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In rare cases where Rosuvastatin Sandoz at doses higher than 20 mg is indicated, initiation of therapy should be under close specialist supervision. The physician who elects to use Rosuvastatin Sandoz at doses higher than 20 mg should periodically re-evaluate the long-term risk/benefit of Rosuvastatin Sandoz for the individual patient.
Race: Pharmacokinetic studies show an increase in exposure in Asian subjects including subjects of Japanese, Chinese, Malay and Indian ancestry compared with Caucasians (see Dosage & Administration and Pharmacology: Pharmacokinetics under Actions). A population pharmacokinetic analysis revealed no clinically relevant differences in pharmacokinetics between Caucasian, Hispanic, Black and Afro-Caribbean groups.
Renal Effects: Proteinuria, detected by dipstick testing and mostly tubular in origin, has been observed in patients treated with higher doses of rosuvastatin, in particular 40 mg. The effects were generally transient and not associated with worsening of renal function. Although the clinical significance of this finding is unknown, a dose reduction should be considered in patients with unexplained persistent proteinuria during routine urinalysis testing. An assessment of renal function is recommended during routine follow-up of patients treated with a dose of 40 mg.
Skeletal Muscle: 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. As with other HMG-CoA reductase inhibitors, the reporting rate for rhabdomyolysis in post-marketing use is higher at the highest marketed dose. Rare cases of rhabdomyolysis, which were occasionally associated with impairment of renal function, have been reported with rosuvastatin and with other marketed statins.
There have been very rare reports of an immune-mediated necrotising myopathy clinically characterized by persistent proximal muscle weakness and elevated serum creatine kinase during treatment or following discontinuation of statins, including rosuvastatin. Additional neuromuscular and serologic testing may be necessary. Treatment with immunosuppressive agents may be required.
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.
Before Treatment: If CK levels are significantly elevated at baseline (>10xULN) treatment should not be started.
Rosuvastatin Sandoz, as with other HMG-CoA reductase inhibitors, should be prescribed with caution in patients with pre-disposing factors for myopathy/rhabdomyolysis. Such factors include: renal impairment, hypothyroidism, personal or family history of hereditary muscular disorders, previous history of muscular toxicity with another HMG-CoA reductase inhibitor, fibrate or niacin, alcohol abuse, age ≥ 65 years, situations where an increase in plasma levels may occur, concomitant use of fibrates and niacin.
In such patients the risk of treatment should be considered in relation to possible benefit and clinical monitoring is recommended.
In patients with secondary hypercholesterolaemia caused by hypothyroidism or nephrotic syndrome, the underlying disease should be treated prior to initiating therapy with Rosuvastatin Sandoz.
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 (>10xULN) or if muscular symptoms are severe and cause daily discomfort (even if CK levels are ≤ 10xULN). If symptoms resolve and CK levels return to normal, then consideration should be given to re-introducing Rosuvastatin Sandoz 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.
The risk of myopathy during treatment with Rosuvastatin Sandoz may be increased in circumstances which increase rosuvastatin drug levels (see Pharmacology: Pharmacokinetics under Actions).
In clinical trials there was no evidence of increased skeletal muscle effects in the small number of patients dosed with rosuvastatin 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, ciclosporin, nicotinic acid, azole antifungals, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when given concomitantly with some HMG-CoA reductase inhibitors. The benefit of further alterations in lipid levels by the combined use of Rosuvastatin Sandoz with fibrates or niacin should be carefully weighed against the potential risks of such combinations. When used in combination with fibrates or lipid lowering doses of niacin (≥ 1 g/day), the dose of Rosuvastatin Sandoz should not exceed 10 mg/day (see Interactions and Adverse Reactions).
Rosuvastatin Sandoz should be temporarily withheld 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).
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 (see Adverse Reactions and Pharmacology: Pharmacodynamics under Actions).
Liver Effects: As with other HMG-CoA reductase inhibitors, Rosuvastatin Sandoz 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 treatment and any increase of dose, and periodically (semi-annually) thereafter.
Patients with increased transaminases levels should be monitored until abnormalities resolve. Rosuvastatin Sandoz should be discontinued or the dose reduced if the level of serum transaminases is > 3 ULN.
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 Rosuvastatin Sandoz in HIV patients receiving protease inhibitors and the potential for increased rosuvastatin plasma concentrations when initiating and up titrating Rosuvastatin Sandoz doses in patients treated with protease inhibitors. The concomitant use with certain protease inhibitors is not recommended unless the dose of Rosuvastatin Sandoz is adjusted (see Dosage & Administration and Interactions).
Endocrine Effects: Increases in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including rosuvastatin (see Adverse Reactions).
Effects on ability to drive and use machines: Studies to determine the effect of rosuvastatin on the ability to drive and use machines have not been conducted. However, based on its pharmacodynamic properties, rosuvastatin 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 and Adolescents 10 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 paediatric patients taking rosuvastatin is limited to a one year period. (See Pharmacology: Pharmacodynamics under Actions).
