Niacin / simvastatin Disease Interactions

There are 9 disease interactions with niacin / simvastatin:

Hmg-Coa Reductase Inhibitors (Includes Niacin/simvastatin) ↔ Liver Disease

Severe Potential Hazard, High plausibility

Applies to: Liver Disease, Alcoholism

The use of HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease or unexplained, persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual product package labeling is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of therapy.

References

  1. Mauro VF "Clinical pharmacokinetics and practical applications of simvastatin." Clin Pharmacokinet 24 (1993): 195-202
  2. "Lovastatin 5-year safety and efficacy study. Lovastatin Study Groups I through IV." Arch Intern Med 153 (1993): 1079-87
  3. Pan HY, Morrison RA, Singhvi SM, Frantz BM, Waclawski AP, Willard DA "Disposition of pravastatin sodium (SQ 31,000), a tissue-selective HMG-CoA reductase inhibitor, in healthy subjects." Clin Res 36 (1988): a368
View all 41 references

Hmg-Coa Reductase Inhibitors (Includes Niacin/simvastatin) ↔ Rhabdomyolysis

Severe Potential Hazard, Moderate plausibility

Applies to: Myopathy, Myoneural Disorder

Severe myopathy, including rhabdomyolysis with acute renal failure secondary to myoglobinuria, has been reported rarely with the use of HMG-CoA reductase inhibitors. The myopathy may be dose-related and is characterized by muscle aches and/or weakness in conjunction with increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy or a myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

References

  1. Norman DJ, Illingworth DR, Munson J, Hosenpud J "Myolysis and acute renal failure in a heart-transplant recipient receiving lovastatin." N Engl J Med 318 (1988): 46-7
  2. Vanpuijenbroek EP, Dubufvereijken PWG, Spooren PFMJ, Vandoormaal JJ "Possible increased risk of rhabdomyolysis during concomitant use of simvastatin and gemfibrozil." J Intern Med 240 (1996): 403-4
  3. van Puijenbroek EP, Du Buf-Vereijken PW, Spooren PF, van Doormaal JJ "Possible increased risk of rhabdomyolysis during concomitant use of simvastatin and gemfibrozil." J Intern Med 240 (1996): 403-4
View all 33 references

Niacin/Niacinamide (Includes Niacin/simvastatin) ↔ Coronary Artery Disease

Severe Potential Hazard, Moderate plausibility

Applies to: Ischemic Heart Disease, Arrhythmias

The Coronary Drug Project (1975) reported a significant increase in cardiac arrhythmias associated with the use of niacin at lipid-lowering dosages. Treatment using pharmacologic dosages of niacin and niacinamide (nicotinamide) should be administered cautiously in patients with coronary heart disease or arrhythmias. Particular caution is advised in the presence of unstable angina or in the acute phase of myocardial infarction, especially if the patient is also receiving vasoactive drugs such as nitrates, calcium channel blockers, or adrenergic blocking agents.

References

  1. DiPalma JR, Thayer WS "Use of niacin as a drug." Annu Rev Nutr 11 (1991): 169-87
  2. Pasternak RC, Kolman BS "Unstable myocardial ischemia after the initiation of niacin therapy." Am J Cardiol 67 (1991): 904-6
  3. Darby WJ, McNutt KW, Todhunter EN "Niacin." Nutr Rev 33 (1975): 289-97
View all 13 references

Niacin/Niacinamide (Includes Niacin/simvastatin) ↔ Hepatotoxicity

Severe Potential Hazard, High plausibility

Applies to: Liver Disease, Alcoholism, Gallbladder Disease

The use of nicotinic acid and its derivatives at dosages substantially exceeding those for physiologic requirements is contraindicated in patients with active liver disease or unexplained, persistent elevations of serum transaminases. Hepatotoxicity, including biochemical abnormalities of liver function, cholestatic jaundice, increased prothrombin time, and fulminant hepatic necrosis and failure, has been reported during therapy with niacin and niacinamide (nicotinamide), particularly in patients who have substituted sustained-release nicotinic acid products for immediate-release preparations at equivalent dosages. Treatment using pharmacologic dosages (e.g., lipid-lowering dosages) of these agents should be administered cautiously in patients with gallbladder disease or a history of jaundice, liver disease and/or heavy alcohol use. Liver transaminase levels should be evaluated prior to initiation of therapy, every 6 to 12 weeks for the first year, and periodically thereafter (e.g., semiannually). Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, therapy should be withdrawn. Liver biopsy should be considered in patients with elevations that persist beyond cessation of therapy.

