P - Caution when used during pregnancy
L - Caution when used during lactation
LI - Lab *
Niacin, also known as vitamin B3 or nicotinic acid, is an organic compound with the formula C5H4NCO2H. This colourless, water-soluble solid is a derivative of pyridine, with a carboxyl group (COOH) at the 3-position. Other forms of vitamin B3 include the corresponding amide, nicotinamide ("niacinamide"), where the carboxyl group has been replaced by a carboxamide group (CONH2), as well as more complex amides and a variety of esters. The terms niacin, nicotinamide, and vitamin B3 are often used interchangeably to refer to any member of this family of compounds, since they have the same biochemical activity.
Niacin is converted to nicotinamide and then to NAD and NADP in vivo. Although the two are identical in their vitamin activity, nicotinamide does not have the same pharmacological effects as niacin, which occur as side-effects of niacin's conversion. Nicotinamide does not reduce cholesterol or cause flushing. Nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults. Niacin is a precursor to NADH, NAD+, NADP+ and NADPH, which play essential metabolic roles in living cells. Niacin is involved in both DNA repair, and the production of steroid hormones in the adrenal gland.
Niacin is one of five vitamins associated with a pandemic deficiency disease: these are niacin (pellagra), vitamin C (scurvy), thiamin (beriberi), vitamin D (rickets), and vitamin A deficiency, a syndrome which has no common name but is one of the most common symptomatic deficiencies worldwide. In larger doses, niacin can reverse atherosclerosis by lowering low density lipoprotein (LDL) and favorably affecting other compounds.
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Vomiting, diarrhoea, peptic ulceration, jaundice, abnormal LFTs, decreased glucose- tolerance hyperuricaemia, gout, toxic amblyopia, flushing, pruritus, hyperpigmentation, dry skin & headache, artial fibrillation, orthostatis, cystoid macular oedema.
Monitor
Monitor creatine phosphokinase and potassium in patients taking niacin and HMG-CoA reductase inhibitors.
Assess uric acid level before starting therapy. If patient has gout or a history of gouty arthritis, periodically evaluate uric acid during long-term treatment. Monitor blood sugar in diabetic patients when drug is started or dose is changed.
Assess fasting blood glucose before starting therapy and periodically thereafter during therapy in patients with risk factors for diabetes mellitus (eg, obesity, family history of diabetes). Assess transaminase levels before starting therapy, every 6 to 12 wk for the first 12 months of therapy, and periodically (eg, every 6 months) thereafter, as clinically indicated.
Closely monitor PT and platelet counts in patients undergoing surgery and/or receiving oral anticoagulant therapy; periodically monitor phosphorus levels in patients at risk of hypophosphatemia.
Gout; cases of severe hepatic toxicity, including fulminant hepatic necrosis have occured in patients who have substituted SR nicotine acid products for immediate- release nicotinic acid at equiv doses. Monitor LFT. DM, diabetic patients may experience a dose- related rise in glucose intolerance. Children, adolescents. Pregnancy, lactation (contraindications at high doses)
Potentiates the effects of ganglionic blocking agents & vasoactive drugs resulting in postural hypotension. Increased risk of rhabdominal with resulting in postural hypotension. Increased risk or rhaabdominal with concominant admin of HMG- CoA reductase inhibitors. Alcohol or hot drinks may increase the side effects of flushing & pruritis & should be avoided at the time of drug ingestion.
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Caution when used during pregnancy
Caution when used during lactation
Safety and efficacy not established for doses exceeding nutritional requirements. Extended-release preparations not recommended for children.
Use with caution in patients who consume substantial quantities of alcohol or who have a history of liver disease.
Liver disease; active peptic ulcer; severe hypotension; arterial bleeding.
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