Atorvastatin Tablets

Hypercholesterolaemia Atorvastatin Alkem is indicated:

• As an adjunct to diet for reduction of elevated total-cholesterol, LDL-cholesterol, apolipoprotein- B, triglyceride levels and to moderately increase HDL-cholesterol in patients with primary hypercholesterolaemia (heterozygous familial and non-familial hypercholesterolaemia) and combined/ mixed dyslipidaemia,
• To reduce total-C and LDL-C in patients with homozygous familial hypercholesterolaemia as an adjunct to other lipid-lowering treatments (e.g., LDL apheresis) or if such treatments are unavailable.

Paediatric patients (10 u2013 17 years of age): Atorvastatin Alkem is indicated as an adjunct to diet to reduce total-C, LDL-C, and apo B levels in boys and postmenarchal girls, > 10 to 17 years of age, with heterozygous familial hypercholesterolaemia if after an adequate trial of diet therapy, the following findings are present:

• a) LDL- C remains u2265 4,98 mmol/L (190 mg/dL) or
• b) LDL- C remains u2265 4,04 mmol/L (160 mg/dL) and:
• - There is a positive family history of premature cardiovascular disease or
• - Two or more other CVD risk factors are present in the paediatric patient.

Reduction of cardiovascular complications: In patients without clinically evident cardiovascular disease, and with or without dyslipidaemia, but with multiple risk factors for coronary heart disease such as smoking, hypertension, diabetes, low HDL-C, or a family history of early coronary heart disease, Atorvastatin Alkem is indicated to:

• Reduce the risk of ischaemic cardiovascular and cerebrovascular diseases.

Secondary reduction: Reduction of cardiovascular events in patients with clinically evident coronary heart disease and increased cholesterol levels. Therapy with lipid-lowering medicines should be a component of multiple-risk-factor intervention in individuals at increased risk of atherosclerotic vascular disease due to hypercholesterolaemia. Lipid-altering medicines should be used in addition to a diet restricted in saturated fat and cholesterol only when the response to diet and other non-pharmacological measures has been inadequate.

Prior to initiating therapy with Atorvastatin Alkem, secondary causes for hypercholesterolaemia (e.g., poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinaemia, obstructive liver disease, other medicine therapy, and alcoholism) should be excluded, and a lipid profile performed to measure total-C, LDL-C, HDL-C, and TG.

The patient should be placed on a standard cholesterol-lowering diet before receiving Atorvastatin Alkem and should continue with this diet during treatment with Atorvastatin Alkem.

Posology: The usual starting dose is 10 mg once a day and should be individualised according to the baseline LDL-C levels, the goal of therapy, and patient response. Adjustment of dosage should only be made after an interval of 4 weeks or more. The maximum recommended daily dose will depend on the indication (see below). Doses may be given at any time of day with or without food.

Primary hypercholesterolaemia and combined (mixed) hyperlipidaemia: Most patients are controlled with Atorvastatin Alkem 10 mg once a day. 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.

Heterozygous familial hypercholesterolaemia in paediatric patients (> 10 u2013 17 years of age): Experience in paediatrics is limited to a small number of patients (age 10 u2013 17 years) with severe dyslipidaemias, such as familial hypercholesterolaemia. Patients should be started with Atorvastatin Alkem 10 mg daily; the maximum recommended dose is 20 mg/day.

Homozygous familial hypercholesterolaemia: Most patients responded to a dose of Atorvastatin Alkem 80 mg, with a greater than 15 % reduction in LDL-C (18 % u2013 45 %).

Reduction of cardiovascular complications: The dosage range is 10 mg to 80 mg once daily.

Dosage in patients with renal insufficiency: Renal disease has no influence on the plasma concentrations or on the lipid effects of Atorvastatin Alkem; thus, no adjustment of dose is required (see section 4.4).

Dosage in patients with hepatic dysfunction: In patients with moderate to severe hepatic dysfunction, the therapeutic response to Atorvastatin Alkem is unaffected but serum levels of the medicine are greatly increased. In patients with chronic alcoholic liver disease, plasma concentrations of atorvastatin are markedly increased. Cmax and AUC are each 4-fold greater in patients with Child-Pugh A disease. Cmax and AUC are approximately 16-fold and 11-fold increased, respectively, in patients with Child-Pugh B disease. Therefore, caution with dosage should be exercised in patients who consume substantial quantities of alcohol and/or have a history of liver disease (see sections 4.4).

