Source: Medicines & Healthcare Products Regulatory Agency (GB) Revision Year: 2026 Publisher: AstraZeneca UK Limited, 1 Francis Crick Avenue, Cambridge, CB2 0AA, UK
Crestor is contraindicated:
The 40 mg dose is contraindicated in patients with pre-disposing factors for myopathy/rhabdomyolysis. Such factors include:
(See sections 4.4, 4.5 and 5.2)
Proteinuria, detected by dipstick testing and mostly tubular in origin, has been observed in patients treated with higher doses of Crestor, in particular 40 mg, where it was transient or intermittent in most cases. Proteinuria has not been shown to be predictive of acute or progressive renal disease (see section 4.8). The reporting rate for serious renal events in post-marketing use is higher at the 40 mg dose. An assessment of renal function should be considered during routine follow-up of patients treated with a dose of 40 mg.
Effects on skeletal muscle e.g. myalgia, myopathy and, rarely, rhabdomyolysis have been reported in Crestor-treated patients with all doses and in particular with doses >20 mg. Very rare cases of rhabdomyolysis have been reported with the use of ezetimibe in combination with HMG-CoA reductase inhibitors. A pharmacodynamic interaction cannot be excluded (see section 4.5) and caution should be exercised with their combined use. As with other HMG-CoA reductase inhibitors, the reporting rate for rhabdomyolysis associated with Crestor in post-marketing use is higher at the 40 mg dose.
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 (>5xULN) a confirmatory test should be carried out within 5–7 days. If the repeat test confirms a baseline CK >5xULN, treatment should not be started.
Crestor, as with other HMG-CoA reductase inhibitors, should be prescribed with caution in patients with pre-disposing factors for myopathy/rhabdomyolysis. Such factors include:
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 (>5xULN) treatment should not be started.
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 (>5xULN) or if muscular symptoms are severe and cause daily discomfort (even if CK levels are ≤5xULN). If symptoms resolve and CK levels return to normal, then consideration should be given to re-introducing Crestor 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 characterised by proximal muscle weakness and elevated serum creatine kinase, which persist despite discontinuation of statin treatment.
In few cases, statins have been reported to induce de novo or aggravate pre-existing myasthenia gravis or ocular myasthenia (see section 4.8). Crestor should be discontinued in case of aggravation of symptoms. Recurrences when the same or a different statin was (re-) administered have been reported.
In clinical trials, there was no evidence of increased skeletal muscle effects in the small number of patients dosed with Crestor 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. Therefore, the combination of Crestor and gemfibrozil is not recommended. The benefit of further alterations in lipid levels by the combined use of Crestor with fibrates or niacin should be carefully weighed against the potential risks of such combinations. The 40 mg dose is contraindicated with concomitant use of a fibrate (see sections 4.5 and 4.8).
Crestor must not be co-administered with systemic formulations of fusidic acid or within 7 days of stopping fusidic acid treatment. In patients where the use of systemic fusidic acid is considered essential, statin treatment should be discontinued throughout the duration of fusidic acid treatment. There have been reports of rhabdomyolysis (including some fatalities) in patients receiving fusidic acid and statins in combination (see section 4.5). Patients should be advised to seek medical advice immediately if they experience any symptoms of muscle weakness, pain or tenderness. Statin therapy may be re-introduced seven days after the last dose of fusidic acid. In exceptional circumstances, where prolonged systemic fusidic acid is needed, e.g. for the treatment of severe infections, the need for co-administration of Crestor and fusidic acid should only be considered on a case by case basis and under close medical supervision.
Crestor 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).
Severe cutaneous adverse reactions including Stevens-Johnson syndrome (SJS) and drug reaction with eosinophilia and systemic symptoms (DRESS), which could be life-threatening or fatal, have been reported with rosuvastatin (see section 4.8). At the time of prescription, patients should be advised of the signs and symptoms of severe skin reactions and be closely monitored. If signs and symptoms suggestive of this reaction appear, Crestor should be discontinued immediately and an alternative treatment should be considered.
