胺碘酮联合阿托伐他汀治疗非缺血性心衰伴恶性心律失常疗效观察

目的观察胺碘酮联合阿托伐他汀治疗非缺血性心衰伴恶性心律失常的临床疗效。方法将本院2010年1月～2012年9月期间非缺血性慢性心衰伴恶性心律失常患者57例随机分为2组，治疗组常规抗心衰治疗基础上加用阿托伐他汀及胺碘酮控制心律失常，对照组常规心衰治疗基础上仅加用胺碘酮控制心律失常。结果两组对心律失常均有效，治疗组总有效率89．2％，显著高于对照组72．1％（P〈0．05）结论胺碘酮联合阿托伐他汀治疗非缺血性恶性心律失常安全有效，优于单用胺碘酮。     

阿托伐他汀钙片与胺碘酮联合治疗慢性心力衰竭并室性心律失常的效果

目的探讨和分析阿托伐他汀钙片与胺碘酮联合治疗慢性心力衰竭并室性心律失常的效果。方法选择2013年1月至2016年12月间在盘锦市中医医院接受治疗的125例慢性心力衰竭并室性心律失常患者,遵循患者的入院顺序分甲组、乙组,甲组患者为63例,乙组患者为62例。所有患者均通过胺碘酮进行治疗,而甲组患者在胺碘酮治疗的基础上加用阿托伐他汀钙片进行治疗,评价甲乙两组患者的疗效、心功能、细胞因子和不良反应发生率。结果甲组患者的疗效、心功能指标、细胞因子水平均明显优于乙组患者,差异显著(P<0.05)。甲乙两组患者不良反应间差异不明显(P>0.05)。结论在慢性心力衰竭合并室性心律失常患者的治疗中,胺碘酮联合阿托伐他汀钙片的效果确切、安全性高,改善患者的心功能、细胞因子水平。     

阿托伐他汀引起肝损害的不良反应及监护

目的通过对阿托伐他汀所致肝损害不良反应病例不良反应进行分析,了解阿托伐他汀所致肝损害不良反应病例的表现和特点。方法临床药师通过阿托伐他汀所致肝损害不良反应进行分析及观察,判断肝损害与药物的因果关系,为临床提出合理用药建议,保障患者的安全合理用药。结果经过医生和药师的治疗和监护,患者病情好转出院。结论临床药师在参与临床治疗工作的过程中,要密切结合临床,注重细节的观察和分析,为患者合理安全用药,缩短病程,提高疗效,发挥临床药师的作用。     

辛伐他汀和阿托伐他汀与CYP3A4酶抑制剂/诱导剂在心内科患者中联用情况调查

目的:调查临床治疗中辛伐他汀和阿托伐他汀与CYP3A4酶抑制剂/诱导剂联合使用的情况。方法:随机抽取某三甲医院2012年度心内科应用辛伐他汀和阿托伐他汀的病例各50份,应用SPSS18.0统计软件,对患者的一般状况、用药情况及化验指标进行统计分析,计算各项指标的平均值或比例。结果:本调查纳入100名患者,66%的患者在使用辛伐他汀或阿托伐他汀的同时使用CYP3A4酶抑制剂,其中,辛伐他汀占30%,阿托伐他汀占36%,平均联合用药时间为(7.04±0.29)d。联合使用的CYP3A4酶抑制剂药物有氨氯地平片、地尔硫片、雷尼替丁片、胺碘酮、银杏叶片;CYP3A4酶诱导剂药物主要有卡马西平和醋酸泼尼松龙片。辛伐他汀或阿托伐他汀与CYP3A4酶抑制剂联合使用频率远远多于与CYP3A4酶诱导剂联合使用频率。比较合用和无合用CYP3A4酶抑制剂患者的主要生化指标,差异无统计学意义(P>0.05)。结论:辛伐他汀或阿托伐他汀与CYP3A4酶抑制剂联合使用情况在该医院较常见。建议尽量避免联用具有相互作用的药物,如必须使用,应按说明书要求不超剂量用药,并充分关注药物相互作用导致的不良反应,对患者后续情况定期随访。     

