Abstract
Only a few cases of type 3 hyperlipoproteinemia secondary to diabetes have been documented in Japan.
Three cases of diabetic coma which developed type 3 hyperlipoproteinemia are reported here.
Case 1: A 21-yr-old female was admitted due to diabetic ketoacidosis. On admission, her serum cholesterol and triglyceride levels were 332 mg/dl and 226 mg/dl, respectively. Agarose gel electrophoresis of serum lipoproteins showed a broad-β pattern. The VLDL (d<1.006) obtained by ultracentrifugation according to the method of Havel showed a floating-β band on agarosegel electrophoresis. VLDL-cholesterol was 57 mg/dl and the cholesterol/triglyceride ratio in the VLDL was 0.50. These data met the criteria for diagnosis of type 3 hyperlipoproteinemia. After treatment of the diabetic ketoacidosis, serum lipids and VLDL returned to normal levels and the VLDL showed normal pre-β mobility on electrophoresis. However, 2 weeks later, the VLDL showed a late-pre-β band, suggesting type 3 hyperlipoproteinemia. One month after the onset of diabetic ketoacidosis, hepatic triglyceride lipase activity was decreased to the level of 3.36 μEq FFA/ml/hr (normal: 9.20±3.70), while the extra-hepatic triglyceride lipase activity (4.33 μEq FFA/ml/hr) was slightly high (normal: 2.32±1.41).
Case 2: An 18-yr-old female was admitted due to diabetic ketoacidosis. On admission, her serum cholesterol and triglyceride levels were 367 mg/dl and 255 mg/dl, respectively. Agarose gel electrophoresis of serum lipoproteins showed a broad-β band which consisted of two bands migrating between β and pre-β bands. After treatment of the diabetic ketoacidosis, the electrophoretic pattern changed from type 3 to 2b and then to 2a.
Case 3: A 62-yr-old man was admitted due to hyperosmolar nonketotic diabetic coma. On admission, his serum cholesterol and triglyceride levels were 177 mg/dl and 406 mg/dl, respectively. Agarose gel electrophoresis of serum lipoproteins showed a broad-β band. After treatment of the diabetic coma, the electrophoretic pattern changed from type 3 to 4 and then to 2a. One month before the onset of diabetic coma, hepatic triglyceride lipase activity was decreased to the level of 3.23 μEq FFA/ml/hr, while extra-hepatic triglyceride lipase activity was normal (1.63μEq FFA/ml/hr), and the VLDL showed a late-pre-β band on electrophoresis.
These results indicate that deficiency of lipoprotein lipase activity, especially of hepatic triglyceride lipase activity, might play some role in the pathogenesis of type 3 hyperlipoproteinemia.
