Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/807
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Niaspan (Tablet, Extended Release)
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| dailymed-instance:dosage |
NIASPAN should be taken at bedtime, after a low-fat snack, and doses should
be individualized according to patient response. Therapy with NIASPAN must be initiated at 500 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 13 below.<br/>Maintenance Dose: The daily dosage of NIASPAN should not be increased by more than 500
mg in any 4-week period. The recommended maintenance dose is 1000
mg (two 500 mg tablets or one 1000 mg tablet) to 2000 mg (two 1000
mg tablets or four 500 mg tablets) once daily at bedtime. Doses greater than 2000 mg daily are not recommended. Women may
respond at lower NIASPAN doses than men (see CLINICAL PHARMACOLOGY, Gender
Effect). Single-dose bioavailability studies have demonstrated that two of
the 500 mg and one of the 1000 mg tablet strengths are interchangeable
but three of the 500 mg and two of the 750 mg tablet strengths are
not interchangeable. If lipid response to NIASPAN alone is insufficient
(see NCEP treatment guidelines; Table 10), or if higher doses of NIASPAN are not well tolerated,
some patients may benefit from combination therapy with a bile acid
binding resin or an HMG-CoA reductase inhibitor (see WARNINGS, PRECAUTIONS, Drug Interactions, Concomitant Therapy below, and CLINICAL PHARMACOLOGY, NIASPAN
Clinical Studies). Flushing of the skin may be reduced
in frequency or severity by pretreatment with aspirin (taken 30 minutes
prior to NIASPAN dose) or non-steroidal anti-inflammatory
drugs. 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. Equivalent doses of NIASPAN should not be substituted for sustained-release
(modified-release, timed-release) niacin preparations or immediate-release
(crystalline) niacin . Patients previously receiving
other niacin products should be started with the recommended NIASPAN titration schedule (see Table
13), and the dose should subsequently be individualized
based on patient response. If NIASPAN therapy is discontinued for an extended
period, reinstitution of therapy should include a titration phase
(see Table 13). NIASPAN tablets should be taken whole and should
not be broken, crushed or chewed before swallowing.<br/>Concomitant Therapy:<br/>Concomitant Therapy with Lovastatin: Patients
already receiving a stable dose of lovastatin who require further
TG-lowering or HDL-raising (e.g., to achieve NCEP non-HDL-C goals),
may receive concomitant dosage titration with NIASPAN per NIASPAN recommended initial titration schedule
. For
patients already receiving a stable dose of NIASPAN who require further LDL-lowering (e.g., to achieve NCEP LDL-C goals; Table 10), the usual recommended starting dose
of lovastatin is 20 mg once a day. Dose adjustments should be made
at intervals of 4 weeks or more. Combination therapy with NIASPAN and lovastatin should not exceed doses of 2000 mg and
40 mg daily, respectively.<br/>Dosage in Patients with Renal or Hepatic Insufficiency: Use of NIASPAN in patients with renal or hepatic insufficiency has
not been studied. NIASPAN is contraindicated in
patients with significant or unexplained hepatic dysfunction. NIASPAN should be used with caution in patients with renal insufficiency
.
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| dailymed-instance:descripti... |
NIASPAN (niacin extended-release tablets), contains niacin, which at therapeutic
doses is an antihyperlipidemic agent. Niacin (nicotinic acid, or
3-pyridinecarboxylic acid) is a white, crystalline powder, very soluble
in water, with the following structural formula: NIASPAN is an unscored, medium-orange, film-coated
tablet for oral administration and is available in three tablet strengths
containing 500, 750, and 1000 mg niacin. NIASPAN tablets also contain the inactive ingredients hypromellose, povidone,
stearic acid, and polyethylene glycol, and the following coloring
agents: FD&C yellow #6/sunset yellow FCF Aluminum Lake, synthetic
red and yellow iron oxides, and titanium dioxide.