阿托伐他汀致肝功能异常的危险因素分析

目的探讨阿托伐他汀致肝功能异常的危险因素,指导临床为患者提供药学监护,保证临床安全合理用药。方法选取2013年1月至12月在本院使用阿托伐他汀且资料完整的500例患者作为研究对象,对可能影响肝功能的诸多因素进行χ2检验、单因素分析和Cox多因素分析。结果肝功能异常的发生率为5.4%(27/500)。经单因素和多因素分析后显示,年龄≥60岁、饮酒≥500 g·周-1、合并用药(胺碘酮)与肝功能异常有关,是阿托伐他汀致肝功能异常的独立危险因素。结论老年人、饮酒和合并用药(胺碘酮)是阿托伐他汀致肝功能异常的危险因素,选用他汀类药物时应结合患者的个体情况,保证用药安全。     

胺碘酮联合阿托伐他汀治疗老年人阵发性房颤临床疗效观察

目的探讨胺碘酮联合阿托伐他汀治疗老年性阵发性房颤的临床效果。方法选择南通市通州区人民院2008年9月至2010年9月阵发性房颤老年患者82例,将上述患者随机分为两组,观察组和对照组。对照组患者给予胺碘酮治疗,观察组给予胺碘酮和阿托伐他汀治疗。均治疗6个月。测定两组患者治疗前血脂情况、血浆C反应蛋白水平及窦性心律的维持情况。结果观察组治疗后C反应蛋白水平显著低于对照组,差异有统计学意义(P<0.05);观察组治疗后血脂改善情况显著优于对照组,差异有统计学意义(P<0.05);观察组治疗后窦性心律维持率明显高于对照组,差异有统计学意义(P<0.05)。结论胺碘酮联合阿托伐他汀合用治疗老年人阵发性房颤临床效果显著,值得借鉴。     

胺碘酮联合阿托伐他汀钙片治疗心力衰竭合并心绞痛的效果研究

目的探讨胺碘酮联合阿托伐他汀钙片治疗心力衰竭(心衰)合并心绞痛的效果研究。方法将本院2010年5月至2011年5月收治的64例心衰合并心绞痛患者随机分为对照组和治疗组,两组均给予胺碘酮治疗,仅治疗组加用阿托伐他汀钙片治疗。观察两组治疗8周后的心绞痛症状改善、心衰症状改善及不良反应情况。结果①治疗组的心绞痛治疗有效率高于对照组(P<0.05),且硝酸甘油停药例数多于对照组(P<0.01);②治疗组的心衰治疗总有效率高于对照组,LVEF(P<0.05)和E/A(P<0.01)水平高于对照组;③两组的不良反应无差异,但治疗组的头晕发生率低于对照组(P<0.05)。结论胺碘酮联合阿托伐他汀钙片治疗心衰合并心绞痛的效果较好,可提高心衰合并心绞痛治疗有效率,且不良反应少,耐受性好。     

阿托伐他汀不良反应及合理应用

目的对临床一线调脂药阿托伐他汀所致药品不良反应(ADR)进行分析,为临床合理用药提供参考。方法文献检索2001年6月—2011年6月国内医药期刊报道的有关阿托伐他汀的不良反应案例,共收集34例,进行统计分析和归纳。结果 34例不良反应临床表现以肌损害最常见(47.06%),其次是肝-胆异常(29.41%),老年患者(≥61岁)发生率较高(64.71%)。结论多种药物合用是导致阿托伐他汀不良反应的重要危险因素。提示应注意药物相互作用,加强用药监测,以减少或避免ADR的发生。     

胺碘酮联合厄贝沙坦和阿托伐他汀治疗130例阵发性心房颤动患者的临床疗效观察

目的观察胺碘酮联合厄贝沙坦、阿托伐他汀治疗阵发性房颤的临床疗效。方法将130例阵发性房颤患者随机分为两组：胺碘酮加阿托伐他汀组（对照组）65例;在对照组用药基础上加用厄贝沙坦组（治疗组）65例。观察两组患者治疗后的窦性心律维持率及治疗前、治疗后6、12、18个月后左心房内径（LA）的变化情况。结果两组治疗后窦性心律维持率均较治疗前显著改善,差异有统计学意义（P〈0.05）,但组间比较,差异无统计学意义（P〉0.05）,治疗12个月后治疗组窦性心律维持率明显大于对照组（P〈0.05）;治疗6个月后两组左心房内径差异无统计学意义,但18个月后治疗组的左心房内径较明显小于对照组（P〈0.05）。结论胺碘酮联合厄贝沙坦、阿托伐他汀治疗阵发性心房颤动,其维持窦性心律的疗效优于胺碘酮联合阿托伐他汀,并能延缓左心房的扩大。     