Method of administration: For oral use.

Atorvastatin Alkem is contraindicated in:

• Patients exhibiting hypersensitivity to the atorvastatin or to any of the excipients of Atorvastatin Alkem, listed in section 6.1,
• Active liver disease or unexplained persistent elevations of serum transaminases exceeding three times the upper limit of normal (see section 4.4),
• Concomitant use with rifampicin, diltiazem and grapefruit juice (see section 4.5),
• Patients with Child-Pugh B and C (liver cirrhosis),
• Patients treated with the hepatitis C antivirals glecaprevir/ pibrentasvir,
• Pregnancy and Lactation (see Section 4.6).

Liver effects: Persistent elevations (> 3 times the upper limit of normal (ULN) which occurred on 2 or more occasions) in serum transaminases occurred in 0,7 % of patients who received atorvastatin, as in Atorvastatin Alkem, in clinical trials. The incidence of these abnormalities was 0,2 %, 0,2 %, 0,6 % and 2,3 % for 10, 20, 40 and 80 mg respectively. It is recommended that liver function tests be performed before the initiation of treatment with Atorvastatin Alkem and repeated as clinically indicated. If serious liver injury with clinical symptoms and/or hyperbilirubinaemia or jaundice occurs during treatment with Atorvastatin Alkem, promptly interrupt therapy. If an alternate aetiology is not found, do not restart Atorvastatin Alkem. Atorvastatin Alkem should be used with caution in patients who consume substantial quantities of alcohol and/or have a history of liver disease. Active liver disease or unexplained persistent transaminase elevations are contraindications to the use of Atorvastatin Alkem (see Section 4.3).

Haemorrhagic stroke: Patients without coronary heart disease (CHD) who had a recent stroke or transient ischemic attack (TIA), within the preceding 6 months, and who were initiated on atorvastatin 80 mg, exhibited a high incidence of haemorrhagic stroke. The increased risk is evident in patients with prior haemorrhagic stroke or lacunar infarct at study entry. For patients with prior haemorrhagic stroke or lacunar infarct, the balance of risks and benefits of atorvastatin 80 mg is uncertain, and the potential risk of haemorrhagic stroke should be carefully considered before initiating treatment (see section 5.1).

Skeletal muscle: Rhabdomyolysis with or without renal impairment has been reported with the use of Atorvastatin Alkem. A history of renal impairment may be a risk factor for the development of rhabdomyolysis. Such patients merit closer monitoring for skeletal muscle effects. Myalgia has been reported in patients treated with Atorvastatin Alkem (see section 4.8). Myopathy, defined as muscle aching or muscle weakness in conjunction with increases in creatine phosphokinase (CPK) values greater than 10 times the upper limit of normal, should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevation of CPK. Patients should be advised to report promptly any unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Atorvastatin Alkem therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed or suspected. The risk of myopathy during treatment with Atorvastatin Alkem is increased with concurrent administration of immunosuppressive medicines, including ciclosporin, fibric acid derivatives, nicotinic acid, azole antifungals or erythromycin, colchicine, the hepatitis C protease inhibitor telaprevir, boceprevir, combinations of HIV protease inhibitors, including saquinavir plus ritonavir, lopinavir plus ritonavir, tipranavir plus ritonavir, darunavir plus ritonavir, fosamprenavir, and fosamprenavir plus ritonavir and cytochrome P450 inhibitors. Medical practitioners considering combined therapy with Atorvastatin Alkem and fibric acid derivatives, erythromycin, a combination of saquinavir plus ritonavir, lopinavir plus ritonavir, darunavir plus ritonavir, fosamprenavir, or fosamprenavir plus ritonavir, immunosuppressive medicines, azole antifungals, or lipid-modifying doses of niacin should carefully weigh the potential benefits and risks and should carefully monitor patients for any signs and symptoms of muscle pain, tenderness, or weakness, particularly during the initial months of therapy and during any periods of upward dosage titration of either medicine. Muscle-related adverse events have been reported with concomitant Atorvastatin Alkem and fusidic acid. Temporary suspension of Atorvastatin Alkem may be appropriate during fusidic acid therapy (see section 4.5). Atorvastatin Alkem therapy should be withdrawn in any patient with an acute, serious condition suggestive of a myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis, (e.g., severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures).

