Hepatic Effects
As with other lipid-lowering agents of the same class, moderate (>3 x upper limit of normal [ULN]) elevations of serum transaminases have been reported following therapy with atorvastatin. Liver function was monitored during pre-marketing as well as post-marketing clinical studies of atorvastatin given at doses of 10, 20, 40 and 80 mg. 
Persistent increase in serum transaminases (>3 x ULN on two or more occasions) occurred in 0.7% of patients of who received atorvastation in these clinical trials. The incidence of these abnormalities was 0.2%, 0.2%, 0.6%, and 2.3% for the 10 mg, 20 mg, 40 mg, and 80 mg doses, respectively. 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 pre-treatment levels. Most patients continued treatment on a reduced dose of atorvastatin without sequelae.
Liver enzyme tests should be performed before initiated with statin and as required by clinic condition. Patients who develop increased transaminase levels should be monitored until the abnormality(ies) resolve(s). Should an increase in ALT or AST of >3 x ULN persist, reduction of dose or withdrawal of atorvastatin is recommended. Atorvastatin can cause an elevation in transaminases (see section Undesirable effects)
Atorvastatin 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 (see section Contraindications)
Skeletal Muscle Effects 
Myalgia has been reported in atorvastatin-treated patients (see section Undesirable effects). Creatine phosphokinase (CPK) should be performed before treatment in such cases as: kidney dysfunction, hypothyroidism, personal or family history of hereditary myopathy, history of myopathy acquired due to prior statin and fibrate use, history of liver disease and/or alcohol abuse, elderly patients (over 70 years old) at risk of rhabdomyolysis. If CPK result is 5 times higher than the normal level, treatment with statin should not be initiated. Myopathy, defined as muscle ache or muscle weakness in conjunction with increases in CPK values >10 x ULN, should be considered in any patient with diffuse myalgia, muscle tenderness or weakness, and/or marked elevation of CPK. Patients should be avoided to promptly report unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Atorvastatin therapy should be discontinued of markedly elevated CPK levels occur or if myopathy is diagnosed or suspected. The risk of myopathy during treatment with drugs in this class is increased with concurrent administration of cyclosporine, fibric acid derivatives, erythromycin, niacin, or azole antifungals, colchicine, telaprevir, boceprevir, or the combination of tipranavir/ritonavir. Many of these drugs inhibit cytochrome P450 3A4 metabolism and/or drug-transport. CYP 3A4 is the primary hepatic isozymes known to be involved in the biotransformation of atorvastatin.
Physicians considering combined therapy with atorvastatin and fibric acid derivatives, gemfibrozil, erythromycin, immunosuppressive drugs, azole antifungals, or lipid-modifying doses of niacin at high level (>1g/day), colchicine 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 drug. Therefore, lower starting and maintenance doses of atorvastatin should also be considered when taken concomitantly with the aforementioned drugs. The concurrent use of atorvastatin fusidic acid is not recommended, therefore, temporary suspension of atorvastation is advised during fusidic acid therapy (see section Interactions). Periodic CPK determinations may be considered in such situations, but there is no assurance that such monitoring will prevent the occurrence of severe myopathy. Atorvastatin may cause an elevation of CPK (see section Undesirable effects).
As with other drugs in this class, rare cases of rhabdomyolysis with acute renal failure secondary to myoglobinuria, have 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. Atorvastatin therapy should be temporarily withheld or discontinued 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).
Hemorrhagic Stroke 
In a post-hoc analysis of a clinical study in 4731 patients without CHD who had a stroke or transient ischemic attack (TIA) within the preceding 6 months and were initiated on atorvastatin 80 mg revealed a higher incidence of haemorrhagic stroke in the atorvastatin 80 mg group compared to placebo (55 atorvastatin vs. 33 placebo). Patients with haemorrhagic stroke on entry appeared to be at increased risk of recurrent haemorrhagic stroke (7 atorvastatin vs. 2 placebo). However, in patients treated with atorvastatin 80 mg, there were fewer stroke of any type (265 vs. 311) and fewer CHD events (123 vs. 204) (see section Pharmacodynamic properties and Pharmacokinetic properties)
Endocrine Function
Increase in hemoglobin A1c (HbA1c) and fasting serum glucose levels have been reported with 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, including atorvastatin. The risk of hyperglycemia, however, is outweighed by the reduction in vascular risk with statin.
The use of statin drugs for patients with risk factors leading muscle damage should be considered. Statin drugs pose the risks to cause adverse reactions on musculature, such as muscular atrophy, myositis, especially on patients with risk factors, such as over 65 years of age, patients with uncontrolled hypothyroidism, and patients with renal disease. Adverse reactions should be monitored closely during administration.
Before treatment, creatine kinase (CK) test should be performed in case of potential drug interactions and for some special patients. In these cases, benefits/risks should be considered and patients should be monitored clinically with statins. During treatment with statin, patients should inform their doctors if muscle signs are noticed, such as muscle pain, muscle stiffness, muscle weakness, etc. When those signs appear, CK test should be performed to take appropriate interventions.
Concomitant treatment with other medicinal products
Risk of rhabdomyolysis is increased when atorvastatin is administered concomitantly with certain medicinal products that may increase the plasma concentration of atorvastatin such as potent inhibitors of CYP3A4 or transport proteins (e.g. ciclosporin, telithromycin, clarithromycin, delavirdine, stiripentol, ketoconazole, voriconazole, itraconazole, posaconazole, letermovir and HIV protease inhibitors including ritonavir, lopinavir, atazanavir, indinavir, darunavir, tipranavir/ritonavir, etc). The risk of myopathy may also be increased with the concomitant use of gemfibrozil and other fibric acid derivates, antivirals for the treatment of hepatitis C (HCV) (boceprevir, telaprevir, elbasvir/grazoprevir), erythromycin, niacin or ezetimibe. If possible, alternative (non-interacting) therapies should be considered instead of these medicinal products.
In cases where co-administration of these medicinal products with atorvastatin is necessary, the benefit and the risk of concurrent treatment should be carefully considered. When patients are receiving medicinal products that increase the plasma concentration of atorvastatin, a lower maximum dose of atorvastatin is recommended. In addition, in the case of potent CYP3A4 inhibitors, a lower starting dose of atorvastatin should be considered and appropriate clinical monitoring of these patients is recommended (see section Interactions).   
Atorvastatin 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 Interactions). 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 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 Atorvastatin and fusidic acid should only be considered on a case by case basis and under close medical supervision.
Paediatric population
No clinically significant effect on growth and sexual maturation was observed in a 3-year study based on the assessment of overall maturation and development, assessment of Tanner Stage, and measurement of height and weight (see section Undesirable effects).
Interstitial lung disease
Exceptional cases of interstitial lung disease have been reported with some statins, especially with long term therapy (see section Undesirable effects). 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.
Excipient 
Lactose: Since lactose is found in the ingredients of the drug, do not use atorvastatin to patients with problems of lactose intolerance, lactase deficiency or glucose-galactose malabsorption.