|Composition||Atorvastatin 10,20,40 and 80mg Tablets.|
|Indication||Mixed dyslipidaemia; Heterozygous familial; Nonfamilialhypercholesterolaemia|
|Mechanism of Action||
Atorvastatin competitively inhibits HMG-CoA reductase, the enzyme that catalyses the conversion of HMG-CoA to mevalonate. This results in the induction of the LDL receptors and stimulation of LDL catabolism, leading to lowered LDL-cholesterol levels.
Absorption: Readily absorbed from the GI tract. Bioavailability: Approx 12%.
Distribution: Volume of distribution: Approx 381 L. Plasma protein binding: 98%.
Metabolism: Metabolised by CYP3A4 isoenzyme to active ortho- and parahydroxylatedderivates and an inactive β-oxidation product.
Excretion: Via faeces (as metabolites); urine 2% as unchanged drug). Elimination half-life: Approx 14 hr.
Headache, flatulence, constipation, dyspepsia, nausea, diarrhoea, vomiting, anorexia. Pain in extremity, musculoskeletal and pharyngolaryngeal; myopathy, muscle spasms, myalgia, arthralgia, nasopharyngitis, insomnia, UTI. Increased serum aminotransferase, glycosylated haemoglobin and fasting serum glucose levels.
Potentially Fatal: Severe rhabdomyolysis w/ acute renal failure. Hepatitis, pancreatitis. Rarely, Stevens-Johnson syndrome, anaphylaxis, toxic epidermal necrolysis.
|Drug drug interaction||
May increase risk of myopathy and rhabdomyolysis w/ CYP3A4 potent inhibitor (e.g. HIV or HCV protease inhibitors, itraconazole, clarithromycin), fenofibrate, colchicines, fixed combination of lopinavir/ritonavir. May decrease plasma concentration w/ CYP3A4 inducer (e.g. rifampicin, efavirenz). May significantly increase AUC and peak plasma concentration of digoxin. Increased AUC for norethindrone and ethinylestradiol.
Potentially Fatal: Increased risk of myopathy or rhabdomyolysis w/ ciclosporin, gemfibrozil, telaprevir, tipranavir.
History of liver disease; patients who consume substantial quantities of alcohol; patients w/ risk factors for myopathy or rhabdomyolysis. Hypothyroidism should be properly managed prior to statin therapy initiation. Renal impairment. Childn 10 yr. Premenarcheal females. Monitoring Parameters Monitor creatine kinase (CK) periodically and LFT. Discontinue if there is significant or persistent increase in CK levels, serum aminotransferase levels or evidence of myopathy.
Mixed dyslipidaemia ; Heterozygous familial
Adult: Initially, 10 or 20 mg once daily, may be adjusted at 4-wk interval. May initiate 40 mg once daily in patients who require >45% reduction in LDL-cholesterol. Max: 80 mg/day.
Child: Heterozygous familial hypercholesterolaemia: 10-17 yr 10 mg once daily, may increase at intervals of at least 4 wk to max 20 mg/day.
Elderly: No dosage adjustment needed.
Renal impairment: No dosage adjustment needed..