阿托伐他汀促卡马西平致皮肤不良反应的临床分析

目的：探讨阿托伐他汀促卡马西平致皮肤不良反应的临床特点及可能性机制。方法回顾性分析16例患者因同时服用卡马西平及阿托伐他汀而出现的皮肤不良反应。结果16例患者中剥脱性皮炎7例,荨麻疹型5例,大疱性表皮松解型药疹2例, Stevens-Johnson syndrome 2例。结论阿托伐他汀对肝酶的影响是其促卡马西平致皮肤不良反应的可能性机制。     

Safety and efficacy of HMG-CoA reductase inhibitors for treatment of hyperlipidemia in patients with HIV infection

STUDY OBJECTIVE: To assess the efficacy and safety of HMG-CoA reductase inhibitors (statins) in patients with human immunodeficiency virus (HIV) infection and hyperlipidemia. DESIGN: Retrospective analysis. SETTING: HIV clinic. PATIENTS: Twenty-six HIV-infected patients with hyperlipidemia. INTERVENTION: Five patients received pravastatin, 13 lovastatin, 10 simvastatin, and 2 atorvastatin (total 30 courses). MEASUREMENTS AND MAIN RESULTS: Reductions in cholesterol and triglycetides were used to assess efficacy; creatine kinase (CK), liver enzymes, and myalgia were markers of statin toxicity. After a median of 8.2 and 7.2 months of treatment, the agents collectively reduced median baseline total cholesterol 27% (354 to 263 mg/dl) and triglycerides 15% (513 to 438 mg/dl), respectively. Two patients, one with marked CK elevations, experienced myalgias with lovastatin, and two experienced transaminase elevations 3 or more times the upper limit of normal. CONCLUSION: Statins are effective in reducing total cholesterol and triglycerides in HIV-infected patients, although lipid levels infrequently return to normal. Lovastatin should be avoided in patients receiving concomitant drugs that may potentiate skeletal muscle toxicity with this agent.     

Acute hepatic injury with atorvastatin: An unusual occurrence

Atorvastatin, a commonly used and well-tolerated hypolipidemic drug, belongs to the class of statins or hydroxymethylglutaryl-coenzyme A reductase inhibitors. Use of atorvastatin may be associated with minor asymptomatic elevations in serum aminotransferases, but clinically significant hepatotoxicity is usually infrequent. Here we present a case of self-limiting clinically apparent acute hepatic injury attributable to atorvastatin occurring at recommended daily dose of 20 mg once a day. This case was postulated to be an unusual idiosyncratic reaction of the drug.KEY WORDS: Acute hepatotoxicity, aminotransferase enzymes, atorvastatin     

Liver function test abnormalities and pruritus in a patient treated with atorvastatin: case report and review of the literature

The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (also known as statins) are associated with elevated transaminase levels in 1-3% of patients. Therapy with these drugs requires monitoring of alanine aminotransferase (ALT) levels because animal studies and premarketing clinical trials showed signs of hepatotoxicity that were primarily minor elevations of ALT. Nevertheless, postmarketing experience suggests that hepatotoxicity is rare, and that elevated ALT levels are reversible with continued therapy and probably are related to cholesterol lowering. Based on the low occurrence of ALT elevations and the lack of clinical evidence of hepatotoxicity, some clinicians are calling for a change in the current practice of monitoring liver function tests. We report, however, the case of a 71-year-old woman who was receiving atorvastatin and experienced elevated transaminase levels on two occasions, and developed pruritus on rechallenge with the drug. Thus, clinicians should be aware of asymptomatic elevations in liver function tests in patients receiving atorvastatin who do not have known risk factors for liver damage.     

