Medically reviewed on May 1, Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hyperlipidemia. Niacin therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate. Niacin extended-release tablets should be taken at bedtime, after a low-fat snack, and doses should be individualized according to patient response.
Therapy with Niacin extended-release tablets must be initiated at mg at bedtime in order to reduce the incidence and severity of side effects which may occur during early therapy. The recommended dose escalation is shown in Table 1 below. If response to 1, mg daily is inadequate, increase dose adjustment for lipitor and hypothyroidism to dose adjustment for lipitor and hypothyroidism, mg daily; may subsequently increase dose to 2, mg daily.
Daily dose should not be increased more than mg in a 4-week period, and doses above 2, mg daily are not recommended. Women may respond at lower doses than men, dose adjustment for lipitor and hypothyroidism. Maintenance Dose The daily dosage of Niacin extended-release tablets should not be increased by more than mg in any 4-week period.
The recommended maintenance dose is 1, mg two mg tablets or one 1, mg tablet to 2, mg two 1, mg tablets or four mg tablets once daily at bedtime. Doses greater than 2, dose adjustment for lipitor and hypothyroidism, mg daily are not recommended. Women may respond at lower Niacin extended-release tablets doses than men [ see Clinical Studies Single-dose bioavailability studies have demonstrated that two of the mg and one of the 1, dose adjustment for lipitor and hypothyroidism, mg tablet strengths are interchangeable but three of the mg and two of the mg tablet strengths are not interchangeable.
Flushing of the skin [see Adverse Reactions 6. Tolerance to this flushing develops rapidly over the course of several weeks. Flushing, pruritus, and gastrointestinal distress are also greatly reduced by slowly increasing the dose of Niacin and avoiding administration on an empty stomach.
Concomitant alcoholic, hot drinks or spicy foods may increase the side effects of flushing and pruritus and should be avoided around the time of Niacin extended-release tablets ingestion. Equivalent doses of Niacin extended-release tablets should not be substituted for sustained-release modified-release, timed-release Niacin preparations or immediate-release crystalline Niacin [see Warnings and Precautions 5 ]. Patients previously receiving other Niacin products should be started with the recommended Niacin extended-release tablets titration schedule see Table 1and the dose should subsequently be individualized based on patient response.
If Niacin extended-release tablets therapy is discontinued for an extended period, reinstitution of therapy should include a titration phase see Table 1.
Niacin extended-release tablets should be taken whole and should not be broken, crushed or chewed before swallowing. Dosage in Patients with Renal or Hepatic Impairment Use of Niacin extended-release tablets in patients with renal or hepatic impairment has not been studied.
Niacin extended-release tablets are contraindicated in patients with significant or unexplained hepatic dysfunction. Niacin extended-release tablets should be used with caution in patients with renal impairment [see Warnings and Precautions 5 ]. Light orange to orange colored, capsule shaped, film coated tablets debossed with "CNI" on one side and plain on the other side. Niacin preparations should not be substituted for equivalent doses of immediate-release crystalline Niacin.
For patients switching from immediate-release Niacin to Niacin extended-release, therapy with Niacin extended-release should be initiated with low doses i. Caution should also be used when Niacin is used in patients with unstable angina or in the acute phase of an MI, particularly when such patients are also receiving vasoactive drugs such as nitrates, calcium channel blockers, or adrenergic blocking agents.
Niacin is rapidly metabolized by the liver, and excreted through the kidneys. Niacin is contraindicated in patients with significant or unexplained hepatic impairment [see Contraindications 4 and Warnings and Precautions 5. Patients with a past history of jaundice, hepatobiliary disease, or peptic ulcer should be observed closely during Niacin therapy.
Niacin extended-release tablets have not been shown to reduce cardiovascular morbidity or mortality among patients already treated with a statin. Dose adjustment for lipitor and hypothyroidism percent of patients were on background statin therapy prior to entering the trial.
On-treatment lipid changes at two years for LDL-C were HDL-C increased by Triglyceride levels decreased by The primary outcome was an ITT composite of the first study occurrence of coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, hospitalization for acute coronary syndrome or symptom-driven coronary or cerebral revascularization procedures.
The trial was stopped after a mean follow-up period of 3 years owing to a lack of efficacy. The primary outcome occurred in patients in the simvastatin plus Niacin group In an ITT analysis, there were 42 cases of first occurrence of ischemic stroke reported, 27 1.
The on-treatment ischemic stroke events were 19 for the simvastatin plus Niacin group and 15 for the simvastatin plus placebo group [see Adverse Reactions 6.
Elderly patients and patients with diabetes, renal failure, or uncontrolled dose adjustment for lipitor and hypothyroidism are particularly at risk. 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. Periodic serum creatine phosphokinase CPK and potassium determinations should be considered in such situations, dose adjustment for lipitor and hypothyroidism, but there is no assurance that such monitoring will prevent the occurrence of severe myopathy.
Cases of severe hepatic toxicity, including fulminant hepatic necrosis, have occurred in patients who have substituted sustained-release modified-release, timed-release Niacin products for immediate-release crystalline Niacin at equivalent doses.