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| dailymed-instance:clinicalP... |
Niacin functions in the
body after conversion to nicotinamide adenine dinucleotide (NAD) in
the NAD coenzyme system. Niacin (but not nicotinamide) in gram doses
reduces total cholesterol (TC), low-density lipoprotein cholesterol
(LDL-C) and triglycerides (TG), and increases high-density lipoprotein
cholesterol (HDL-C). The magnitude of individual lipid and lipoprotein
responses may be influenced by the severity and type of underlying
lipid abnormality. The increase in total HDL-C is associated with
an increase in apolipoprotein A-I (Apo A-I) and a shift inthe distribution
of HDL subfractions. These shifts include an increase in the HDL:HDLratio, and an elevation in lipoprotein A-I
(Lp A-I, an HDL particle containing only Apo A-I). Niacin treatment
also decreases serum levels of apolipoprotein B-100 (Apo B), the major
protein component of the very low-density lipoprotein (VLDL) and LDL
fractions, and of Lp(a), a variant form of LDL independently associated
with coronary risk.In addition, preliminary reports
suggest that niacin causes favorable LDL particle size transformations,
although the clinical relevance of this effect requires further investigation.
The effect of niacin-induced changes in lipids/lipoproteins on cardiovascular
morbidity or mortality in individuals without pre-existing coronary
disease has not been established. A variety of clinical studies have demonstrated that elevated levels
of TC, LDL-C, and Apo B promote human atherosclerosis. Similarly,
decreased levels of HDL-C are associated with the development of atherosclerosis.
Epidemiological investigations have established that cardiovascular
morbidity and mortality vary directly with the level of TC and LDL-C,
and inversely with the level of HDL-C. Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including
VLDL, intermediate-density lipoprotein (IDL), and their remnants,
can also promote atherosclerosis. Elevated plasma TG are frequently
found in a triad with low HDL-C levels and small LDL particles, as
well as in association with non-lipid metabolic risk factors for coronary
heart disease (CHD). As such, total plasma TG have not consistently
been shown to be an independent risk factor for CHD. Furthermore,
the independent effect of raising HDL-C or lowering TG on the risk
of coronary and cardiovascular morbidity and mortality has not been
determined.<br/>Mechanism of Action: The mechanism by
which niacin alters lipid profiles has not been well defined. 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.<br/>Pharmacokinetics/Metabolism:<br/>Absorption: Niacin is
rapidly and extensively absorbed (at least 60 to 76% of dose) when
administered orally. To maximize bioavailability and reduce the risk
of gastrointestinal (GI) upset, administration of NIASPAN with a low-fat meal or snack is recommended. Single-dose bioavailability studies have demonstrated that the 500
mg and 1000 mg tablet strengths are dosage form equivalent but the
500 mg and 750 mg tablet strengths are not dosage form equivalent.<br/>Distribution: Studies
using radiolabeled niacin in mice show that niacin and its metabolites
concentrate in the liver, kidney and adipose tissue.<br/>Metabolism: The pharmacokinetic
profile of niacin is complicated due to rapid and extensive first-pass
metabolism, which is species and dose-rate specific. In humans, one
pathway is through a simple conjugation step with glycine to form
nicotinuric acid (NUA). NUA is then excreted in the urine, although
there may be a small amount of reversible metabolism back to niacin.
The other pathway results in the formation of nicotinamide adenine
dinucleotide (NAD). It is unclear whether nicotinamide is formed
as a precursor to, or following the synthesis of, NAD. Nicotinamide
is further metabolized to at least N-methylnicotinamide (MNA) and
nicotinamide-N-oxide (NNO). MNA is further metabolized to two other
compounds, N-methyl-2-pyridone-5-carboxamide (2PY) and N-methyl-4-pyridone-5-carboxamide
(4PY). The formation of 2PY appears to predominate over 4PY in humans.
At the doses used to treat hyperlipidemia, these metabolic pathways
are saturable, which explains the nonlinear relationship between niacin
dose and plasma concentrations following multiple-dose NIASPAN administration. Nicotinamide does not have hypolipidemic activity; the activity of
the other metabolites is unknown.<br/>Elimination: Niacin and
its metabolites are rapidly eliminated in the urine. Following single
and multiple doses, approximately 60 to 76% of the niacin dose administered
as NIASPAN was recovered in urine as niacin and metabolites;
up to 12% was recovered as unchanged niacin after multiple dosing.