If the patient has developed a serious reaction such as SJS or DRESS with the use of Crestor, treatment with Crestor must not be restarted in this patient at any time.
As with other HMG-CoA reductase inhibitors, Crestor 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 carried out prior to, and 3 months following, the initiation of treatment. Crestor 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 Crestor.
Pharmacokinetic studies show an increase in exposure in Asian subjects compared with Caucasians (see sections 4.2, 4.3 and 5.2).
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 Crestor in HIV patients receiving protease inhibitors and the potential for increased rosuvastatin plasma concentrations when initiating and up titrating Crestor doses in patients treated with protease inhibitors. The concomitant use with certain protease inhibitors is not recommended unless the dose of Crestor is adjusted. (See sections 4.2 and 4.5).
Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
Exceptional cases of interstitial lung disease have been reported with some statins, especially with long-term therapy (see section 4.8). Presenting features can include dyspnoea, non-productive cough and deterioration in general health (fatigue, weight loss and fever). If it is suspected a patient has developed interstitial lung disease, statin therapy should be discontinued.
Some evidence suggests that statins as a class raise blood glucose and in some patients, at high risk of future diabetes, may produce a level of hyperglycaemia where formal diabetes care is appropriate. This risk, however, is outweighed by the reduction in vascular risk with statins and therefore should not be a reason for stopping statin treatment. Patients at risk (fasting glucose 5.6 to 6.9 mmol/l, BMI >30 kg/m², raised triglycerides, hypertension) should be monitored both clinically and biochemically according to national guidelines.
In the JUPITER study, the reported overall frequency of diabetes mellitus was 2.8% in rosuvastatin and 2.3% in placebo, mostly in patients with fasting glucose 5.6 to 6.9 mmol/l.
The evaluation of linear growth (height), weight, BMI (body mass index), and secondary characteristics of sexual maturation by Tanner staging in paediatric patients 6 to 17 years of age taking rosuvastatin is limited to a two-year period. After two years of study treatment, no effect on growth, weight, BMI or sexual maturation was detected (see section 5.1).
In a clinical trial of children and adolescents receiving rosuvastatin for 52 weeks, CK elevations >10xULN and muscle symptoms following exercise or increased physical activity were observed more frequently compared to observations in clinical trials in adults (see section 4.8).
Rosuvastatin is a substrate for certain transporter proteins including the hepatic uptake transporter OATP1B1 and efflux transporter BCRP. Concomitant administration of Crestor with medicinal products that are inhibitors of these transporter proteins may result in increased rosuvastatin plasma concentrations and an increased risk of myopathy (see sections 4.2, 4.4 and 4.5 Table 1).
During concomitant treatment with Crestor and ciclosporin, rosuvastatin AUC values were on average 7 times higher than those observed in healthy volunteers (see Table 1). Crestor is contraindicated in patients receiving concomitant ciclosporin (see section 4.3). Concomitant administration did not affect plasma concentrations of ciclosporin.
Although the exact mechanism of interaction is unknown, concomitant protease inhibitor use may strongly increase rosuvastatin exposure (see Table 1). For instance, in a pharmacokinetic study, co-administration of 10 mg rosuvastatin and a combination product of two protease inhibitors (300 mg atazanavir/100 mg ritonavir) in healthy volunteers was associated with an approximately three-fold and seven-fold increase in rosuvastatin AUC and Cmax respectively. The concomitant use of Crestor and some protease inhibitor combinations may be considered after careful consideration of Crestor dose adjustments based on the expected increase in rosuvastatin exposure (see sections 4.2, 4.4 and 4.5 Table 1).
Concomitant use of Crestor and gemfibrozil resulted in a 2-fold increase in rosuvastatin Cmax and AUC (see section 4.4).