Active liver diseases or unexplained transaminase elevations are contraindications to the use of Niacin extended-release tablets. Niacin preparations have been associated with abnormal liver tests.
In three placebo-controlled clinical trials involving titration to final daily Niacin doses ranging from to 3, mg, patients received Niacin for a mean duration of 17 weeks. Liver-related tests should be performed on all patients dose adjustment for lipitor and hypothyroidism therapy with Niacin.
Special attention should be paid to patients who develop elevated serum transaminase levels, and in these patients, measurements should be repeated promptly and then performed more frequently.
Increase in Blood Glucose: Niacin treatment can increase fasting blood glucose. Frequent monitoring of blood glucose should be performed to ascertain that the drug is producing no adverse effects. Diabetic patients may experience a dose-related increase in glucose intolerance. Reduction in platelet count: Caution should be observed when Niacin is administered concomitantly with anticoagulants; platelet counts should be monitored closely in such patients. Increase in Prothrombin Time PT: Caution should be observed when Niacin is administered concomitantly with anticoagulants; prothrombin time should be monitored closely in such patients.
Increase in Uric Acid: Elevated uric acid levels have occurred with Niacin therapy, therefore use with caution in patients predisposed to gout. Although these reductions were transient, phosphorus levels should be monitored periodically in patients at risk for hypophosphatemia. Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice.
In the placebo-controlled clinical trials, flushing episodes i. In comparisons of immediate-release IR Niacin and Niacin extended-release, although the proportion of patients who flushed was similar, fewer flushing episodes were reported by patients who received Niacin extended-release. Following 4 weeks of maintenance therapy at daily doses of 1, mg, the incidence of flushing over the 4-week period averaged 8. In general, the incidence of adverse events was higher in women compared to men.
There were 5 cases of rhabdomyolysis reported, 4 0. Because the below reactions are diabetes and alcohalism voluntarily from a population of uncertain size, it is generally not possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
The following additional adverse reactions have been identified during post-approval use of Niacin: Clinical Laboratory Abnormalities Chemistry: Elevations in serum transaminases [see Warnings and Precautions 5. Slight reductions in platelet counts and prolongation in prothrombin time [see Warnings and Precautions 5.
An in vitro study results suggest that the bile acid-binding resins have high Niacin binding capacity. Therefore, 4 to 6 hours, or as great an interval as possible, should elapse between the ingestion of bile acid-binding resins and the administration of Niacin [see Clinical Pharmacology Concomitant aspirin may decrease the metabolic clearance of nicotinic acid. The clinical relevance of this finding is unclear.
Niacin may potentiate the effects of ganglionic blocking agents and vasoactive drugs resulting in postural hypotension. Vitamins or other nutritional supplements containing large doses of Niacin or related compounds such as nicotinamide may potentiate the adverse effects of Niacin. Niacin may produce false elevations in some fluorometric determinations of plasma or urinary catecholamines.
Animal reproduction studies have not been conducted with Niacin or dose adjustment for lipitor and hypothyroidism Niacin extended-release tablets. If a woman receiving Niacin for primary hyperlipidemia becomes pregnant, the drug should be discontinued. If a woman being treated with Niacin for hypertriglyceridemia conceives, the benefits and risks of continued therapy should be assessed on an individual basis.
Niacin is excreted into human milk but the actual infant dose or infant dose as a percent of the maternal dose is not known. Because of the potential for serious adverse reactions in nursing infants from lipid-altering doses of nicotinic acid, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
No studies have been conducted with Niacin in nursing mothers. No overall differences in safety and effectiveness were observed between these patients and dose adjustment for lipitor and hypothyroidism patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out.
No studies have been performed in this population. Niacin should be used with caution in patients with renal impairment [see Warnings and Precautions 5 ]. Active liver disease, unexplained transaminase elevations and significant or unexplained hepatic dysfunction are contraindications to the use of Niacin [see Contraindications 4. Data from the clinical trials suggest that women have a greater hypolipidemic response than men at equivalent doses of Niacin. Niacin USP nicotinic acid, dose adjustment for lipitor and hypothyroidism, or 3-pyridinecarboxylic acid is a white crystals or crystalline powder, freely soluble in boiling water, and in solutions of alkali hydroxides and carbonate, sparingly soluble in water and practically insoluble in ether.
It is odourless or has a slight odour with the following structural formula:. Niacin extended-release tablets USP also contain the inactive ingredients: The mechanism by which Niacin alters lipid profiles has not been well defined, dose adjustment for lipitor and hypothyroidism.
It may involve several actions including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity, which may increase the rate of chylomicron triglyceride removal from plasma. Niacin decreases the rate of hepatic synthesis of VLDL and LDL, and does not appear to affect fecal excretion of fats, sterols, or bile acids, dose adjustment for lipitor and hypothyroidism. Absorption Due to extensive and saturable first-pass metabolism, Niacin concentrations in the general circulation are dose dependent and highly dose adjustment for lipitor and hypothyroidism. Time to reach the maximum Niacin plasma concentrations was about 5 hours following Niacin.