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Drug Interaction Report

6 potential interactions and/or warnings found for the following 2 drugs:

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Interactions between your drugs

Moderate

metoprolol insulin regular

Applies to: Metoprolol Succinate ER (metoprolol), insulin isophane / insulin regular

MONITOR: Beta-blockers may inhibit some of the normal physiologic response to hypoglycemia. Symptoms of hypoglycemia such as tremor and tachycardia may be absent, making it more difficult for patients to recognize an oncoming episode. In addition, multiple effects on glucose metabolism have been reported, usually with the noncardioselective beta-blockers (e.g., propranolol, pindolol, timolol) but occasionally also with relatively beta-1 selective agents (e.g., atenolol, metoprolol, nebivolol). Specifically, inhibition of catecholamine-mediated glycogenolysis and glucose mobilization in association with beta-blockade can potentiate insulin-induced hypoglycemia in diabetics and delay the recovery of normal blood glucose levels. Prolonged and severe hypoglycemia may occur, although these events have rarely been reported. Significant increases in blood pressure and bradycardia can also occur during hypoglycemia in diabetics treated with insulin and beta-blockers due to antagonism of epinephrine's effect on beta-2 adrenergic receptors, which leads to unopposed alpha-adrenergic effects including vasoconstriction. Other effects reported with various beta-blockers include decreased glucose tolerance and decreased glucose-induced insulin secretion.

MANAGEMENT: In general, cardioselective beta-blockers are considered safer than noncardioselective agents in the treatment of diabetic patients. Nevertheless, caution is advised if they are prescribed to patients treated with insulin or oral antidiabetic agents that can cause hypoglycemia (e.g., insulin secretagogues), as cardioselectivity is not absolute and larger doses of beta-1 selective agents may pose some of the same risks as nonselective agents. Patients should be advised of the need for regular blood glucose monitoring and be aware that certain symptoms of hypoglycemia such as tremor and tachycardia may be masked. However, other symptoms such as headache, dizziness, drowsiness, confusion, nausea, hunger, weakness, and perspiration may be unaffected. The same precautions are applicable in diabetic patients treated with ophthalmic beta-blockers.

References

  1. Shepherd AM, Lin M-S, Keeton TK (1981) "Hypoglycemia-induced hypertension in a diabetic patient on metoprolol." Ann Intern Med, 94, p. 357-8
  2. Micossi P, Pollavini G, Raggi U, et al. (1984) "Effects of metoprolol and propranolol on glucose tolerance and insulin secretion in diabetes mellitus." Horm Metab Res, 16, p. 59-63
  3. Popp DA, Tse TF, Shah SD, et al. (1984) "Oral propranolol and metoprolol both impair glucose recovery from insulin-induced hypoglycemia in insulin-dependent diabetes mellitus." Diabetes Care, 7, p. 243-7
  4. Mann SJ, Krakoff LR (1984) "Hypertensive crisis caused by hypoglycemia and propranolol." Arch Intern Med, 144, p. 2427-8
  5. Groop L, Totterman KJ, Harno K, Gordin A (1982) "Influence of beta-blocking drugs on glucose metabolism in patients with non-insulin dependent diabetes mellitus." Acta Med Scand, 211, p. 7-12
  6. Viberti GC, Keen H, Bloom SR (1980) "Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in insulin-dependent diabetics." Metabolism, 29, p. 873-9
  7. Viberti GC, Keen H, Bloom SR (1980) "Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in normal subjects." Metabolism, 29, p. 866-72
  8. Newman RJ (1976) "Comparison of propranolol, metoprolol, and acebutolol on insulin-induced hypoglycaemia." Br Med J, 2, p. 447-9
  9. Smith U (1978) "Beta blockade in diabetes." N Engl J Med, 299, p. 1467
  10. Zaman R, Kendall MJ, Biggs PI (1982) "The effect of acebutolol and propranolol on the hypoglycaemic action of glibenclamide." Br J Clin Pharmacol, 13, p. 507-12
  11. Munroe WP, Rindone JP, Kershner RM (1985) "Systemic side effects associated with the ophthalmic administratiion of timolol." Drug Intell Clin Pharm, 19, p. 85-9
  12. Ostman J (1983) "B-adrenergic blockade and diabetes mellitus." Acta Med Scand, 672, p. 69-77
  13. Deacon SP, Karunanayake A, Barnett D (1977) "Acebutolol, atenolol, and propranolol and metabolic responses to acute hypoglycaemia in diabetes." Br Med J, 12, p. 1255-7
  14. Pollare T, Lithell H, Selinus I, Berne C (1989) "Sensitivity to insulin during treatment with atenolol and metoprolol: a randomised, double blind study of effects on carbohydrate and lipoprotein metabolism in hypertensive patients." BMJ, 298, p. 1152-7
  15. Sinclair AJ, Davies IB, Warrington SJ (1990) "Betaxolol and glucose-insulin relationships: studies in normal subjects taking glibenclamide or metformin." Br J Clin Pharmacol, 30, p. 699-702
  16. (1975) "New Zealand Committee on Adverse Drug Reactions. Ninth Annual Report." N Z Dent J, 71, p. 28-32
View all 16 references