Based on data from specific interaction studies no pharmacokinetic relevant interaction with fenofibrate is expected, however a pharmacodynamic interaction may occur. Gemfibrozil, fenofibrate, other fibrates and lipid lowering doses (> or equal to 1 g/day) of niacin (nicotinic acid) increase the risk of myopathy when given concomitantly with HMG-CoA reductase inhibitors, probably because they can produce myopathy when given alone. The 40 mg dose is contraindicated with concomitant use of a fibrate (see sections 4.3 and 4.4). These patients should also start with the 5 mg dose.
Concomitant use of 10 mg Crestor and 10 mg ezetimibe resulted in a 1.2-fold increase in AUC of rosuvastatin in hypercholesterolaemic subjects (Table 1). A pharmacodynamic interaction, in terms of adverse effects, between Crestor and ezetimibe cannot be ruled out (see section 4.4).
The simultaneous dosing of Crestor with an antacid suspension containing aluminium and magnesium hydroxide resulted in a decrease in rosuvastatin plasma concentration of approximately 50%. This effect was mitigated when the antacid was dosed 2 hours after Crestor. The clinical relevance of this interaction has not been studied.
Concomitant use of Crestor and erythromycin resulted in a 20% decrease in AUC and a 30% decrease in Cmax of rosuvastatin. This interaction may be caused by the increase in gut motility caused by erythromycin.
Ticagrelor has been shown to increase rosuvastatin AUC by 2.3-fold, which may result in increased risk of myopathy. Consideration should be given to the benefits of prevention of major adverse cardiovascular events by use of rosuvastatin and the risks with increased rosuvastatin plasma concentrations.
Results from in vitro and in vivo studies show that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a poor substrate for these isoenzymes. Therefore, drug interactions resulting from cytochrome P450-mediated metabolism are not expected. No clinically relevant interactions have been observed between rosuvastatin and either fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4).
When it is necessary to co-administer Crestor with other medicinal products known to increase exposure to rosuvastatin, doses of Crestor should be adjusted. Start with a 5 mg once daily dose of Crestor if the expected increase in exposure (AUC) is approximately 2-fold or higher. The maximum daily dose of Crestor should be adjusted so that the expected rosuvastatin exposure would not likely exceed that of a 40 mg daily dose of Crestor taken without interacting medicinal products, for example a 20 mg dose of Crestor with gemfibrozil (1.9-fold increase), and a 10 mg dose of Crestor with combination ritonavir/atazanavir (3.1-fold increase).
If medicinal product is observed to increase rosuvastatin AUC less than 2-fold, the starting dose need not be decreased but caution should be taken if increasing the Crestor dose above 20 mg.
Table 1. Effect of co-administered medicinal products on rosuvastatin exposure (AUC; in order of decreasing magnitude) from published clinical trials:
| 2-fold or greater than 2-fold increase in AUC of rosuvastatin | ||
| Interacting drug dose regimen | Rosuvastatin dose regimen | Change in rosuvastatin AUC* |
| Sofosbuvir/velpatasvir/voxilaprevir (400 mg-100 mg-100 mg) + Voxilaprevir (100 mg) once daily for 15 days | 10 mg, single dose | 7.4 -fold ↑ |