Incidence and prevalence of abnormal liver associated enzymes in patients with atrial fibrillation in a routine clinical care population

The prevalence of elevated liver enzymes has not been described in patients with atrial fibrillation (AF) who may be more likely to develop these abnormalities due to comorbidities and medications. As signals of liver injury lead to termination of drug development programs, an attempt to better define the background prevalence would aid in interpreting these elevations in the setting of exposure to a new drug. The aim of this study was to estimate the prevalence and incidence of alanine aminotransferase (ALT) elevations in a cohort with AF. METHODS: Retrospective cohort of patients with AF using the outpatient medical record of the University of Pennsylvania Health System (UPHS). Primary outcomes were prevalence and incidence of ALT elevations (>40 U/L). We also examined the prevalence of risk factors for ALT elevations. RESULTS: Liver enzymes were measured at least once in 1630 of 2151 patients (76%). The prevalence of ALT >40 U/L was 27.6% (95%CI 25.7-29.5%). The incidence of new ALT elevations was 14.5/100 person-years (95%CI 13.0-16.1) for ALT > 40 U/L and 2.1/100 person-years (95%CI 1.6-2.8) for ALT elevations above twice the upper limit of normal (ULN). New persistent ALT elevations above twice the ULN were identified in 0.2% of patients. CONCLUSION: Elevated ALT is common among patients with AF, although new and persistent elevation greater than twice the ULN is uncommon. In the setting of a new drug, these factors make it difficult to delineate drug-induced liver injury from incident elevations due to comorbidities.     

Atorvastatin: a safety and tolerability profile

Extensive data are available on the safety of atorvastatin from randomised clinical trials, postmarketing analyses and reports to regulatory agencies. Atorvastatin is generally well tolerated across the range of therapeutic dosages, with the exception of a slightly higher rate of liver enzyme elevations with atorvastatin 80 mg/day which does not appear to confer an increased risk of clinically important adverse events. Unlike simvastatin, atorvastatin is associated with a low incidence of muscular toxicity. It is not associated with neurological, cognitive or renal adverse effects and does not require dosage adjustment in patients with renal dysfunction, due to its favourable pharmacokinetic profile, which is unique among the statins. In patients aged > or =65 years, atorvastatin is well tolerated with no dose-dependent increase in adverse events up to the maximum daily dosage of 80 mg/day. Thus, atorvastatin is a safe and well tolerated statin for use in a wide range of patients.     

阿托伐他汀与瑞舒伐他汀对冠心病患者肝功能影响的对比

目的:评估阿托伐他汀与瑞舒伐他汀长期应用对冠心病患者血脂水平和肝功能的影响。方法:采用回顾性分析方法,选择我院住院冠心病患者200例,根据他汀类药物应用情况,分为阿托伐他汀组(102例)和瑞舒伐他汀组(98例),比较两组患者应用他汀后1周、1个月、3个月、6个月和12个月的血脂和肝功能水平变化。结果:两组患者治疗后各时期的TC、LDL-C水平差异均无统计学意义(P>0.05)。两组患者治疗后AST和ALT较治疗前显著升高(P<0.05),但两组间差异均无统计学意义(P>0.05)。结论:两种他汀降脂效果相似,但均可导致肝酶升高。     

Risk factors for alcohol hepatotoxicity among male alcoholics

Alcoholic liver cirrhosis is a leading cause of morbidity and mortality in alcohol dependence. A common precursor to cirrhosis is alcoholic hepatotoxicity evident clinically by elevated serum liver enzymes. In this study 50 male patients with significant (greater than two times upper limits of normal) elevation of liver enzymes attending a veterans inpatient alcohol treatment center were matched by age and time since last drink to 50 male veterans without elevated liver enzymes. Patients with elevated liver enzymes were found to be more likely to be daily drinkers, less likely to indulge in binge drinking patterns or have alcoholic blackouts, and showed a trend towards a less severe pattern of alcoholism. Significant gamma glutamyl transferase (GGT) elevations were found in patients consuming an average of 7 beers/day for 5 years, and significant aspartate aminotransferase (AST) elevations were found in patients consuming a threshold of 12 beers/day for 10 years. These findings are consistent with current research suggesting alcoholic cirrhosis is a result of a threshold exposure to alcohol in alcoholics with an additional environmental or genetic risk factor.     