The ratio of metabolites recovered in the urine was dependent on
the dose administered.<br/>Special Populations:<br/>Niacin Clinical Studies: The role
of LDL-C in atherogenesis is supported by pathological observations,
clinical studies, and many animal experiments. Observational epidemiological
studies have clearly established that high TC or LDL-C and low HDL-C
are risk factors for CHD. Additionally, elevated levels of Lp(a)
have been shown to be independently associated with CHD risk.The efficacy of niacin in improving lipoprotein lipid profiles,
either alone or in combination with other lipid-altering drugs, as
an adjunct to diet therapy in the treatment of hyperlipoproteinemia
has been well documented. Niacin's ability to reduce mortality and the risk of definite,
nonfatal myocardial infarction (MI) has also been assessed in long-term
studies. The Coronary Drug Project,completed in 1975,
was designed to assess the safety and efficacy of niacin and other
lipid-altering drugs in men 30 to 64 years old with a history of MI.
Over an observation period of 5 years, niacin treatment was associated
with a statistically significant reduction in nonfatal, recurrent
MI. The incidence of definite, nonfatal MI was 8.9% for the 1,119
patients randomized to nicotinic acid versus 12.2% for the 2,789 patients
who received placebo (p<0.004). Total mortality was similar in the two groups at 5 years
(24.4% with nicotinic acid versus 25.4% with placebo; p = N.S.). At the time of a 15-year
follow-up, there were 11% (69) fewer deaths in the niacin group compared
to the placebo cohort (52.0% versus 58.2%; p = 0.0004).However, mortality at 15 years
was not an original endpoint of the Coronary Drug Project. In addition,
patients had not received niacin for approximately 9 years, and confounding
variables such as concomitant medication use and medical or surgical
treatments were not controlled. The Cholesterol-Lowering Atherosclerosis Study (CLAS) was a randomized,
placebo-controlled, angiographic trial testing combined colestipol
and niacin therapy in 162 non-smoking males with previous coronary
bypass surgery.The primary, per-subject cardiac endpoint
was global coronary artery change score. After 2 years, 61% of patients
in the placebo cohort showed disease progression by global change
score (n = 82), compared with only 38.8% of drug-treated subjects
(n = 80), when both native arteries and grafts were considered (p<0.005); disease regression also
occurred more frequently in the drug-treated group (16.2% versus 2.4%; p = 0.002). In a follow-up to this
trial in a subgroup of 103 patients treated for 4 years, again, significantly
fewer patients in the drug-treated group demonstrated progression
than in the placebo cohort (48% versus 85%, respectively; p<0.0001). The Familial
Atherosclerosis Treatment Study (FATS) in 146 men ages 62 and younger
with Apo B levels���125 mg/dL, established coronary artery
disease, and family histories of vascular disease, assessed change
in severity of disease in the proximal coronary arteries by quantitative
arteriography.Patients were given dietary counseling
and randomized to treatment with either conventional therapy with
double placebo (or placebo plus colestipol if the LDL-C was elevated);
lovastatin plus colestipol; or niacin plus colestipol. In the conventional
therapy group, 46% of patients had disease progression (and no regression)
in at least one of nine proximal coronary segments; regression was
the only change in 11%. In contrast, progression (as the only change)
was seen in only 25% in the niacin plus colestipol group, while regression
was observed in 39%. Though not an original endpoint of the trial,
clinical events (death, MI, or revascularization for worsening angina)
occurred in 10 of 52 patients who received conventional therapy, compared
with 2 of 48 who received niacin plus colestipol. The Harvard Atherosclerosis Reversibility Project (HARP) was a randomized
placebo-controlled, 2.5-year study of the effect of a stepped-care
antihyperlipidemic drug regimen on 91 patients (80 men and 11 women)
with CHD and average baseline TC levels less than 250 mg/dL and ratios
of TC to HDL-C greater than 4.0.Drug treatment consisted
of an HMG-CoA reductase inhibitor administered alone as initial therapy
followed by addition of varying dosages of either a slow-release nicotinic
acid, cholestyramine, or gemfibrozil. Addition of nicotinic acid
to the HMG-CoA reductase inhibitor resulted in further statistically
significant mean reductions in TC, LDL-C, and TG, as well as a further
increase in HDL-C in a majority of patients (40 of 44 patients).
The ratios of TC to HDL-C and LDL-C to HDL-C were also significantly
reduced by this combination drug regimen .<br/>NIASPAN Clinical
Studies:
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NIASPAN is contraindicated in patients with a known hypersensitivity to
niacin or any component of this medication, significant or unexplained
hepatic dysfunction, active peptic ulcer disease, or arterial bleeding.