| Ciclosporin 75 mg BID to 200 mg BID, 6 months | 10 mg OD, 10 days | 7.1-fold ↑ |
| Darolutamide 600 mg BID, 5 days | 5 mg, single dose | 5.2-fold ↑ |
| Belumosudil 200 mg QD, 8 days | 10 mg, single dose on 2 separate days | 4.6-fold ↑ |
| Regorafenib 160 mg, OD, 14 days | 5 mg, single dose | 3.8-fold ↑ |
| Enasidenib 100 mg OD, 28 days | 10 mg, single dose | 3.4-fold ↑ |
| Atazanavir 300 mg/ritonavir 100 mg OD, 8 days | 10 mg, single dose | 3.1-fold ↑ |
| Roxadustat 200 mg QOD | 10 mg, single dose | 2.9-fold ↑ |
| Momelotinib 200 mg OD, 5 days | 10 mg, single dose | 2.7-fold ↑ |
| Velpatasvir 100 mg OD | 10 mg, single dose | 2.7-fold ↑ |
| Ombitasvir 25 mg/paritaprevir 150 mg/ Ritonavir 100 mg OD/ dasabuvir 400 mg BID, 14 days | 5 mg, single dose | 2.6-fold ↑ |
| Teriflunomide | Not available | 2.5-fold ↑ |
| Vadadustat 600 mg OD, 8 days | 20 mg, single dose on 2 separate days | 2.47-fold ↑ |
| Grazoprevir 200 mg/elbasvir 50 mg OD, 11 days | 10 mg, single dose | 2.3-fold ↑ |
| Glecaprevir 400 mg/pibrentasvir 120 mg OD, 7 days | 5 mg OD, 7 days | 2.2-fold ↑ |
| Lopinavir 400 mg/ritonavir 100 mg BID, 17 days | 20 mg OD, 7 days | 2.1-fold ↑ |
| Capmatinib 400 mg BID | 10 mg, single dose | 2.1-fold ↑ |
| Tafamidis 61 mg BID on Days 1 & 2, followed by OD on Days 3 to 9 | 10 mg, single dose | 2.0-fold ↑ |
| Fostamatinib 100 mg twice daily | 20 mg, single dose | 2.0-fold ↑ |
| Febuxostat 120 mg OD | 10 mg, single dose | 1.9-fold ↑ |
| Gemfibrozil 600 mg BID, 7 days | 80 mg, single dose | 1.9-fold ↑ |
| Less than 2-fold increase in AUC of rosuvastatin | ||
| Interacting drug dose regimen | Rosuvastatin dose regimen | Change in rosuvastatin AUC* |
| Eltrombopag 75 mg OD, 5 days | 10 mg, single dose | 1.6-fold ↑ |
| Darunavir 600 mg/ritonavir 100 mg BID, 7 days | 10 mg OD, 7 days | 1.5-fold ↑ |
| Tipranavir 500 mg/ritonavir 200 mg BID, 11 days | 10 mg, single dose | 1.4-fold ↑ |
| Dronedarone 400 mg BID | Not available | 1.4-fold ↑ |
| Itraconazole 200 mg OD, 5 days | 10 mg, single dose | **1.4-fold ↑ |
| Ezetimibe 10 mg OD, 14 days | 10 mg, OD, 14 days | **1.2-fold ↑ |
| Decrease in AUC of rosuvastatin | ||
| Interacting drug dose regimen | Rosuvastatin dose regimen | Change in rosuvastatin AUC* |
| Erythromycin 500 mg QID, 7 days | 80 mg, single dose | 20% ↓ |
| Baicalin 50 mg TID, 14 days | 20 mg, single dose | 47% ↓ |
* Data given as x-fold change represent a simple ratio between co-administration and rosuvastatin alone. Data given as % change represent % difference relative to rosuvastatin alone.
Increase is indicated as "↑", decrease as "↓".
** Several interaction studies have been performed at different Crestor dosages, the table shows the most significant ratio
AUC = area under curve; OD = once daily; BID = twice daily; TID = three times daily; QD = once a day; QID = four times daily; QOD = every other day.
The following medical product/combinations did not have a clinically significant effect on the AUC ratio of rosuvastatin at coadministration:
Aleglitazar 0.3 mg 7 days dosing; Fenofibrate 67 mg 7 days TID dosing; Fluconazole 200mg 11 days OD dosing; Fosamprenavir 700 mg/ritonavir 100 mg 8 days BID dosing; Ketoconazole 200 mg 7 days BID dosing; Rifampin 450 mg 7 days OD dosing; Silymarin 140 mg 5 days TID dosing.