Protease inhibitors: Co-administration of Atorvastatin Alkem and protease inhibitors was associated with increased plasma concentrations of Atorvastatin Alkem.

Endocrine function: Increases in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including Atorvastatin Alkem.

The risk of myopathy during treatment with Atorvastatin Alkem is increased with concurrent administration of immunosuppressive medicines, including ciclosporin, fibric acid derivatives, niacin or cytochrome P450 3A4 inhibitors (macrolide antibiotics e.g., erythromycin, and azole antifungals e.g., clotrimazole) (see section 4.4 u2013 Skeletal muscle).

Inhibitors of cytochrome P450 3A4: Atorvastatin is metabolised by cytochrome P450 3A4 (CYP3A4), concomitant administration of medicines that are inhibitors of CYP3A4 may lead to increased plasma concentrations of atorvastatin and an increased risk of myopathy. The extent of interaction and potentiation of effects depends on the variability of effect on cytochrome P450 3A4 (see section 4.4). Potent CYP3A4 inhibitors have been shown to lead to markedly increased concentrations of atorvastatin (see Table 1 and specific information below). Co-administration of potent CYP3A4 inhibitors (e.g., ciclosporin, telithromycin, clarithromycin, delavirdine, stiripentol, ketoconazole, voriconazole, itraconazole, posaconazole, some antivirals used in the treatment of HCV (e.g., elbasvir/grazoprevir), and HIV protease inhibitors including ritonavir, lopinavir, atazanavir, indinavir, darunavir, etc.) should be avoided if possible. In cases where co-administration of these medicines with atorvastatin cannot be avoided lower starting and maximum doses of atorvastatin should be considered and appropriate clinical monitoring of the patient is recommended.

Moderate CYP3A4 inhibitors (e.g., erythromycin, diltiazem, verapamil, and fluconazole) may increase plasma concentrations of atorvastatin. An increased risk of myopathy has been observed with the use of erythromycin in combination with statins. Interaction studies evaluating the effects of amiodarone or verapamil on atorvastatin have not been conducted. Both amiodarone and verapamil are known to inhibit CYP3A4 activity and co-administration with atorvastatin may result in increased exposure to atorvastatin. Therefore, a lower maximum dose of atorvastatin should be considered, and appropriate clinical monitoring of the patient is recommended when concomitantly used with moderate CYP3A4 inhibitors. Appropriate clinical monitoring is recommended after initiation or following dose adjustments of the inhibitor.

Transport inhibitors: Inhibitors of transport proteins (e.g., ciclosporin, letermovir) may lead to increased plasma concentrations of atorvastatin and an increased risk of myopathy. The effect of inhibition of hepatic uptake transporters on atorvastatin concentrations in hepatocytes is unknown. If concomitant administration cannot be avoided, a dose reduction and clinical monitoring for efficacy is recommended. Use of atorvastatin is not recommended in patients taking letermovir co-administered with ciclosporin (see section 4.4).

Erythromycin/clarithromycin: Plasma concentrations of Atorvastatin Alkem increased approximately 40 % when co-administered with erythromycin, a known inhibitor of cytochrome P450 3A4 (see section 4.4 u2013 Skeletal muscle).

