ABSTRACT
AIM: To study heterogenic forms of LDLP and LP(a) in blood serum of patients with cholelithiasis (CL) and gallbladder cholesterosis (GBC). MATERIAL AND METHODS: Native gradient (3-12%) electrophoresis in polyacrylamide gel, rocket immunoelectrophoresis with antibodies to apo(a) were made in 20 patients with CL and 20 with GBC, 13 controls without gastrointestinal disease. Correlation of retardation factor (Rf) of LDLP and LP(a) with blood lipids, cholesterol (C) and triglycerides (TG) levels, body mass index (BMI) and age was studied. CL and GBC risk factors were analysed basing on a retrospective assessment in random representative samples of patients (100 CL and 100 GBC patients). RESULTS: There was a shift of the main peak in LDLP spectrum in the direction of smaller particles in GBC (Rf = 0.171 +/- 0.003) which was significant in comparison with CL group (Rf = 0.146 +/- 0.004, p < 0.001) and control (Rf = 0.114 +/- 0.013, p < 0.05). The analysis of LDLP Rf distribution in patients with different C levels has shown that LDLP small particles can occur in a normal C level: 75% in GBC and 50% in CL groups. Prevalence of small dense LDLP was recorded in both groups (87.5% cases) in hypercholesterolemia. Compared to control, LP(a) concentration was significantly elevated both in GBC (23.7 +/- 4.9 mg/dl) and CL (15.7 +/- 4.4 mg/dl) patients (control--7.5 +/- 1.4 mg/dl, p < 0.01), p > 0.5 in comparison between the groups. The correlation analysis found no correlations between LP9(a), other lipids, BMI and age in both study groups while Rf of LDLP correlated with C and TG levels (r = 0.596 and r = 0.226, respectively, p < 0.05), age and BMI (r = 0. 533 and r = 0.363, respectively, p < 0.05) in CL and did not correlate in GBC. CONCLUSION: A C level in CL changes with age and BMI while in GBC high LDLP C level was caused by other factors. No correlation of LP(a), LDLP Rf with age, body mass and blood lipids indicates that the above factors are independent in development of GBC.