Physiologically-based pharmacokinetic modeling (PBPK) predicts no clinically relevant DDI between clopidogrel and rosuvastatin based on a dosage regimen of clopidogrel 300 mg loading dose, followed by 75 mg once a day (QD) maintenance dose.
As with other HMG-CoA reductase inhibitors, the initiation of treatment or dosage up-titration of Crestor in patients treated concomitantly with vitamin K antagonists (e.g. warfarin or another coumarin anticoagulant) may result in an increase in International Normalised Ratio (INR). Discontinuation or down-titration of Crestor may result in a decrease in INR. In such situations, appropriate monitoring of INR is desirable.
Concomitant use of Crestor and an oral contraceptive resulted in an increase in ethinyl estradiol and norgestrel AUC of 26% and 34%, respectively. These increased plasma levels should be considered when selecting oral contraceptive doses. There are no pharmacokinetic data available in subjects taking concomitant Crestor and HRT, therefore, a similar effect cannot be excluded. However, the combination has been extensively used in women in clinical trials and was well tolerated.
Digoxin:
Based on data from specific interaction studies no clinically relevant interaction with digoxin is expected.
Fusidic Acid:
Interaction studies with rosuvastatin and fusidic acid have not been conducted. The risk of myopathy, including rhabdomyolysis may be increased by the concomitant administration of systemic fusidic acid with statins. The mechanism of this interaction (whether it is pharmacodynamic or pharmacokinetic, or both) is yet unknown. There have been reports of rhabdomyolysis (including some fatalities) in patients receiving this combination.
If treatment with systemic fusidic acid is necessary, Crestor treatment should be discontinued throughout the duration of the fusidic acid treatment. Also see section 4.4.
Interaction studies have only been performed in adults. The extent of interactions in the paediatric population is not known.
Crestor is not recommended for use in pregnant women. Crestor should be discontinued as soon as pregnancy is recognized. However, the ongoing therapeutic need and the individual benefit risk in patients with very high risk of cardiovascular events should be considered.
Published data from use of statins in pregnant women have not identified a drug-associated risk of major congenital malformations. However, due to Crestor´s mechanism of action, there is a potential risk for adverse reactions in the foetus. The data is insufficient to assess the risk of miscarriage.
Breastfeeding is not recommended during treatment with CRESTOR. Limited data from published reports indicate that CRESTOR is present in human milk. Due to CRESTOR´s mechanism of action, there is a potential risk for adverse reactions in the infant. There is no available information on the effects of the drug on the breastfed infant or the effects of the drug on milk production.
Studies to determine the effect of Crestor on the ability to drive and use machines have not been conducted. However, based on its pharmacodynamic properties, Crestor is unlikely to affect this ability. When driving vehicles or operating machines, it should be taken into account that dizziness may occur during treatment.
The adverse reactions seen with Crestor are generally mild and transient. In controlled clinical trials, less than 4% of Crestor-treated patients were withdrawn due to adverse reactions.
Based on data from clinical studies and extensive post-marketing experience, the following table presents the adverse reaction profile for rosuvastatin. Adverse reactions listed below are classified according to frequency and system organ class (SOC).
The frequencies of adverse reactions are ranked according to the following convention: Common (≥1/100 to <1/10); Uncommon (≥1/1,000 to <1/100); Rare (≥1/10,000 to <1/1000); Very rare (<1/10,000); Not known (cannot be estimated from the available data).
