Hepatic Subcapsular Steatosis in a Diabetic CAPD Patient Receiving Intraperitoneal Insulin
A 46-year-old woman presented with general weakness that had lasted for several weeks. She was diagnosed with type 2 diabetes mellitus (DM) 15 years ago and began continuous ambulatory peritoneal dialysis (CAPD) three years ago. An abdominal sonography obtained before CAPD began revealed a normal liver. The patient received CAPD with four daily exchanges of 2 L each time and switched to three exchanges with 2.5% glucose and one with 4.25% glucose solution; this was required because the ultrafiltration capacity was not sufficient and she became volume overloaded. A peritoneal equilibrium test was not performed. The patient had insulin administered subcutaneously when she started the CAPD but changed to intraperitoneal insulin treatment combined with subcutaneous treatment two years later. Hyperlipidemia treated with simvastatin and fenofibrate were started one year previously but stopped three months later because the drugs caused rhabdomyolysis. Lipid profiles began to worsen and she had to resume with atovastatin but did not develop rhabdomyolysis. Plasma glucose was poorly controlled despite the combination therapy of subcutaneous and intraperitoneal insulin injections. Insulin doses increased from 102 units daily up to 110 units daily during the previous month. The patient was 158 cm tall and weighed 58 kg. When she visited our clinic, her body mass index was 23 kg/m2. Vital signs were a blood pressure of 130/80 mmHg, pulse rate 68/min, respiratory rate 20/min, and body temperature 36.6℃. Her abdomen was soft and mildly distended. The initial complete blood count was white blood cells 8,000/mm3 (neutrophils 70.7%, lymphocytes 18.5%, eosinophils 3.2%), hemoglobin 11.5 g/dL, hematocrit 33.3%, and platelet 288,000/mm3. Her blood chemistry values were, fasting glucose 293 mg/dL, blood urea nitrogen 46.6 mg/dL, creatinine 10.3 mg/dL, sodium 134 mEq/L, potassium 4.4 mEq/L, chloride 90 mEq/L, AST 119 IU/L, ALT 192 IU/L, alkaline phosphatase 850 IU/L, amylase 110 U/L, total protein 6.8 g/dL, albumin 4.0 g/dL, calcium 11.1 mg/dL, phosphorus 6.2 mg/dL, CPK 43 IU/L, LDH 468 IU/L, total cholesterol 450 mg/dL, and triglyceride 1,096 mg/dL. Hepatitis B antigen and hepatitis C antibody were negative. ANCA, anti-liver kidney microsome antibody, and anti-smooth muscle antibody were all negative. Sonography of the abdomen revealed an increased echogenicity of the liver. A CT scan of the abdomen showed extensive low attenuated lesions in the liver capsule, the parenchyma of the left hepatic lobe and a small nodular lesion in the capsular area of the right lobe of the liver (). The MRI findings were consistent with the CT findings. The hepatic subcapsular area showed bright signals in the on-phase T1weighted images, but a marked signal decrease in the off-phase T1-weighed sequences; these findings suggested that the subcapsular area was composed of fat tissue. Hepatic subcapsular steatosis due to high dose intraperitoneal insulin was suspected; the patient was changed from CAPD to HD. Insulin was given only subcutaneously after changing to HD. A CT scan performed two months after starting HD showed complete resolution of the hepatic subcapsular steatosis (). Laboratory values were also improved: AST 34 IU/L, ALT 81 IU/L, alkaline phosphatase 733 IU/L, total cholesterol 259 mg/dL, and triglyceride 177 mg/dL. The blood sugar has been well controlled insulin therapy could be discontinued. Six months after changing from CAPD to HD, oral hypoglycemic agents have been sufficient to maintain adequate plasma glucose levels. Furthermore, liver enzyme levels are within normal range; the total cholesterol level was 206 mg/dL, and triglyceride level 157 mg/dL without requirement for lipid-lowering agents.