Prevalence of elevated liver enzymes in Type 2 diabetes mellitus and its association with the metabolic syndrome.

The occurrence of liver disease and raised liver enzymes is common in Type 2 diabetes, and may be multifactorial in origin. Very few studies are available on the exact prevalence of the phenomenon, however. We carried out an observational point-prevalence study of elevated liver enzymes in eight hospital-based Italian diabetes units. Data of 9621 consecutive Type 2 diabetes patients (males, 52.4%; median age, 65 yr) were analyzed, and alanine and aspartate aminotransferase (ALT, AST) and gamma-glutamyltransferase (GGT) levels were related to body mass index (BMI), metabolic control and the presence of the metabolic syndrome. ALT, AST, and GGT levels exceeding the upper limit of normal were present in 16.0%, 8.8%, 23.1%, respectively, the prevalence being higher in males, increasing with obesity class and poor metabolic control, and decreasing with age. Elevated enzymes were systematically associated with most parameters of the metabolic syndrome. After correction for age, gender, BMI, and differences across centers, elevated triglyceride levels/fibrate treatment [odds ratio (OR), 1.57; 95% confidence interval (CI), 1.34- 1.84] and an enlarged waist circumference (OR, 1.47; 95% CI, 1.17-1.85) were the only parameters independently associated with high ALT. In a separate analysis, the presence of metabolic syndrome (Adult Treatment Panel III criteria) was highly predictive of raised liver enzymes. After exclusion of hepatitis B and C positive cases, tested in 2 centers, the prevalence of raised enzymes decreased by approximately 4%, but the association with the metabolic syndrome did not change significantly. In conclusion, the high prevalence of elevated liver enzymes in Type 2 diabetes is in keeping with the well-demonstrated risk of progressive liver disease. A large amount of diabetes patients may require a thorough clinical, laboratory and histological investigation.

Hyperinsulinism reduction associated with icodextrin treatment in continuous ambulatory peritoneal dialysis patients.

Glucose absorption from peritoneal dialysis solutions causes a chronic stimulation of insulin secretion, which leads to hyperinsulinism. The use of solutions without glucose should correct this metabolic derangement together with the associated cardiovascular risk. To verify this hypothesis, we studied the entire non diabetic continuous ambulatory peritoneal dialysis (CAPD) population of our center: 27 patients with a mean age of 62 +/- 15 years, and a median 17 months on treatment. Morning fasting serum insulin was 32.8 +/- 9.3 microU/mL; glucose, 104.4 +/- 21.8 mg/dL; triglycerides, 162.4 +/- 125.7 mg/dL; cholesterol, 221.9 +/- 54.7 mg/dL; intact parathyroid hormone (iPTH), 212 +/- 189 pg/mL; fibrinogen, 519 +/- 112 mg/dL; body mass index, 24.1 +/- 4.1; and daily erythropoietin subcutaneous therapy dose, 17 +/- 6 U/kg. Insulin sensitivity, measured as ISI-HOMA (insulin sensitivity index, derived from the homeostasis model assessment) was 2.4 +/- 0.7. Daily glucose load, calculated from dialytic schedules, was 135 +/- 38 g. Of the 27 patients, 12 were treated with standard glucose solutions during the day and with one icodextrin dwell during the night for a median of 9 months (range: 1-28). The remaining 15 patients were treated with standard glucose solutions. The icodextrin group showed significantly lower serum insulin levels (28.6 +/- 6.0 microU/mL vs 36.1 +/- 10.2 microU/mL, p = 0.021) and significantly higher ISI-HOMA values (2.7 +/- 0.5 vs 2.2 +/- 0.7, p = 0.041) than the control group. The two groups showed no significant differences for glucose, triglycerides, cholesterol, iPTH, fibrinogen, body mass index, or erythropoietin therapy dose. Daily glucose load was lower in the icodextrin group, but without reaching statistical significance (128 +/- 31 g vs 142 +/- 43 g). This study shows, in a preliminary way, that the chronic use of icodextrin in the long nighttime dwell can reduce serum insulin levels and increase insulin sensitivity in CAPD patients.