Vivacor Special Precautions

Renal Effects: In the rosuvastatin clinical trial program, dipstick-positive proteinuria and microscopic hematuria were observed among rosuvastatin treated patients, predominantly in patients dosed above the recommended dose range (i.e., 80 mg). However, this finding was more frequent in patients taking rosuvastatin 40 mg, when compared to lower doses of rosuvastatin or comparator statins, though it was generally transient and was not associated with worsening renal function. An assessment of renal function should be considered during routine follow-up of patients treated with a dose of 40 mg.
Skeletal Muscle Effects: As with other HMG-CoA reductase inhibitors, effects on skeletal muscle e.g. myalgia, myopathy and, rarely, rhabdomyolysis, have been reported in patients treated with rosuvastatin. As with other HMG-CoA reductase inhibitors, the reporting rate for rhabdomyolysis in post-marketing use is higher at the highest marketed dose. Additional neuromuscular and serologic testing may be necessary. Treatment with immunosuppressive agents may be required.
Statins may in rare instances induce or aggravate myasthenia gravis or ocular myasthenia (see Adverse Reactions) including reports of recurrence when the same or a different statin was administered. CRESTOR should be used with caution in patients with these conditions and should be discontinued if they are induced or aggravated.
Creatine Kinase Measurement: Creatine Kinase (CK) should not be measured following strenuous exercise or in the presence of a plausible alternative cause of CK increase which may confound interpretation of the result. If CK levels are significantly elevated at baseline (>5x Upper Limit of Normal) a confirmatory test should be carried out within 5-7 days. If the repeat test confirms a baseline CK >5x Upper Limit of Normal, treatment should not be started.
Before Treatment: VIVACOR, as with other HMG-CoA reductase inhibitors, should be prescribed with caution in patients with pre-disposing factors for rhabdomyolysis, such as, renal impairment, hypothyroidism, personal or family history of hereditary muscular disorders, previous history of muscular toxicity with another HMG-CoA reductase inhibitor or fibrate, alcohol abuse, age >70 years, situations where an increase in plasma levels may occur (see Dosage & Administration, Interactions and Pharmacology: Pharmacokinetics under Actions), concomitant use of fibrates.
In such patients the risk of treatment should be considered in relation to possible benefit and clinical monitoring is recommended. If CK levels are significantly elevated at baseline (>5x Upper Limit of Normal) treatment should not be started.
Whilst on Treatment: Patients should be asked to report inexplicable muscle pain, weakness or cramps immediately, particularly if associated with malaise or fever. CK levels should be measured in these patients. Therapy should be discontinued if CK levels are markedly elevated (>5x Upper Limit of Normal) or if muscular symptoms are severe and cause daily discomfort (even if CK levels are ≤5x Upper Limit of Normal). If symptoms resolve and CK levels return to normal, then consideration should be given to re-introducing VIVACOR or an alternative HMG-CoA reductase inhibitor at the lowest dose with close monitoring. Routine monitoring of CK levels in asymptomatic patients is not warranted. There have been very rare reports of an immune-mediated necrotising myopathy (IMNM) during or after treatment with statins, including rosuvastatin. IMNM is clinically characterized by proximal muscle weakness and elevated serum creatine kinase, which persist despite discontinuation of statin treatment.
In clinical trials there was no evidence of increased skeletal muscle effects in the small number of patients dosed with VIVACOR and concomitant therapy. However, an increase in the incidence of myositis and myopathy has been seen in patients receiving other HMG-CoA reductase inhibitors together with fibric acid derivatives including gemfibrozil, cyclosporin, nicotinic acid, azole antifungals, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when given concomitantly with some HMG-CoA reductase inhibitors. Therefore, the combination of VIVACOR and gemfibrozil is not recommended. The benefit of further alterations in lipid levels by the combined use of VIVACOR with fibrates or niacin should be carefully weighed against the potential risks of such combinations (see Interactions and Adverse Reactions).
VIVACOR should be prescribed with caution in patients with pre-disposing factors for myopathy, such as, renal impairment, advanced age and hypothyroidism, or situations where an increase in plasma levels may occur (see Interactions and Pharmacology: Pharmacokinetics under Actions).
VIVACOR should not be used in any patient with an acute, serious condition suggestive of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (e.g. sepsis, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders; or uncontrolled seizures).
Liver Effects: As with other HMG-CoA reductase inhibitors, VIVACOR should be used with caution in patients who consume excessive quantities of alcohol and/or have a history of liver disease.
It is recommended that liver function tests be performed before and at 3 months following both the initiation of therapy and any elevation of dose, and periodically thereafter. VIVACOR should be discontinued or the dose reduced if the level of serum transaminases is greater than 3 times the upper limit of normal. The reporting rate for serious hepatic events (consisting mainly of increased hepatic transaminases) in post-marketing use is higher at the 40 mg dose.
In patients with secondary hypercholesterolaemia caused by hypothyroidism or nephrotic syndrome, the underlying disease should be treated prior to initiating therapy with VIVACOR.
Race: Pharmacokinetic studies show an increase in exposure in Asian subjects compared with Caucasians (see Dosage & Administration and Pharmacology: Pharmacokinetics under Actions).
Diabetes Mellitus: As with other HMG-CoA reductase inhibitors, increases in HbA1c and serum glucose levels have been observed in patients treated with rosuvastatin, and in some instances these increases may exceed the threshold for the diagnosis of diabetes mellitus, primarily in patients already at high risk for developing diabetes (see Adverse Reactions and Pharmacology: Pharmacodynamics under Actions).
Protease inhibitors: Increased systemic exposure to rosuvastatin has been observed in subjects receiving rosuvastatin concomitantly with various protease inhibitors in combination with ritonavir. Consideration should be given both to the benefit of lipid lowering by use of VIVACOR in HIV patients receiving protease inhibitors and the potential for increased rosuvastatin plasma concentrations when initiating and up titrating VIVACOR doses in patients treated with protease inhibitors. The concomitant use with certain protease inhibitors is not recommended unless the dose of VIVACOR is adjusted (see Dosage & Administration and Interactions).
Effects on ability to drive and use machines: Studies to determine the effect of VIVACOR on the ability to drive and use machines have not been conducted. However, based on its pharmacodynamic properties, VIVACOR is unlikely to affect this ability. When driving vehicles or operating machines, it should be taken into account that dizziness may occur during treatment.
Use in Children: Children and adolescents 6 to 17 years of age: The evaluation of linear growth (height), weight, BMI (body mass index), and secondary characteristics of sexual maturation by Tanner staging in pediatric patients taking rosuvastatin is limited to a two-year period (see Pharmacology: Pharmacodynamics under Actions).