Combination of protease inhibitors: Plasma concentrations of atorvastatin increased significantly when co-administered with several combinations of HIV protease inhibitors, as well as with the hepatitis C protease inhibitor telaprevir, compared to that of Atorvastatin Alkem alone. Therefore, in patients taking the HIV protease inhibitor tipranavir plus ritonavir, or the hepatitis C protease inhibitor telaprevir, concomitant use of Atorvastatin Alkem should be avoided. Concomitant administration of Atorvastatin Alkem 10 mg single dose with tipranavir 500 mg twice daily plus ritonavir 200 mg twice daily for seven days, resulted in significant increase in atorvastatin AUC and Cmax. Atorvastatin Alkem does not change in pharmacokinetics of tipranavir plus ritonavir. Concomitant administration of Atorvastatin Alkem 20 mg single dose with telaprevir 750 mg every eight hours, for 10 days, resulted in similar increases in atorvastatin AUC and Cmax. Caution should be used when prescribing Atorvastatin Alkem in patients taking the HIV protease inhibitor lopinavir plus ritonavir, and the lowest dose necessary should be used. Concomitant administration of Atorvastatin Alkem 20 mg with lopinavir plus ritonavir (400 mg + 100 mg twice daily) resulted in a 5,9-fold increase in atorvastatin AUC. In patients taking the HIV protease inhibitors saquinavir plus ritonavir, darunavir plus ritonavir, fosamprenavir, or fosamprenavir plus ritonavir, the dose of Atorvastatin Alkem should not exceed 20 mg and should be used with caution. Concomitant administration of Atorvastatin Alkem 40 mg once a day for 4 days with saquinavir 400 mg twice daily plus ritonavir 400 mg twice daily for 15 days resulted in a 3,9-fold increase in atorvastatin AUC and 4,3-fold increase in atorvastatin Cmax. The dose of saquinavir plus ritonavir in this study is not the clinically used dose. The increase in atorvastatin exposure when used clinically is likely to be higher than what was observed in this study. Therefore, caution should be applied and the lowest dose necessary should be used. Concomitant administration of Atorvastatin Alkem 10 mg once a day for 4 days with darunavir 300 mg twice daily plus ritonavir 100 mg twice daily for 9 days resulted in a 3,4-fold increase in atorvastatin AUC and 2,3-fold increase in atorvastatin Cmax. Concomitant administration of Atorvastatin Alkem 10 mg once a day for 4 days with fosamprenavir 1 400 mg twice a day for 14 days resulted in a 2,3-fold increase in atorvastatin AUC and 4,0-fold increase in atorvastatin Cmax. Atorvastatin Alkem resulted in a 1,27-fold increase in fosamprenavir. Concomitant administration of Atorvastatin Alkem 10 mg once a day for 4 days with fosamprenavir 700 mg twice a day plus ritonavir 100 mg twice a day for 14 days resulted in a 2,5-fold increase in atorvastatin AUC and 2,8-fold increase in atorvastatin Cmax. Atorvastatin Alkem did not result in a change in pharmacokinetics of fosamprenavir 700 mg plus ritonavir. In patients taking nelfinavir, the dose of Atorvastatin Alkem should not exceed 40 mg daily. Concomitant administration of Atorvastatin Alkem 10 mg once a day for 28 days with nelfinavir 1 250 mg twice a day for 14 days resulted in a 74 % increase in atorvastatin AUC and 2,2-fold increase in atorvastatin Cmax. Concomitant administration of Atorvastatin Alkem 40 mg single dose with boceprevir 800 mg three times a day for 7 days resulted in a 2,3-fold increase in atorvastatin AUC and 2,66-fold increase in atorvastatin Cmax (see section 4.4 u2013 Skeletal muscle).

Gemfibrozil / fibric acid derivatives: The use of fibrates alone is occasionally associated with muscle related events, including rhabdomyolysis. The risk of these events may be increased with the concomitant use of fibric acid derivatives and atorvastatin. If concomitant administration cannot be avoided, the lowest dose of atorvastatin to achieve the therapeutic objective should be used and the patients should be appropriately monitored (see section 4.4).

Ezetimibe: The use of ezetimibe alone is associated with muscle related events, including rhabdomyolysis. The risk of these events may therefore be increased with concomitant use of ezetimibe and atorvastatin. Appropriate clinical monitoring of these patients is recommended.

Colestipol: Plasma concentrations of atorvastatin and its active metabolites were lower (ratio of atorvastatin concentration: 0.74) when colestipol was co-administered with Atorvastatin Alkem. However, lipid effects were greater when Atorvastatin Alkem and colestipol were co-administered than when either medicine was given alone.

Fusidic acid: 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, atorvastatin treatment should be discontinued throughout the duration of the fusidic acid treatment (see section 4.4).