Table 2. Adverse reactions based on data from clinical studies and post-marketing experience:
| System organ class | Common | Uncommon | Rare | Very rare | Not known |
| Blood and lymphatic system disorders | Thrombocytopenia | ||||
| Immune system disorders | Hypersensitivity reactions including angioedema | ||||
| Endocrine disorders | Diabetes mellitus1 | ||||
| Psychiatric disorders | Depression | ||||
| Nervous system disorders | Headache Dizziness | Polyneuropathy Memory loss | Peripheral neuropathy Sleep disturbances (including insomnia and nightmares) Myasthenia gravis | ||
| Eye disorders | Ocular myasthenia | ||||
| Respiratory, thoracic and mediastinal disorders | Cough Dyspnoea | ||||
| Gastro-intestinal disorders | Constipation Nausea Abdominal pain | Pancreatitis | Diarrhoea | ||
| Hepatobiliary disorders | Increased hepatic transaminases | Jaundice Hepatitis | |||
| Skin and subcutaneous tissue disorders | Pruritus Rash Urticaria | Stevens-Johnson syndrome, Drug reaction with eosinophilia and systemic symptoms (DRESS) Lichenoid drug eruption | |||
| Musculo-skeletal and connective tissue disorders | Myalgia | Myopathy (including myositis) Rhabdomyolysis Lupus-like syndrome Muscle rupture | Arthralgia | Tendon disorders, sometimes complicated by rupture Immune-mediated necrotising myopathy | |
| Renal and urinary disorders | Haematuria | ||||
| Reproductive system and breast disorders | Gynaecomastia | ||||
| General disorders and administration site conditions | Asthenia | Oedema |
1 Frequency will depend on the presence or absence of risk factors (fasting blood glucose ≥5.6 mmol/L, BMI >30 kg/m², raised triglycerides, history of hypertension).
As with other HMG-CoA reductase inhibitors, the incidence of adverse drug reactions tends to be dose dependent.
Renal effects: Proteinuria, detected by dipstick testing and mostly tubular in origin, has been observed in patients treated with Crestor. Shifts in urine protein from none or trace to ++ or more were seen in <1% of patients at some time during treatment with 10 and 20 mg, and in approximately 3% of patients treated with 40 mg. A minor increase in shift from none or trace to + was observed with the 20 mg dose. In most cases, proteinuria decreases or disappears spontaneously on continued therapy. Review of data from clinical trials and post-marketing experience to date has not identified a causal association between proteinuria and acute or progressive renal disease.
Haematuria has been observed in patients treated with Crestor and clinical trial data show that the occurrence is low.
Skeletal muscle effects: Effects on skeletal muscle e.g. myalgia, myopathy (including myositis) and, rarely, rhabdomyolysis with and without acute renal failure have been reported in Crestor-treated patients with all doses and in particular with doses >20 mg.
A dose-related increase in CK levels has been observed in patients taking rosuvastatin; the majority of cases were mild, asymptomatic and transient. If CK levels are elevated (>5xULN), treatment should be discontinued (see section 4.4).
A Cholesterol Treatment Trialists' (CTT) Collaboration meta-analysis in 2022 assessed 19 double-blind trials of statin versus placebo (n=123,940) and four double-blind trials of a more intensive versus a less intensive statin regimen (n=30,724).
The meta-analysis demonstrated statin therapy caused a small relative increase (3%) in the number of first reports of mild muscle pain or weakness largely confined to the first year of treatment. The meta-analysis also demonstrated an increase in first episode of muscle pain or weakness symptoms being more likely for intensive statin regimens compared to moderate/less intense statin regimens. Most (>90%) of all reports of muscle symptoms by participants allocated statin therapy were not due to the statin.
Liver effects: As with other HMG-CoA reductase inhibitors, a dose-related increase in transaminases has been observed in a small number of patients taking rosuvastatin; the majority of cases were mild, asymptomatic and transient.
The following adverse events have been reported with some statins:
Sexual dysfunction.
Exceptional cases of interstitial lung disease, especially with long term therapy (see section 4.4).
The reporting rates for rhabdomyolysis, serious renal events and serious hepatic events (consisting mainly of increased hepatic transaminases) is higher at the 40 mg dose.
Creatine kinase elevations >10xULN and muscle symptoms following exercise or increased physical activity were observed more frequently in a 52-week clinical trial of children and adolescents compared to adults (see section 4.4). In other respects, the safety profile of rosuvastatin was similar in children and adolescents compared to adults.
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme, Website: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.
Not applicable.
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