Antifibrotic effect of AT‐1 blocker and statin in rats with hepatic fibrosis

Hepatic fibrosis is an outcome of chronic liver injury. Angiotensin II (ANG II) may play a role in the pathogenesis of hepatic fibrosis. Certain drugs such as ACE inhibitors, ANG II antagonists, and even statins could interfere with the renin angiotensin system and modulate its deleterious effects. This study was carried out to investigate the possible role of losartan and atorvastatin in liver fibrosis. Liver fibrosis was induced in rats by i.p. injection of 50% CCl₄ twice per week for 8 weeks. The rats intoxicated with CCl₄ were divided into four groups: fibrosis control; losartan group; atorvastatin group; and co‐treated group. A fifth group of normal healthy rats served as a control group. The results showed that losartan and atorvastatin, either alone or in combination, significantly decreased ALT, AST, hyaluronic acid and hydroxyproline levels in their groups compared to those of the fibrosis control group. A significant decrease in TGF‐β was found in the losartan and co‐treated groups but not in the atorvastatin group. These biochemical data were supported by liver histopathology and α‐SMA. The results indicate that the combined treatment with both losartan and atorvastatin produced a greater effect than either drug alone and proved a beneficial role in inhibiting or reversing liver fibrosis.     

A comparison of simvastatin and atorvastatin up to maximal recommended doses in a large multicenter randomized clinical trial

OBJECTIVE: At higher doses, simvastatin has been shown to produce significantly greater increases in high-density lipoprotein (HDL) cholesterol and apolipoprotein (apo) A-I than atorvastatin. To extend and confirm these findings, a 36-week, randomized, double-blind, dose-titration study was performed in 826 hypercholesterolemic patients to compare the effects of simvastatin and atorvastatin on HDL cholesterol, apo A-I, and clinical and laboratory safety. PRIMARY HYPOTHESIS: Simvastatin, across a range of doses, will be more effective than atorvastatin at raising HDL cholesterol and apo A-I levels. METHODS: A total of 826 hypercholesterolemic patients were enrolled in this double-blind, randomized, parallel, 36-week, dose-escalation study. Patients randomized to simvastatin received 40 mg/day for the first 6 weeks, 80 mg/day for the next 6 weeks, and remained on 80 mg/day for the final 24 weeks. Patients randomized to atorvastatin received 20 mg/day for the first 6 weeks, 40 mg/day for the next 6 weeks, and 80 mg/day for the remaining 24 weeks. RESULTS: During the first 12 weeks of the study, simvastatin increased HDL cholesterol and apo A-I more than the comparative doses of atorvastatin, while producing slightly lower reductions in low-density lipoprotein (LDL) cholesterol and triglycerides. At the maximal dose comparison, simvastatin 80 mg and atorvastatin 80 mg, the HDL cholesterol and apo A-I differences favoring simvastatin were larger than at the lower doses. In addition, at the maximal dose comparison, the incidence of drug-related clinical adverse experiences was approximately two-fold higher with atorvastatin 80 mg than with simvastatin 80 mg (23 versus 12%, p < 0.001), due predominantly to a greater incidence of gastrointestinal symptoms with atorvastatin (10 versus 3%, p < 0.001). The incidence of clinically significant alanine aminotransferase elevations was also higher with atorvastatin 80 mg than with simvastatin 80 mg (3.8 versus 0.5%, p < 0.010), especially in women (6.0 versus 0.6%). CONCLUSIONS: At the doses compared in this study, simvastatin led to greater increases in HDL cholesterol and apo A-I levels than atorvastatin. At the maximum dose comparison, there were fewer drug-related gastrointestinal symptoms and clinically significant aminotransferase elevations with simvastatin.     

Subacute liver failure induced by adalimumab

Most cases of liver toxicity associated with TNF-antagonists have been linked to infliximab and to a lesser extent to etanercept. So far only mild elevations of liver enzymes during therapy with adalimumab have been reported. In general, patients who developed ALT and AST elevations were asymptomatic and the abnormalities decreased or resolved with either continuation or discontinuation of adalimumab, or modification of concomitant medications. In this case report, we are presenting the first case of a patient without previous history of liver disease or concomitant risk factors for liver disease who developed subacute liver failure during therapy with adalimumab for psoriatic arthritis.