1.
Case report. Hyperlipoproteinaemia(a): which is the optimal therapy? A case report.
Lupattelli, G, Roscini, AR, Siepi, D, Mannarino, E
Journal of clinical pharmacy and therapeutics. 2010;(5):613-5
Abstract
This case report presents the clinical history of a patient with elevated lipoprotein(a) and small size isoform, associated with mixed hyperlipaemia, which was probably familial combined hyperlipaemia. After premature myocardial infarction, the subject was treated with fibrates. Niacin was started after recurrence. One year ago, after another episode of acute coronary syndrome, rosuvastatin was added to niacin. The atherogenicity of this lipid disorder, along with the different options for therapy is discussed.
2.
Rosuvastatin-induced rhabdomyolysis probably via CYP2C9 saturation.
Gallelli, L, Ferraro, M, Spagnuolo, V, Rende, P, Mauro, GF, De Sarro, G
Drug metabolism and drug interactions. 2009;(1):83-7
Abstract
A 66 year-old woman with no history of renal or liver disease presented with progressive asthenia and diffuse myalgia. She cited 5 months history of mild hyperlipidemia under treatment with rosuvastatin (10 mg/day). Clinical examination documented both an increase in liver size and proximal muscle weakness, with difficulty in raising arms above the head. Blood tests showed the presence of renal, liver and muscle failure, with no evidence of virological, immunological or haematological diseases. Rosuvastatin treatment was stopped and blood values normalised within five days; but because of an increase in cholesterol plasma levels, rosuvastatin (10 mg/day) was restarted. Two days later, the patient returned to our observation due to the development of asthenia and muscle weakness, with an increase in creatine phosphokinase, 12,165 U/l. Rosuvastatin was discontinued and replaced with pravastatin (40 mg/day) with a complete resolution of clinical and laboratory findings in about six days. Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.
3.
A multimodal, evidence-based approach to achieve lipid targets in the treatment of antiretroviral-associated dyslipidemia: case report and review of the literature.
Bain, AM, White, EA, Rutherford, WS, Rahman, AP, Busti, AJ
Pharmacotherapy. 2008;(7):932-8
Abstract
Metabolic abnormalities associated with the treatment of human immunodeficiency virus (HIV) infection are well-recognized problems that increase cardiovascular risk. As a result of the complexity of treating both HIV- and antiretroviral-related comorbidities, strategies that improve adverse drug events while maintaining viral control are in critical need. Although guidelines have somewhat helped in the general approach and in first-line strategies for managing dyslipidemia in patients receiving antiretrovirals, a paucity of data exist to guide clinicians in treating patients whose conditions are refractory to first-line options or who are at substantial risk for cardiovascular events. Further complicating the choice of lipid-lowering strategy is the lack of randomized controlled data from the HIV-affected population and a concern about clinically significant drug-drug interactions. We describe an HIV-infected patient with efavirenz-associated dyslipidemia at very high cardiovascular risk who had not achieved his primary or secondary lipid goals despite 2 years of treatment in a lipid specialty clinic. Lipid control was accomplished in 10 weeks with a targeted, stepwise approach of switching efavirenz to nevirapine, followed by rosuvastatin 20 mg/day, which was sustained for at least 10 months. Of most importance, this outcome was achieved without any clinically significant alteration in virologic or immunologic control. This case report highlights the potential for a pharmacist-guided, multistep approach that addresses HIV-related dyslipidemia and incorporates the pharmacokinetic literature to guide lipid-lowering therapy and promote the attainment of goals based on current standards of care.
4.
Reduction of intima-media thickness in subjects with asymptomatic carotid disease: two cases from the Asymptomatic Carotid Atherosclerosis DIsease Manfredonia Study (ACADIM Study).
Riccioni, G, D'Orazio, N
La Clinica terapeutica. 2007;(5):431-3
Abstract
The intima-media thickness (IMT) of carotid common arteries (CCA) represents an important step of carotid plaque formation and progression, and is a characteristic marker of atherosclerosis, one of the most principal determinants of coronary artery disease (CAD). Change in IMT is one of the currently used markers to evaluate the progression of atherosclerotic process. In particular rosuvastatin (ROS) has demonstrated in a large scale controlled study with placebo a significant reduction of coronary atherosclerosis. Two subjects with normal lipidic profile underwent a carotid ultrasound investigations (CUI) and received ROS (10 mg/day). The CUI documented a bilateral IMT of CCDX and CCSX for the case A (0.101 cm dx-0.105 cm sx; mean 0.103 cm) and B (0.114 cm dx-0.108 cm sx; mean 0.111 cm), in absence of stenosis or occlusion. After 16 treatment-weeks with ROS it has found a significant reduction of IMT for both case A (0.081 cm dx -0.096 cm sx; mean 0.088 cm) than case B (0.082 cm dx-0.084 cm sx; mean 0.083 cm). The treatment with ROS has been well tolerated and no adverse effects has been reported. ROS represents an efficacious IMT-lowering agent of the statin class. The two presented case reports confirm the benefit of ROS in the IMT reduction in subjects with normal LDL-C values.
5.
Short-term memory loss associated with rosuvastatin.
Galatti, L, Polimeni, G, Salvo, F, Romani, M, Sessa, A, Spina, E
Pharmacotherapy. 2006;(8):1190-2
Abstract
Memory loss and cognitive impairment have been reported in the literature in association with several 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), but we found no published case reports associated with rosuvastatin. To our knowledge, this is the first reported case of rosuvastatin-related short-term memory loss. A 53-year-old Caucasian man with hypercholesterolemia experienced memory loss after being treated with rosuvastatin 10 mg/day. He had no other concomitant conditions or drug therapies. After discontinuation of rosuvastatin, the neuropsychiatric adverse reaction resolved gradually, suggesting a probable drug association. During the following year, the patient remained free from neuropsychiatric disturbances. Clinicians should be aware of possible adverse cognitive reactions during statin therapy, including rosuvastatin.