| Objective: Metabolic Syndrome (MS) is a clinical syndrome, which iscaused by certain high-risk environmental factors as the starting factor.Abdominal obesity and insulin resistance is the main pathological basis. Itconsequences result serious cardiovascular damage.In recent years, a series ofstudies have shown that the MS may led to a series of metabolic disorders, thefinal clinical consequences is suffering from an increased risk of CHD andDM, which characterized by high incidence, morbidity and mortality.Atpresent, studies have shown that central obesity and insulin resistance may bethe basic of the MS[1]. Pathological, obesity performance is increasing of thenumber and volume of fat cells,and studies discoverd that leptin secreted byfat cells.Leptin play an important role in pro-inflammatory and promoteatherosclerosis, which extremely closely related to Insulin Resistance[2-3].Some studies have shown[4-5]that, the serum leptin in obese people is twotimes higher than the normal and three times than the thinner. Elevated serumleptin associated with MS risk factors, and can be forecast as an independentpredictor of MS and Cardiovascular disease. Statins (HMG-CoA), because oftheir good TC-lowering effect more and more widely used in the clinical, hasbeen proven in Epidemiology and Clinical studies, the addition to loweringLDL and TG has become a consensus. Lipoprotein disorders in patientswithout metabolic syndrome use moderate statin drugs can make the lipidnormal, but patients with metabolic syndrome need intensive lipid-loweringtherapy. Studies have demonstrated that statins not only act on lipid-lowering,but also protect in endothelial function,anti-inflammatory.In short, a lot ofstudies has not agreed on understanding MS completely in pathophysiological,clinical prognosis, prevention and treatment strategies, but there is no idealtreatment to the MS is an urgent problem. Before the ideal drug has not yet been developed, statins drugs for MS patients, whether lower lipid or reduceleptin safely and effectively, is an open question. In MS patients, applicationof different statins reduced serum level of lipid and leptin, is rarely reported.This study was designed by recording the dynamic changes of serum leptinand lipid levels in MS patients who used different statins, and to explorewhether leptin act as to a new biological indicator in the MS, and provide atheoretical basis for statins therapy on MS.Methods: Sixty patients of metabolic syndrome durnning December2010to December2011, in Department of Cardiology or Endocrinology,TheSecond Hospital of Hebei Medical University, Diagnosis to Ms were in linewith the global consensus on the definition of the IDF. The patients included27males,33female, average age (58.05±8.67) years, BMI (26.35±1.27) kg/m2. Condition and test results are admitted to the MS were randomly dividedinto group A and B. Group A (Atorvastatin calcium group), consisted30cases(13males,17females), average age (57.72±7.64) years old, BMI (26.43±1.33)kg/m2, and received Atorvastatin statins calcium10mg daily orale. Group B(Rosuvastatin calcium group), consisted30cases (14male,16females),average age (58.41±9.72) years old, BMI (26.27±1.23) kg/m2, and receivedrosuvastatin calcium10mg daily oral. Two groups in age, sex, BMI, bloodglucose, blood pressure were not statistically significant.All patients routinelycollect history,serum lipids (TC,TG,HDL,LDL),and leptin, blood pressure,height, weight and body mass index (BMI) measured on the same day, andwere given to all the patients MS conventional treatments. Every selectedcollected venous blood durning before treatment,(12hours without eating),after six and twelve weeks treatment, respectively.One5ml blood to determinlipid levels by ELISA; Another5ml blood, sandwich enzyme-linkedimmunosorbent assay of serum leptin levels. Observe before and aftertreatment between group A and B, and analysised the dynamic changes oflipid and leptin levels.Results:1TC：Before treatment,group B and A had no differences (6.14±0.79 vs6.12±0.87mmol/L,P>0.05). Six weeks, group B and A had no differences(5.56±0.80vs5.61±0.87mmol/L, P>0.05). Twelve weeks, group B wassignificantly lower than group A (4.91±0.51vs5.03±0.62mmol/L, P>0.05).Compared with six weeks, after12weeks treatment group A and B weresignificantly lower (5.03±0.62vs5.61±0.87mmol/L,P<0.05;4.91±0.51vs5.56±0.80mmol/L, P<0.05).2TG：Before treatment, group B and A had no differences (2.21±0.62vs2.23±0.67mmol/L,P>0.05). Six weeks, group B and A had nodifferences (2.12±0.68vs2.15±0.79mmol/L, P>0.05). Twelve weeks: group Bwas significantly lower than group A (1.76±0.35vs1.93±0.45mmol/L,P>0.05). Compared with six weeks, after12weeks treatment group A and Bwere significantly lower (1.93±0.45vs2.15±0.79mmol/L,P<0.05;1.76±0.35vs2.12±0.68mmol/L,P<0.05).3HDL：Before treatment, group B and A had no differences (0.83±0.26vs0.84±0.24mmol/L,P>0.05). Six weeks: group B and A had nodifferences (0.97±0.22vs0.95±0.27mmol/L,P>0.05). Twelve weeks: group Bwas significantly higher than group A (1.14±0.31vs1.05±0.29mmol/L,P>0.05). Compared with six weeks, after12weeks treatment group A and Bwere significantly higher (1.05±0.29vs0.95±0.27mmol/L,P<0.05;1.14±0.31vs0.97±0.22mmol/L, P<0.05).4LDL：Before treatment: group B and A had no differences (4.11±0.85vs4.08±0.92mmol/L,P>0.05). Six weeks: group B and A had nodifferences (3.61±0.36vs3.69±0.33mmol/L,P>0.05). Twelve weeks: group Bwas significantly lower than group A (2.71±0.61vs2.96±0.63mmol/L,P>0.05). Compared with six weeks, after12weeks treatment group A andB were significantly lower(2.96±0.63vs3.69±0.33mmol/L, P<0.05;2.71±0.61vs3.61±0.36mmol/L,P<0.05).5Leptin levels：Before treatment group B and A had no differences(9.96±1.23vs10.05±1.07mmol/L,P>0.05); Six weeks, group B was significan-tly lower than group A (8.32±0.98vs8.83±0.76mmol/L, P<0.05). Twelveweeks: group B was significantly lower than group A (7.16±0.79vs7.76±0.63 mmol/L, P<0.05). Compared with six weeks, after12weeks treatment groupA and B were significantly lower (7.76±0.63vs8.83±0.76mmol/L, P<0.05;7.16±0.79vs8.32±0.98mmol/L, P<0.05).Conclusion:1After treated for6weeks,12weeks,the TC, TG and LDL in group A andB decreased, however HDL increased; The adverse reactions in rosuvastatincalcium and atorvastatin calcium group were mild, show both were reliableand effective lipid lowering drugs. After treated for12weeks was better thansix weeks. For MS patients, after treated for12weeks, rosuvastatin calciumwas better than atorvastatin calcium in lipid-lowering.2After treated for6weeks,12weeks the leptin levels were significantlylower than before treatment in group A and B, after treated for12weeks wasbetter than six weeks；Rosuvastatin calcium and atorvastatin calcium hadeffect on MS patients in serum leptin level, and also had safely andeffectively treatment for MS. In comparison, rosuvastatin calcium was betterto reduce serum leptin levels in MS patients than atorvastatin calcium. |
PDF Full Text Request