NIACIN SUSTAINED RELEASE
Action And Clinical Pharmacology: Nicotinic acid, when released, is readily absorbed from the gastrointestinal tract following oral administration and widely distributed in the body fluids and tissues, even in the breast milk. The main route of metabolism in the liver is conversion first to nicotinamide then to N-methyl nicotinamide, the 2-pyridone and 4-pyridone derivatives and nicotinuric acid formed which are excreted in the urine. Small amounts of nicotinic acid and nicotinamide are excreted unchanged in the urine following therapeutic doses; however, the amount excreted unchanged is increased with larger doses.
Both nicotinic acid and nicotinamide have vitamin activity but only nicotinic acid induces vasodilation resulting in flushing, a sensatiokn of heat, faintness and a pounding of the head. This vasodilation occurs within 20 minutes of oral administration and persists for about 20 to 60 minutes. Tolerance usually develops after 2 weeks of treatment. Sustained release niacin tablets induce less vasodilation than unmodified-release forms.
Nicotinic acid is converted to nicotinamide which is a constituent of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) which are co-enzymes involved in glycogenolysis, lipid metabolism and tissue respiration for electron transfer reactions. Deficiency results in pellagra, characterized by skin lesions, gastrointestinal, neurological and mental distrubances. Hence use as prophylactic and therapeutic vitamin.
Nicotinic acid also lowers both total serum cholesterol and triglyceride concentrations probably by reducing the synthesis of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). It also elevates the high-density lipoprotein cholesterol (HDL). This effect on the plasma lipids occurs at daily dosages exceeding 1 g.
Niacin may also increase gastric motility and acid secretion via the release of histamine, therein may aggravate or initiate peptic ulcer. High dosages of niacin may decrease uric acid excretion or impair glucose tolerance thereby precipitating a bout of gout or hypoglycemia. Postural hypotension may occur in patients already hypotensive due to the additional vasodilative effect.
Indications And Clinical Uses: For the prophylaxis and treatment of vitamin B3 deficiency states such as pellagra; and supplementation due to increased requirements in conditions such as diabetes mellitus; malignancy; inborn errors of metabolism (Hartup disease); malabsorption syndromes associated with pancreatic insufficiency; diseases of the small intestines (e.g. celiac and tropical sprue); hyperthyroidism and others.
Niacin has also been used in the treatment of primary hyperlipidemia (Type IIa & b, III, IV or V hyperlipoproteinemia) as a drug of first choice for initiating therapy to redule LDL-cholesterol concentrations and triglycerides and to increase HDL-cholesterol concentrations. Slow release niacin has particularly been used where it was desirable to minimize flushing and associated symptoms which occur at initiation of therapy; but therapy must be carefully monitored by a physician particularly for liver enzymes.
Contra-Indications: Contraindication is not absolute but careful risk-benefit consideration must be given when treating patients with a history of gout, diabetes mellitus, peptic ulcer, liver dysfunction, sever hypotension or arterial bleeding or hemorrhage. Not recommended for persons hypersensitive to niacin and children below the age of 12.
Precautions: Pregnancy, Lactation, Children and Geriatrics: Problems during pregnancy and breastfeeding, when treating pediatrics and geriatrics have not been well documented; therefore, appropriate monitoring should be observed particularly during initiation of therapy.
Isoniazid may cause deficiency by inhibiting niacin incorporation into nicotinamide adenine dinucleotide (NAD). Also chenodiol’s effect may be reduced because of the resulting increase in cholesterol in the bile.
Urinary catecholamine concentration measurements by fluorimetric methods may be falsely elevated by niacin, while a positive urine glucose determination using Benedict’s reagent (cupric sulfate) may be falsely produced by niacin.
All subjects should be monitored for liver function during niacin therapy.
Adverse Reactions: Water soluble vitamins seldom cause toxicity in persons with normal renal function. However, flushing or redness of the skin, especially on face and neck; feeling of warmth, headache or an allergic reaction may occur but usually subside in 2 weeks.
At higher doses, diarrhea, dizziness or faintness, dryness of skin or eyes; nausea or vomiting; aggravation of peptic ulcer causing stomach pain; pruritus; hyperglycemia; hyperuricemia; cardiac arrhythmias and hepatotoxicity are more likely to occur.
Dosage And Administration: Vitamin: Use up to 500 mg a day taken with milk or meals. Swallow whole without crushing or chewing but tablet may be broken in half if a smaller dose is desired.
Antihyperlipidemic: 1 g 2 or 3 times a day, the dosage being increased in increments of 500 mg a day every 2 to 4 weeks as needed and tolerated. Maintenance dosages range from 1 to 2 g 2 or 3 times a day to a maximum of 6 g a day. Tablets may be broken but not crushed or chewed before swallowing. Flushing may be reduced by taking a 325 mg ASA tablet, 1 hour prior to the niacin tablet.
Availability And Storage: Each elongated, oval, sustained release tablet contains: nicotinic acid (niacin) 500 mg. Nonmedicinal ingredients: carnauba wax, glyceryl behenate and magnesium stearate. Bottles of 100.
NIACIN SUSTAINED RELEASE Stanley Nicotinic Acid Vitamin