NIACIN (VITAMIN B3, NICOTINIC ACID)

NIACIN (VITAMIN B₃, NICOTINIC ACID)
(nye'a-sin)
Niacor, Niaspan, Nicobid, Nico-400, Nicotinex, Novoniacin

, Slo-Niacin, Tri-B3

NIACINAMIDE (NICOTINAMIDE)
Classifications: vitamin b₃; antilipemic; lipid-lowering agent;
Therapeutic: vitamin b₃; lipid-lowering agent
Pregnancy Category: C

Availability

50 mg, 100 mg, 250 mg, 500 mg tablets; 125 mg, 250 mg, 400 mg, 500 mg, 750 mg, 1000 mg sustained release tablets, capsules

Action

Water-soluble, heat-stable, B-complex vitamin (B₃) that functions with riboflavin as a control agent in coenzyme system that converts protein, carbohydrate, and fat to energy through oxidation-reduction. Niacinamide, an amide of niacin, is used as an alternative in the prevention and treatment of pellagra.

Therapeutic Effect

Produces vasodilation by direct action on vascular smooth muscles. Inhibits hepatic synthesis of VLDL, cholesterol, and triglyceride, and, indirectly, LDL. Large doses effectively reduce elevated serum cholesterol and total lipid levels in hypercholesterolemia and hyperlipidemic states.

Uses

In prophylaxis and treatment of pellagra, usually in combination with other B-complex vitamins, and in deficiency states accompanying carcinoid syndrome, isoniazid therapy, Hartnup's disease, and chronic alcoholism. Also in adjuvant treatment of hyperlipidemia (elevated cholesterol or triglycerides) in patients who do not respond adequately to diet or weight loss. Also as vasodilator in peripheral vascular disorders, M?nière's disease, and labyrinthine syndrome, as well as to counteract LSD toxicity and to distinguish between psychoses of dietary and nondietary origin.

Contraindications

Hypersensitivity to niacin; hepatic impairment; severe hypotension; hemorrhaging or arterial bleeding; active peptic ulcer; pregnancy (category C), lactation, and children <16 y.

Cautious Use

History of gallbladder disease, liver disease, and peptic ulcer; severe renal impairment; glaucoma; angina; coronary artery disease; diabetes mellitus; predisposition to gout; allergy; thrombocytopenia.

Route & Dosage

Niacin Deficiency
Adult: PO 10–20 mg/d

Pellagra
Adult: PO 50–100 mg 3–4 times/d
Child: PO 50–100 mg t.i.d.

Hyperlipidemia
Adult: PO 1.5–3 g/d in divided doses, may increase up to 6 g/d if necessary
Child: PO 100–250 mg/d in 3 divided doses, may increase by 250 mg/d q2–3wk as tolerated

Administration

Oral

Give oral drug with meals to decrease GI distress. Give with cold water (not hot beverage) to facilitate swallowing.
Ensure that sustained release form is not chewed or crushed. It must be swallowed whole.
Store at 15°–30° C (59°–86° F) in a light and moisture proof container.

Adverse Effects (≥1%)

CNS: Transient headache, tingling of extremities, syncope. With chronic use: nervousness, panic, toxic amblyopia, proptosis, blurred vision, loss of central vision. CV: Generalized flushing with sensation of warmth, postural hypotension, vasovagal attacks, arrhythmias (rare). GI: Abnormalities of liver function tests; jaundice, bloating, flatulence, nausea, vomiting, GI disorders, activation of peptic ulcer, xerostomia. Skin: Increased sebaceous gland activity, dry skin, skin rash, pruritus, keratitis nigricans. Metabolic: Hyperuricemia, hyperglycemia, glycosuria, hypoprothrombinemia, hypoalbuminemia.

Diagnostic Test Interference

Niacin causes elevated serum bilirubin, uric acid, alkaline phosphatase, AST, ALT, LDH levels and may cause glucose intolerance. Decreases serum cholesterol 15–30% and may cause false elevations with certain fluorometric methods of determining urinary catecholamines. Niacin may cause false-positive urine glucose tests using copper sulfate reagents, (e.g., Benedict's solution).

Interactions

Drug: Potentiates hypotensive effects of antihypertensive agents.

Pharmacokinetics

Absorption: Readily from GI tract. Peak: 20–70 min. Distribution: Into breast milk. Metabolism: In liver. Elimination: Primarily in urine. Half-Life: 45 min.

Nursing Implications

Assessment & Drug Effects

Monitor therapeutic effectiveness and record effect of therapy on clinical manifestations of deficiency (fiery red tongue, excessive saliva secretion and infection of oral membranes, nausea, vomiting, diarrhea, confusion). Therapeutic response usually begins within 24 h.
Lab tests: Obtain baseline and periodic tests of blood glucose and liver function in patients receiving prolonged high dose therapy.
Monitor diabetics and patients on high doses closely. Hyperglycemia, glycosuria, ketonuria, and increased insulin requirements have been reported.
Observe patients closely for evidence of liver dysfunction (jaundice, dark urine, light-colored stools, pruritus) and hyperuricemia in patients predisposed to gout (flank, joint, or stomach pain; altered urine excretion pattern).

Patient & Family Education

Be aware that you may feel warm and flushed in face, neck, and ears within first 2 h after oral ingestion and immediately after parenteral administration and may last several hours. Effects are usually transient and subside as therapy continues.
Sit or lie down and avoid sudden posture changes if you feel weak or dizzy. Report these symptoms and persistent flushing to your physician. Relief may be obtained by reduction of dosage, increasing subsequent doses in small increments, or by changing to sustained release formulation.
Be aware that alcohol and large doses of niacin cause increased flushing and sensation of warmth.
Avoid exposure to direct sunlight until lesions have entirely cleared if you have skin manifestations.

Common adverse effects in italic, life-threatening effects underlined; generic names in bold; classifications in SMALL CAPS; Canadian drug name; Prototype drug

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