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Reversible Focal Hepatic Steatosis in Type 1 Diabetic Patients Treated With Intraperitoneal Insulin Implantable Pump Therapy

  1. Laurent Meyer, MD12,
  2. Jeremy Jeantroux, MD34,
  3. Jean Pierre Riveline, MD5,
  4. François Moreau, MD12,
  5. Sophie Boivin, MD12,
  6. Thomas Moser, MD34,
  7. Michel Pinget, MD12 and
  8. Nathalie Jeandidier, MD, PHD12
  1. 1Centre Hospitalier Régional Universitaire de Strasbourg, Service d'Endocrinologie, Diabète et Maladies Métaboliques, Hôpital Civil, Strasbourg, France
  2. 2Université Louis Pasteur, Faculté de Médecine, Strasbourg, France
  3. 3Centre Hospitalier Régional Universitaire de Strasbourg, Service de Radiologie Hôpital Civil, Strasbourg, France
  4. 4Université Louis Pasteur, Faculté de Médecine, Strasbourg, France
  5. 5Department of Diabetology, Hospital of Corbeil Essonnes, Corbeil Essonnes, France
  1. Corresponding author: Laurent Meyer, MD, Service d’Endocrinologie, Diabète et Maladies Métaboliques, Pavillon Leriche, 1 Place de l'Hôpital, 67000, Strasbourg, France. E-mail: laurent.meyer{at}chru-strasbourg.fr

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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