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Cardiovascular disease is one of the most comon cause of death in patients undergoing hemodialysis. Long standing hypertension, volume overload, anemia and hyperliprlipidemia lead to dys- function of heart in these patients. Recently, lipo- protein(a) (Lp(a) ) reported as a major risk factor of ischemic heart disease and peripheral vascular disease. So we reviewed hyperlipidemic feature and serum Lp(a) concentrations of patients undergoing hemodialysis to evalualuate their functional and structural features of heart and the effects of hyperlipidemia and Lp(a) to the heart. The results are as followings'. 1) Serum Lp(a) concentrations are significantly higher in patients undergoing hemodialysis with 26.5?18.6 mg/dl than normal control subjects with 10.9?5.2 mg/dl (median value.' 22.05 mg/dl ' vs 10 mg/dl, p$lt;0.01). 2) Serum Lp(a) concentrations are significantly higher in patients with ischemic heart disease with 36.0?18.5 mg/dl than other patients with 14.9? 10.6 mg/dl (median value. 37 mg/dl vs 9.75 dl, p$lt;0.01) and show positive correlations with thickness of posterior wall of left ventricle and ejection fraction (r=0.61, r=0.49). Serum triglyc- eride concentrations show positive correlations with ejection fraction (r=0.52), serum cholesterol concentrations show positive correlatior with thickness of posterior wall of left ventricle and ejection fraction (r = 0.50, r = 0.48) and apolipo- protein A I concentrations show negative correla- tions with internal dimension of left atrium during diastole(r = 0.54) 3) Serum Lp(a) concentrations are significantly higher in patients with occlusion of arteriovenous fistula with 39.9?17.1 mg/dl than other patients with 21.5?16.8 mg/dl (median value'. 37.5 mg/dl vs 15 mg/dl, p$lt;0.01) and show positive correla- tions with thickenss of posterior wall of left ventri- cle and ejection fraction (r=0.51, r=0.65) and negative correlations with internal dimension of left atrium during diastole(r= 0.67). Triglyceride and cholesterol correlate positively with ejection fraion (r=0.49, r=0.65), and LDL cholesterol shows positive correlations with thickness of pos- terior wall of left ventricle and ejection fraction (r =0.57, r=0.70). 4) Serum Lp(a) concentrations are significantly higher in patients with arrhythmia with 30.2?20.2 mg/dl than other patients with 17.9?10.0 mg/dl (median value'. 33 mg/dl vs 15.8 mg/dl, p$lt;0.01), serum cholesterol (172.3?67.5 mg/dl vs 130.3? 22.3 mg/dl, p$lt;0.01) and LDL cholesterol(79.5? 34.6 mg/dl vs 59.1?17.6 mg/dl, p$lt;0.05) concen- trations are higher in patients with arrhythmia than other patients. Concentrations of triglyceride and cholesterol show positive correlation ehection fraction (r =0.48, r = 0.70) in patients with arrhythmia. From above results, we suggest that hyperlipidemia may acclerate the cardiovascular disease and Lp(a) may influence to the development of cardiovascular complications and survival of arteriovenous fistula in the patients undergoing hemodialysis.
The rate of remission induction with initial steroid therapy in children with minimal change disease is known to be above 90%, of which 40% is frequently relapsing type. In long-term steroid treatment, significant side effects occur during the course of therapy such as osteoprosis, growth retardation, obesity, Cushing syndrome and diabetes mellitus. By binding to steroid receptor, deflazacort(Calcort), an oxazoline derivative of prednisolone, exhibit antiinflammatory and immune suppressive effects, but decreases incidence of osteoporosis by lesser effect on calcium homeostasis and osteoclast activation than prednisolone. Thus the authors investingated 38 patients who need long term steroid therapy because of nephrotic syndrome to see the efficacy and the effect of deflazacort on bone metabolisrn. The 38 patients were randomly divided in two groups with classic drug, prednisolone and new drug, deflazacort. Beside laboratory parameters to ensure the effect of treatment of the nephrotic syndrome, all had measu rements of the bone densitometry, serum levels of parathyroid hormone and osteocalcin at 0 and 3 months of treatrnent. The therapeutic effects on the nephrotic syndrome were not different between the two drugs. The bone loss in the prednisolne-treated group was significantly higher than that of the deflazacort-treated group(Bone mineral content, 0 month vs. 3 month: 0.644±0.133 vs 0.615±0.159 g/cm in prednisolone-treated group, 0.581±0.127 vs 0.599±0.144 g/cm in deflazacort-treated group). There was a more marked fall in osteocalcin in prednisolone-treated group(0 month vs. 3 month: 60.45±47.19 vs 28.69±25.61 ng/ml) compared to deflazacort-treated group(0 month vs. 3 month: 44.20± 33.74 vs 39.33±24.83 ng/rnl). No significant difference was demonstrated between the two groups concerning serum PTH and cortisol. Thus, the detrimental effect of long-term steroid treatment on the bone may not be abolished, but it is significantly reduced by using deflazacort instead of prednisolone.