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| dailymed-instance:supply |
NIASPAN tablets are supplied as unscored, medium-orange, film-coated, capsule-shaped
tablets containing 500, 750 or 1000 mg of niacin in an extended-release
formulation. Tablets are debossed KOS on one side and the tablet
strength (500, 750 or 1000) on the other side. Tablets are supplied
in bottles of 90 and 100 as shown below. 500
mg tablets: bottles of 90 - NDC# 0074-3074-90500 mg tablets: bottles of 100 - NDC# 0074-3074-11 750
mg tablets: bottles of 90 - NDC# 0074-3079-90750 mg tablets: bottles of 100 - NDC# 0074-3079-11 1000
mg tablets: bottles of 90 - NDC# 0074-3080-901000
mg tablets: bottles of 100 - NDC# 0074-3080-11 Store
at room temperature (20 to 25��C or 68 to 77��F).
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| dailymed-instance:inactiveI... |
dailymed-ingredient:FD&C_yellow_#6/sunset_yellow_FCF_Aluminum_Lake,
dailymed-ingredient:hypromellose,
dailymed-ingredient:polyethylene_glycol,
dailymed-ingredient:povidone,
dailymed-ingredient:stearic_acid,
dailymed-ingredient:synthetic_red_and_yellow_iron_oxides,
dailymed-ingredient:titanium_dioxide
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| dailymed-instance:precautio... |
General: Before instituting
therapy with NIASPAN an attempt should be made to
control hyperlipidemia with appropriate diet, exercise, and weight
reduction in obese patients, and to treat other underlying medical
problems (see INDICATIONS
AND USAGE). Patients with a past history of jaundice, hepatobiliary disease,
or peptic ulcer should be observed closely during NIASPAN therapy. Frequent monitoring of liver function tests and blood
glucose should be performed to ascertain that the drug is producing
no adverse effects on these organ systems. Diabetic patients may
experience a dose-related rise in glucose intolerance, the clinical
significance of which is unclear. Diabetic or potentially diabetic
patients should be observed closely. Adjustment of diet and/or hypoglycemic
therapy may be necessary. Caution should also be used when NIASPAN 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. Elevated uric acid levels
have occurred with niacin therapy, therefore use with caution in patients
predisposed to gout. NIASPAN has been associated with small but statistically
significant dose-related reductions in platelet count (mean of -11%
with 2000 mg). In addition, NIASPAN has been associated
with small but statistically significant increases in prothrombin
time (mean of approximately +4%); accordingly, patients undergoing
surgery should be carefully evaluated. Caution should be observed
when NIASPAN is administered concomitantly with anticoagulants;
prothrombin time andplatelet counts should be monitored closely in
such patients. In placebo-controlled trials, NIASPAN has been associated
with small but statistically significant, dose-related reductions
in phosphorus levels (mean of -13% with 2000 mg). Although these
reductions were transient, phosphorus levels should be monitored periodically
in patients at risk for hypophosphatemia. Niacin is rapidly metabolized by the liver, and excreted through
the kidneys. NIASPAN is contraindicated in patients
with significant or unexplained hepatic dysfunction and should be used with caution in patients with renal
dysfunction.<br/>Information for Patients: Patients should
be advised:<br/>Drug Interactions: HMG-CoA Reductase Inhibitors: See WARNINGS, Skeletal Muscle. Antihypertensive
Therapy: Niacin may potentiate the effects of ganglionic
blocking agents and vasoactive drugs resulting in postural hypotension. Aspirin: Concomitant
aspirin may decrease the metabolic clearance of nicotinic acid. The
clinical relevance of this finding is unclear. Bile Acid Sequestrants: An in vitro study was carried out investigating the niacin-binding
capacity of colestipol and cholestyramine. About 98% of available
niacin was bound to colestipol, with 10 to 30% binding to cholestyramine.
These results suggest that 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 NIASPAN. Other: Concomitant alcohol or hot drinks
may increase the side effects of flushing and pruritus and should
be avoided around the time of NIASPAN ingestion.