References

  1. Witztum JL "Current approaches to drug therapy for the hypercholesterolemic patient." Circulation 80 (1989): 1101-14
  2. Dearing BD, Lavie CJ, Lohmann TP, Genton E "Niacin-induced clotting factor synthesis deficiency with coagulopathy." Arch Intern Med 152 (1992): 861-3
  3. Knapp TR, Middleton RK "Adverse effects of sustained-release niacin." DICP 25 (1991): 253-4
View all 37 references

Niacin/Niacinamide (Includes Niacin/simvastatin) ↔ Hypotension

Severe Potential Hazard, High plausibility

Applies to: Hypotension, Syncope

The use of niacin and niacinamide (nicotinamide) is contraindicated in patients with severe hypotension. These agents have peripheral vasodilating effects and may commonly cause flushing at dosages substantially exceeding those for physiologic requirements (e.g., lipid-lowering dosages).

References

  1. Knapp TR, Middleton RK "Adverse effects of sustained-release niacin." DICP 25 (1991): 253-4
  2. Florkowski CM, Cramb R "Approaches to the management of hypercholesterolaemia." J Clin Pharm Ther 17 (1992): 81-9
  3. Truswell AS "ABC of nutrition. Vitamins I." Br Med J (Clin Res Ed) 291 (1985): 1033-5
View all 25 references

Niacin/Niacinamide (Includes Niacin/simvastatin) ↔ Peptic Ulcer Disease

Severe Potential Hazard, High plausibility

Applies to: Peptic Ulcer, History - Peptic Ulcer

The use of niacin and niacinamide (nicotinamide) at dosages substantially exceeding those for physiologic requirements is contraindicated in patients with active peptic ulcer disease. These agents have been reported to activate peptic ulcer. Treatment using pharmacologic dosages (e.g., lipid-lowering dosages) should be administered cautiously in patients with a history of peptic ulcer disease.

References

  1. Goldstein MR "Potential problems with the widespread use of niacin." Am J Med 85 (1988): 881
  2. Gray DR, Morgan T, Chretien SD, Kashyap ML "Efficacy and safety of controlled-release niacin in dyslipoproteinemic veterans." Ann Intern Med 121 (1994): 252-8
  3. "Product Information. Slo-Niacin (niacin)." Upsher-Smith Laboratories Inc, Minneapolis, MN.
View all 22 references

Simvastatin (Includes Niacin/simvastatin) ↔ Renal Dysfunction

Severe Potential Hazard, High plausibility

Applies to: Renal Dysfunction

Although simvastatin itself is not eliminated by the kidney, the plasma concentrations of total HMG-CoA reductase inhibitors after a single dose of simvastatin may be increased in patients with significant renal impairment, presumably due to the accumulation of active metabolites. Increased HMG-CoA reductase inhibitory activity may be associated with a greater risk of adverse effects, including hepatic and musculoskeletal toxicities. Therapy with simvastatin should be administered cautiously at a reduced dosage in patients with severe renal impairment. Close clinical monitoring is recommended.

References

  1. Mauro VF "Clinical pharmacokinetics and practical applications of simvastatin." Clin Pharmacokinet 24 (1993): 195-202
  2. Lennernas H, Fager G "Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences." Clin Pharmacokinet 32 (1997): 403-25
  3. "Product Information. Zocor (simvastatin)." Merck & Co, Inc, West Point, PA.

Niacin/Niacinamide (Includes Niacin/simvastatin) ↔ Hyperglycemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Diabetes Mellitus

Elevated fasting blood sugars and decreased glucose tolerance have been reported during niacin and niacinamide (nicotinamide) therapy at dosages substantially exceeding those for physiologic requirements. Patients with diabetes mellitus should be monitored more closely during therapy with these agents, and adjustments made accordingly in their antidiabetic regimen.

References

  1. Witztum JL "Current approaches to drug therapy for the hypercholesterolemic patient." Circulation 80 (1989): 1101-14
  2. Schwartz ML "Severe reversible hyperglycemia as a consequence of niacin therapy." Arch Intern Med 153 (1993): 2050-2
  3. Truswell AS "ABC of nutrition. Vitamins I." Br Med J (Clin Res Ed) 291 (1985): 1033-5
View all 16 references

Niacin/Niacinamide (Includes Niacin/simvastatin) ↔ Hyperuricemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Gout

Large doses of niacin and niacinamide (nicotinamide) can compete with uric acid for excretion by the kidney. Hyperuricemia and precipitation of gout have been reported during long-term therapy. Treatment using pharmacologic dosages (e.g., lipid-lowering dosages) of these agents should be administered cautiously in patients with or predisposed to gout.

References

  1. "Product Information. Slo-Niacin (niacin)." Upsher-Smith Laboratories Inc, Minneapolis, MN.
  2. Blum CB, Levy RI "Rational drug therapy of the hyperlipoproteinemias, Part II." Ration Drug Ther 20 (1986): 1-4
  3. Hunninghake DB "The pharmacology and therapeutics of lipid-lowering drugs." Am Pharm ns27 (1987): s18-25
View all 14 references

You should also know about...

niacin / simvastatin drug Interactions

There are 343 drug interactions with niacin / simvastatin

niacin / simvastatin alcohol/food Interactions

There are 3 alcohol/food interactions with niacin / simvastatin

Drug Interaction Classification

The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.

Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.

Do not stop taking any medications without consulting your healthcare provider.

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