Colchicine: Cases of myopathy have been reported with atorvastatin co-administered with colchicine, and caution should be exercised when prescribing atorvastatin with colchicine.

Diltiazem: Co-administration of Atorvastatin Alkem with diltiazem was associated with an increase in AUC of 51 % of Atorvastatin Alkem (see Section 4.4).

Cimetidine: Atorvastatin plasma concentrations and LDL-C reduction were not altered by co-administration of cimetidine.

Itraconazole: Co-administration of Atorvastatin Alkem 40 mg, single dose and itraconazole 200 mg, once daily, was associated with a 3,3-fold increase in AUC and a 20 % increase in Cmax.

Grapefruit juice: Contains one or more components that inhibit CYP 3A4 and can increase plasma concentrations of Atorvastatin Alkem by 2,5 to 3,3-fold and the combination should be avoided (see Section 4.4).

Digoxin: When multiple doses of digoxin and 10 mg atorvastatin were co-administered, steady-state digoxin concentrations increased slightly. Patients taking digoxin should be monitored appropriately.

Oral contraceptives: Co-administration of Atorvastatin Alkem with an oral contraceptive produced increases in plasma concentrations of norethindrone and ethinyl oestradiol.

Warfarin: Patients receiving chronic warfarin therapy, co-administration of atorvastatin 80 mg daily with warfarin caused a small decrease of about 1.7 seconds in prothrombin time during the first 4 days of dosing which returned to normal within 15 days of atorvastatin treatment. Although only less frequent cases of clinically significant anticoagulant interactions have been reported, prothrombin time should be determined before starting atorvastatin in patients taking coumarin anticoagulants and frequently enough during early therapy to ensure that no significant alteration of prothrombin time occurs. Once a stable prothrombin time has been documented, prothrombin times can be monitored at the intervals usually recommended for patients on coumarin anticoagulants. If the dose of atorvastatin is changed or discontinued, the same procedure should be repeated. Atorvastatin therapy has not been associated with bleeding or with changes in prothrombin time in patients not taking anticoagulants.

Inducers of cytochrome P450 3A: Concomitant administration of Atorvastatin Alkem with inducers of cytochrome P450 3A4 (e.g., efavirenz, rifampicin) can lead to variable reductions in plasma concentrations of Atorvastatin Alkem. Due to the dual interaction mechanism of rifampicin, simultaneous co-administration of Atorvastatin Alkem with rifampicin is not recommended as delayed administration of Atorvastatin Alkem after administration of rifampicin has been associated with a significant reduction in Atorvastatin Alkem plasma concentrations.

Antacids: Co-administration of an oral antacid suspension containing magnesium and aluminium hydroxides decreased plasma concentrations of Atorvastatin Alkem approximately 35 %; however, LDL-C reduction was not altered.

Antipyrine: Because Atorvastatin Alkem does not affect the pharmacokinetics of antipyrine, interactions with other medicines metabolised via the same cytochrome isozymes are not expected.

Azithromycin: Co-administration of Atorvastatin Alkem (10 mg once daily) and azithromycin (500 mg once daily) did not alter the plasma concentrations of Atorvastatin Alkem.

Amlodipine: Atorvastatin Alkem pharmacokinetics were not altered by the co-administration of Atorvastatin Alkem 80 mg and amlodipine 10 mg at steady state.

Other concomitant therapy: Atorvastatin Alkem used concomitantly with antihypertensive medicines and oestrogen replacement therapy does not show significant adverse interactions.

Women of child-bearing potential: Atorvastatin Alkem contraindicated in women of child-bearing potential not using adequate contraceptive measures. Atorvastatin Alkem should be administered to women of child-bearing age only when such patients are using adequate contraception and have been informed of the potential hazards to the foetus. An interval of one month should be allowed from stopping Atorvastatin Alkem treatment to conception in the event of planning a pregnancy.

Pregnancy: Atorvastatin Alkem contraindicated in pregnancy.

Breast-feeding: Atorvastatin Alkem contraindicated in mothers breastfeeding their infants.

Some adverse effects (e.g., dizziness, blurred vision and visual disturbances) may impair the patientu2019s ability to drive or operate or use machines.

