years when a metabolic degradation occurred. A catheter tip obstruction wassuspected. An enhanced computed tomography (CT) scan was performed showing a subcapsular hypoattenuating region in the left lobe of the liver, consistent with focal steatosis. The catheter tip, surrounded by a thickening of tissue, stuck to the liver capsule; hepatic parenchyma was otherwise normal. IPII was stopped. Two months later, a CT scan showed the disappearance of the focal hypodensity.

A 30-year-old type 1 diabetic woman treated with IPII for 3 years saw her insulin needs increase; a catheter obstruction was suspected. A CT scan showed the same hepatic feature: hypodensity and patent catheter tip near the liver capsule. A coelioscopy confirmed that the catheter had not penetrated the capsule and allowed the removal of the tip from the liver vicinity. A histological analysis showed a macrovesicular steatosis (a single vacuole larger than the nucleus per cell). After 6 months, a CT scan showed a dramatic decrease of the steatosis. Liver enzymes levels were always normal in both patients.

A diffuse hepatic steatosis is frequent in insulin-resistant subjects (those with metabolic syndrome or type 2 diabetes), due to the portal compensatory hyperinsulinemia leading to a diffuse accumulation of triglycerides (1). A focal hepatic steatosis was observed surrounding the liver metastasis of insulinoma (2). During a peritoneal dialysis associated with intraperitoneal insulin delivery, a subcapsular steatosis, often mistaken for a hepatic tumor, disappearing after intraperitoneal insulin interruption (3), was observed. A focal macrosteatosis around functioning islets, disappearing when patients became C peptide negative, was described in the hepatic implantation of islets grafts (4), supporting the notion of a causative effect of high concentrations of insulin around the islets. In our C peptide-negative, type 1 diabetic patients, the macrosteatosis (a benign, reversible condition) only occurred near the catheter tip, where the insulin was infused at a concentration of 400 units/ml (sanofi-aventis). The global hepatic parenchyma was normal. Our observations, associated with the cases of insulinoma, peritoneal dialysis, and islet cells, add to the hypothesis that high local insulin levels may induce a focal reversible hepatic steatosis.

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