Vitamins or other nutritional supplements containing large doses
of niacin or related compounds such as nicotinamide may potentiate
the adverse effects of NIASPAN.<br/>Drug/Laboratory Test Interactions: Niacin may produce
false elevations in some fluorometric determinations of plasma or
urinary catecholamines. Niacin may also give false-positive reactions
with cupric sulfate solution (Benedict's reagent) in urine glucose
tests.<br/>Carcinogenesis, Mutagenesis, Impairment of Fertility: Niacin administered
to mice for a lifetime as a 1% solution in drinking water was not
carcinogenic. The mice in this study received approximately 6 to
8 times a human dose of 3000 mg/day as determined on a mg/mbasis. Niacin was negative for mutagenicity in the Ames
test. No studies on impairment of fertility have been performed.
No studies have been conducted with NIASPAN regarding
carcinogenesis, mutagenesis, or impairment of fertility.<br/>Pregnancy:<br/>Pregnancy Category C.: Animal reproduction
studies have not been conducted with niacin or with NIASPAN. It is also not known whether niacin at doses typically used for
lipid disorders can cause fetal harm when administered to pregnant
women or whether it can affect reproductive capacity. If a woman
receiving niacin for primary hypercholesterolemia (Types IIa or IIb)
becomes pregnant, the drug should be discontinued. If a woman being
treated with niacin for hypertriglyceridemia (Types IV or V) conceives,
the benefits and risks of continued therapy should be assessed on
an individual basis.<br/>Nursing Mothers: Niacin has been
reported to be excreted in human milk. 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 NIASPAN innursing mothers.<br/>Pediatric Use: Safety and effectiveness
of niacin therapy in pediatric patients (���16 years) have not
been established. No studies in patients under 21 years of age have
been conducted with NIASPAN.<br/>Geriatric Use: Of 979 patients
in clinical studies of NIASPAN, 21% of the patients
were age 65 and over. No overall differences in safety and effectiveness
were observed between these patients and younger 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.
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Supportive measures should
be undertaken in the event of an overdose.
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niacin
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Niaspan (Tablet, Extended Release)
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NIASPAN is generally well tolerated; adverse reactions have been mild and
transient. In the placebo-controlled clinical trials, flushing episodes
(i.e., warmth, redness, itching and/or tingling) were the most common
treatment-emergent adverse events (reported by as many as 88% of patients)
for NIASPAN. Spontaneous reports suggest that flushing
may also be accompanied by symptoms of dizziness, tachycardia, palpitations,
shortness of breath, sweating, chills, and/or edema, which in rare
cases may lead to syncope. In pivotal studies, fewer than 6% (14/245)
of NIASPAN patients discontinued dueto flushing.
In comparisons of immediate-release (IR) niacin and NIASPAN, although the proportion of patients who flushed was similar, fewer
flushing episodes were reported by patients who received NIASPAN. Following 4 weeks of maintenance therapy at daily
doses of 1500 mg, the incidence of flushing over the 4-week period
averaged 8.56 events per patient for IR niacin versus 1.88 following
NIASPAN. Other adverse events occurring in 5% or greater of patients treated
with NIASPAN, at least remotely related to NIASPAN, are shown in Table 12 below. In general, the incidence
of adverse events was higher in women compared to men. The following adverse events
have also been reported with NIASPAN or other niacin
products, either during clinical trials or in routine patient management. Body as a Whole: generalized edema; face edema; peripheral edema; asthenia;
chills Cardiovascular: atrial fibrillation and other cardiac arrhythmias; tachycardia;
palpitations; orthostasis; syncope; hypotension Eye: toxic amblyopia;
cystoid macular edema Gastrointestinal: activation of peptic ulcers
and peptic ulceration; jaundice; eructation; flatulence Metabolic: decreased
glucose tolerance; gout Musculoskeletal: myalgia;
myasthenia Nervous: dizziness; insomnia; leg cramps; nervousness; paresthesia Respiratory: dyspnea Skin: hyper-pigmentation;
acanthosis nigricans; maculopapular rash; urticaria; dry skin; sweating Other: migraine Hypersensitivity reactions: An
apparent hypersensitivity reaction has been reported rarely that has
included one or more of the following features: anaphylaxis, angioedema,
urticaria, flushing, dyspnea, tongue edema, larynx edema, face edema,