Frequencies of reactions are ranked according to the following convention: Frequent; less frequent and frequency unknown. not known (cannot be estimated from the available data).

Infections and infestations: Frequent: nasopharyngitis. Less frequent: infection and flu syndrome

Blood and lymphatic system disorders: Less frequent: thrombocytopenia.

Injury and poisoning: Less frequent: accidental injury.

Immune system disorders: Frequent: allergic reactions. Less frequent: anaphylaxis.

Metabolism and nutrition disorders: Frequent: hyperglycaemia. Less frequent: hypoglycaemia, weight gain and anorexia.

Psychiatric disorders: Less frequent: nightmare and insomnia.

Nervous system disorders: Frequent: headache. Less frequent: dizziness, paraesthesia, hypoaesthesia, dysgeusia, amnesia and peripheral neuropathy.

Eye disorders: Less frequent: vision blurred and visual disturbance.

Ear and labyrinth disorders: Less frequent: tinnitus and hearing loss.

Respiratory, thoracic and mediastinal disorders: Frequent: pharyngo-laryngeal pain, epistaxis, sinusitis and pharyngitis.

Gastrointestinal disorders: Frequent: constipation, flatulence, dyspepsia, nausea and diarrhoea. Less frequent: vomiting, abdominal pain upper and lower, eructation, pancreatitis.

Hepatobiliary disorders: Less frequent: hepatitis, cholestasis and hepatic failure.

Skin and subcutaneous tissue disorders: Frequent: skin rash. Less frequent: urticaria, pruritus, alopecia, angioneurotic oedema, dermatitis bullous including erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis.

Musculoskeletal and connective tissue disorders: Less frequent: myalgia, arthralgia, pain in extremity, muscle spasms, joint swelling, back pain, neck pain, muscle fatigue, myopathy, myositis, rhabdomyolysis, muscle rupture, tendonopathy, sometimes complicated by rupture and lupus-like syndrome. Frequency unknown: immune mediated necrotizing myopathy (see section 4.4).

Reproductive system and breast disorders: Less frequent: erectile dysfunction, gynecomastia, and impotence.

General disorders and administration site conditions: Less frequent: malaise, asthenia, chest pain, peripheral oedema, fatigue, and pyrexia.

Investigations: Frequent: liver function test abnormal, blood creatine kinase increased. Less frequent: white blood cells urine positive. As with other HMG-CoA reductase inhibitors elevated serum transaminases have been reported in patients receiving Atorvastatin Alkem. These changes were usually mild, transient, and did not require interruption of treatment. Clinically important (> 3 times upper normal limit) elevations in serum transaminases occurred in 0.8 % patients on atorvastatin as in Atorvastatin Alkem. These elevations were dose related and were reversible in all patients. Elevated serum creatine kinase (CK) levels greater than 3 times upper limit of normal may occur on patients on atorvastatin, like other HMG-CoA reductase inhibitors. Levels above 10 times the normal upper range may occur in 0.4 % atorvastatin-treated patients (see section 4.4).

Paediatric population: Paediatric patients aged from 10 to 17 years of age treated with atorvastatin had infections as the most frequent adverse experience. Growth and sexual maturation were not affected when assessed using Tanner Stage tool, and measurement of height and weight. The safety profile in this group is similar to that in adults.

Reporting of suspected adverse reactions: Reporting suspected adverse reactions after authorisation of the medicine is important. It allows continued monitoring of the benefit/risk balance of the medicine. Healthcare professionals are asked to report any suspected adverse reactions to SAHPRA via the u201c6.04 Adverse Drug Reactions Reporting Formu201d, found online under SAHPRAu2019s publications: https://www.sahpra.org.za/Publications/Index/8 Alternatively all adverse events can be reported to Ascend Laboratories vial the e-mail: [email protected].

Specific treatment is not available for Atorvastatin Alkem overdose. Should an overdose occur, the patient should be treated symptomatically, and supportive measures instituted, as required. Liver function tests should be performed and serum CK levels should be monitored. Due to extensive atorvastatin binding to plasma proteins, haemodialysis is not expected to significantly enhance atorvastatin clearance.