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Prior to initiating therapy with atorvastatin, secondary causes of hypercholesterolaemia (e. Lipitor is indicated in hypertensive patients with multiple risk factors for coronary heart disease (CHD) which may include diabetes, history of stroke or other cerebrovascular disease, peripheral vascular disease or existing asymptomatic CHD (see Section 5.

These effects do not replace the need to independently control known causes of cardiovascular (CV) mortality and morbidity such as hypertension, diabetes and smoking. Therapy should be individualised according to the target lipid levels, the recommended goal of therapy and the patient's response. Primary hypercholesterolaemia and mixed dyslipidaemia. The majority of patients are controlled with 10 mg Lipitor once daily. A therapeutic response is evident within 2 weeks, and the maximum response is usually achieved within 4 weeks.

The response is maintained during chronic therapy. Lipitor is for oral administration. It can be taken at any time of the day, with or without food. Use in renal impairment. Use in hepatic impairment. Plasma concentrations of atorvastatin are markedly increased in patients with chronic alcoholic liver disease (Child-Pugh B). The benefits of therapy should be weighed against the risks when atorvastatin is to be given to patients with hepatic insufficiency (see Section 4.

Use in combination with other medicinal compounds. Use of atorvastatin is not recommended in patients taking letermovir co-administered with ciclosporin. When atorvastatin and letermovir are administered concomitantly, do not exceed 20 mg atorvastatin daily (see Section 4. Appropriate clinical assessment is recommended to ensure that the lowest dose of atorvastatin necessary is used.

Hypersensitivity to any component of this medication. Active liver disease or unexplained persistent elevations of serum transaminases (see Section 4.

Pregnancy and lactation (see Section 4. Women of childbearing potential, unless on an effective contraceptive and highly unlikely to conceive. Concomitant use with fusidic acid (see Section 4. The incidence of these abnormalities was 0.

Increases were generally not associated with jaundice or other clinical signs or symptoms. When the dosage of atorvastatin was reduced, or drug treatment interrupted or discontinued, transaminase levels returned to pretreatment levels.

Most patients continued treatment on a reduced dose of Lipitor without sequelae. Patients who develop increased transaminase levels should be monitored until the abnormalities resolve.

Active liver disease or unexplained persistent transaminase elevations are contraindications to the use of atorvastatin (see Section 4. Uncomplicated myalgia has been reported in atorvastatin treated patients (see Section 4.

Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Lipitor therapy should be discontinued if markedly elevated CK levels occur or if myopathy is diagnosed or suspected. The risk of myopathy and rhabdomyolysis is increased with concurrent administration of drugs that increase the systemic concentration of atorvastatin (see Section 4. Lower starting and maintenance doses of atorvastatin should also be considered when taken concomitantly with the other aforementioned drugs (see Section 4.

There have been reports of rhabdomyolysis (including some fatalities) in patients receiving concomitant fusidic acid and statins (see Section 4. In patients where the use of systemic fusidic acid is considered essential, statin treatment should be discontinued throughout the duration of the fusidic acid treatment. The patient should be advised to seek medical advice immediately if they experience any symptoms of muscle weakness, pain or tenderness.

Statin therapy may be reintroduced seven days after the last dose of fusidic acid. Periodic CK determinations may be considered in such situations, although there is no assurance that such monitoring will prevent the occurrence of severe myopathy (see Section 4. As with other drugs in this class, rhabdomyolysis with acute renal failure has been reported. A history of renal impairment may be a risk factor for the development of rhabdomyolysis.

Such patients merit closer monitoring for skeletal muscle effects. Lipitor therapy should be temporarily withheld or discontinued in any patient with an acute, serious condition suggestive of a myopathy or with a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (e. Immune mediated necrotising myopathy. There have been rare reports of an immune-mediated necrotising myopathy (IMNM) during or after treatment with some statins.

IMNM is clinically characterised by persistent proximal muscle weakness and elevated serum creatinine kinase, which persists despite discontinuation of statin treatment. Throughout the study, all cause mortality was numerically higher in the atorvastatin arm than the placebo arm. At study end all cause mortality was 9. The increased risk of haemorrhagic stroke was observed in patients who entered the study with prior haemorrhagic stroke (15.

All cause mortality was also increased in these patients with prior haemorrhagic stroke (15. The potential risk of haemorrhagic stroke should be carefully considered before initiating treatment with atorvastatin in patients with recent (1-6 months) stroke or TIA.

Clinical studies have shown that atorvastatin does not reduce basal plasma cortisol concentration nor impair adrenal reserve. The effects of HMG-CoA reductase inhibitors on male fertility have not been studied in adequate numbers of patients.

The effects, if any, on the pituitary gonadal axis in premenopausal women are unknown. Caution should be exercised if an HMG-CoA reductase inhibitor is administered concomitantly with other drugs that may decrease the levels or activity of endogenous steroid hormones such as ketoconazole, spironolactone and cimetidine. Increases in haemoglobin A1c (HbA1c) and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including atorvastatin.

Effect on ubiquinone levels (COQ10). Significant decreases in circulating ubiquinone levels in patients treated with atorvastatin and other statins have been observed. The clinical significance of a potential long term, statin induced deficiency of ubiquinone has not been established.