peripheral edema, laryngismus, and vesiculobullous rash.<br/>Clinical Laboratory Abnormalities: Chemistry: Elevations in serum transaminases
(see WARNINGS, Liver
Dysfunction), LDH, fasting glucose, uric acid,
total bilirubin, and amylase; reductions in phosphorus Hematology: Slight reductions in platelet
counts and prolongation in prothrombin time
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| dailymed-instance:warning |
NIASPAN preparations
should not be substituted for equivalent doses of immediate-release
(crystalline) niacin. For patients switching from immediate-release
niacin to NIASPAN, therapy with NIASPAN should be initiated with low doses (i.e., 500 mg
at bedtime) and the NIASPAN dose should then be titrated to the desired therapeutic
response .<br/>Liver Dysfunction: 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. NIASPAN should be used with caution in patients who consume
substantial quantities of alcohol and/or have a past history of liver
disease. Active liver diseases or unexplained transaminase elevations
are contraindications to the use of NIASPAN. Niacin preparations,
like some other lipid-lowering therapies, have been associated with
abnormal liver tests. In three placebo-controlled clinical trials
involving titration to final daily NIASPAN doses
ranging from 500 to 3000 mg, 245 patients received NIASPAN for a mean duration of 17 weeks. No patient with normal serum transaminase
levels (AST, ALT) at baseline experienced elevations to more than
3 times the upper limit of normal (ULN) during treatment with NIASPAN. In these studies, fewer than 1% (2/245) of NIASPAN patients discontinued due to transaminase elevations
greater than 2 times the ULN. In three safety and efficacy studies with a combination tablet of
NIASPAN and lovastatin involving titration to final
daily doses (expressed as mg of niacin/ mg of lovastatin) 500 mg/10
mg to 2500 mg/40 mg, ten of 1028 patients (1.0%) experienced reversible
elevations in AST/ALT to more than 3 times the upper limit of normal
(ULN). Three of ten elevations occurred at doses outside the recommended
dosing limit of 2000 mg/40 mg; no patient receiving 1000 mg/20 mg
had 3-fold elevations inAST/ALT. In the placebo-controlled clinical trials and the long-term extension
study, elevations in transaminases did not appear to be related to
treatment duration; elevations in AST levels did appear to be dose
related. Transaminase elevations were reversible upon discontinuation
of NIASPAN. Liver tests should be performed on all patients during therapy with
NIASPAN. Serum transaminase levels, including AST
and ALT (SGOT and SGPT), should be monitored before treatment begins,
every 6 to 12 weeks for the first year, and periodically thereafter
(e.g., at approximately 6-month intervals). 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. If the transaminase levels show evidence
of progression, particularly if they rise to 3 times ULN and are persistent,
or if they are associated with symptoms of nausea, fever, and/or malaise,
the drug should be discontinued.<br/>Skeletal Muscle: Rare cases of rhabdomyolysis
have been associated with concomitant administration of lipid-altering
doses (���1 g/day) of niacin and HMG-CoA reductase inhibitors.
In clinical studies with a combination tablet of NIASPAN and lovastatin, no cases of rhabdomyolysis and one suspected case
of myopathy have been reported in 1079 patients who were treated with
doses up to 2000 mg of NIASPAN and 40 mg of lovastatin
daily for periods up to 2 years. Physicians
contemplating combined therapy with HMG-CoA reductase inhibitors and
NIASPAN 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. Periodic serum creatine phosphokinase (CPK) and potassium determinations
should be considered in such situations, but there is no assurance
that such monitoring will prevent the occurrence of severe myopathy.
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| dailymed-instance:indicatio... |
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 hypercholesterolemia. 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 (see also Table 10 and the NCEP treatment guidelines). Prior to initiating
therapy with niacin, secondary causes for hypercholesterolemia (e.g.,
poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome,
dysproteinemias, obstructive liver disease, other drug therapy, alcoholism)
should be excluded, and a lipid profile obtained to measure TC, HDL-C,
and TG. After the LDL-C goal has
been achieved, if the TG is still���200 mg/dL, non-HDL-C (TC
minus HDL-C) becomes a secondary target of therapy. Non-HDL-C goals
are set 30 mg/dL higher than LDL-C goals for each risk category.
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Niaspan
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