Rostat 10
anti-Hypercholesterolemia
  • Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor for cholesterol. The primary site of action of rosuvastatin is the liver, the target organ for cholesterol lowering.
  • Rosuvastatin increases the number of hepatic LDL receptors on the cell-surface, enhancing uptake and catabolism of LDL and it inhibits the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.
  • Maximum rosuvastatin plasma concentrations are achieved approximately 5 hours after oral administration. The absolute bioavailability is approximately 20%.
  • Rosuvastatin undergoes limited metabolism (approximately 10%). In vitro metabol- ism studies using human hepatocytes indicate that rosuvastatin is a poor substrate for cytochrome P450-based metabolism. The main metabolites identified are the N-desmethyl and lactone metabolites. The N-desmethyl metabolite is approximat- ely 50% less active than rosuvastatin whereas the lactone form is considered clini- cally inactive. Rosuvastatin accounts for greater than 90% of the circulating HMG-CoA reductase inhibitor activity. -
  • Approximately 90% of the rosuvastatin dose is excreted unchanged in the faeces (consisting of absorbed and non-absorbed active substance) and the remaining part is excreted in urine. The plasma elimination half-life is approximately 19 hours.

Each film coated tablet of Rostat® 10 mg contains:

  • Rosuvastatin 10 mg ( rosuvastatin calcium)
  • Primary hypercholesterolaemia (type IIa including heterozygous familial hypercho lesterolaemia).
  •  mixed dyslipidaemia (type IIb) as an adjunct to diet when response to diet.
  • other non-pharmacological treatments (e.g. exercise, weight reduction) is inadequate.
  • Homozygous familial hypercholesterolaemia as an adjunct to diet and other lipid lowering treatments (e.g. LDL apheresis) or if such treatments are not appropriate.

 Rostat® is contraindicated:

  • In patients with hypersensitivity to rosuvastatin or to any of the excipients.
  • In patients with active liver disease including unexplained, persistent elevations of serum transaminases and any serum transaminase elevation exceeding 3 x the upper limit of normal (ULN). 
  • In patients with severe renal impairment (Cr CL < 30 mL/mini).
  • In patients with myopathy.
  • In patients receiving concomitant cyclosporin.
  • During pregnancy and lactation and in women of childbearing potential not using appropriate contraceptive measures.
  • The 40 mg dose is contraindicated in patients with pre-disposing factors for myopathy/ rhabdomyolysis. Such factors include: moderate renal impairment (creatinine clear- ance <60 ml/min), hypothyroidism, personal or family history of hereditary muscular disorders, previous history of muscular toxicity with another HMG-CoA reductase inhibitor or fibrate, alcohol abuse, situations where an increase in plasma levels may occur, Asian patients, or concomitant use of fibrates.
  • Cyclosporin.
  • Vitamin K antagonists.
  • Gemfibrozil and other lipid-lowering products.
  • Antacid.
  • Erythromycin.
  • Oral contraceptive/hormone replacement therapy (HRT).
  • Other medicinal products.
  • Cytochrome P450 enzymes.
  • Rostat® is contraindicated in pregnancy and lactation.

*the incidence of adverse drug reactions tends to be dose dependent.

*The adverse events seen with Rostat® are generally mild and transient. 

  • Common: (headache, dizziness, constipation, nausea, abdominal pain, myalgia, asthenia).
  • Uncommon: (pruritus, rash and urticaria).
  • Rare: (hypersensitivity reactions including angioedema, myopathy and rhabdomyolysis).
  • Renal effects: Proteinuria has been observed in patients treated with Rostat®. In most cases, proteinuria decreases or disappears spontaneously on continued therapy, and has not been shown to be predictive of acute or progressive renal disease.
  • Liver effects: 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.

Overdosage:

  • There is no specific treatment in the event of overdose. In the event of overdose, the patient should be treated symptomatically and supportive measures instituted as required.Liver function and CK levels should be monitored.
  • Haemodialysis is unlikely to be of benefit.

* Before treatment initiation the patient should be placed on a standard cholesterol- lowering diet that should continue during treatment.

*The dose should be individual- ised according to the goal of therapy and patient response.

*The recommended start dose: (5 mg or 10 mg orally once daily) in both 

  • Patients being treated for the first time with statin medicines.

  • patients switched from another HMG CoA reductase inhibitor.

(should take into account the individual patient’s cholesterol level and future cardiovascular risk as well as the potential risk for adverse reactions).

.( A dose adjustment to the next dose level can be made after 4 weeks, if necessary )

*Rostat® may be given at any time of day, with or without food.

*Pediatric use:(Safety and efficacy have not been established in children, therefore Rostat® is not recommended for pediatric use at this time).

*Geriatric use:(No dose adjustment is necessary).

  • should be prescribed Rostat® with caution in patients with pre-disposing factors for myopathy / rhabdomyolysis.
  • Whilst on treatment, patients should be asked to report inexplicable muscle pain, weakness or cramps immediately, particularly if associated with malaise or fever.
  • An assessment of renal function should be considered during routine follow-up of patients treated with a dose of 40 mg.
  • 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 reintroducing Rostat® or an alternative HMG-CoA reductase inhi-bitor at the lowest dose with close monitoring.
  • Routine monitoring of CK levels in asymptomatic patients is not warranted.
  • Rostat® 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).
  • Rostat® 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.
  • Rostat® should be discontinued or the dose reduced if the level of serum transaminases is greater than 3 times the upper limit of normal.
  • In patients with secondary hypercholesterolaemia caused by hypothyroidism or nephrotic syndrome, the underlying disease should be treated prior to initiating therapy with Rostat®.
  • Blister of 10 tablets, pack of 2 blisters.
  • Store below 25ºC, and protect from light.