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Moderate

metoprolol insulin isophane (NPH)

Applies to: Metoprolol Succinate ER (metoprolol), insulin isophane / insulin regular

MONITOR: Beta-blockers may inhibit some of the normal physiologic response to hypoglycemia. Symptoms of hypoglycemia such as tremor and tachycardia may be absent, making it more difficult for patients to recognize an oncoming episode. In addition, multiple effects on glucose metabolism have been reported, usually with the noncardioselective beta-blockers (e.g., propranolol, pindolol, timolol) but occasionally also with relatively beta-1 selective agents (e.g., atenolol, metoprolol, nebivolol). Specifically, inhibition of catecholamine-mediated glycogenolysis and glucose mobilization in association with beta-blockade can potentiate insulin-induced hypoglycemia in diabetics and delay the recovery of normal blood glucose levels. Prolonged and severe hypoglycemia may occur, although these events have rarely been reported. Significant increases in blood pressure and bradycardia can also occur during hypoglycemia in diabetics treated with insulin and beta-blockers due to antagonism of epinephrine's effect on beta-2 adrenergic receptors, which leads to unopposed alpha-adrenergic effects including vasoconstriction. Other effects reported with various beta-blockers include decreased glucose tolerance and decreased glucose-induced insulin secretion.

MANAGEMENT: In general, cardioselective beta-blockers are considered safer than noncardioselective agents in the treatment of diabetic patients. Nevertheless, caution is advised if they are prescribed to patients treated with insulin or oral antidiabetic agents that can cause hypoglycemia (e.g., insulin secretagogues), as cardioselectivity is not absolute and larger doses of beta-1 selective agents may pose some of the same risks as nonselective agents. Patients should be advised of the need for regular blood glucose monitoring and be aware that certain symptoms of hypoglycemia such as tremor and tachycardia may be masked. However, other symptoms such as headache, dizziness, drowsiness, confusion, nausea, hunger, weakness, and perspiration may be unaffected. The same precautions are applicable in diabetic patients treated with ophthalmic beta-blockers.

References

  1. Shepherd AM, Lin M-S, Keeton TK (1981) "Hypoglycemia-induced hypertension in a diabetic patient on metoprolol." Ann Intern Med, 94, p. 357-8
  2. Micossi P, Pollavini G, Raggi U, et al. (1984) "Effects of metoprolol and propranolol on glucose tolerance and insulin secretion in diabetes mellitus." Horm Metab Res, 16, p. 59-63
  3. Popp DA, Tse TF, Shah SD, et al. (1984) "Oral propranolol and metoprolol both impair glucose recovery from insulin-induced hypoglycemia in insulin-dependent diabetes mellitus." Diabetes Care, 7, p. 243-7
  4. Mann SJ, Krakoff LR (1984) "Hypertensive crisis caused by hypoglycemia and propranolol." Arch Intern Med, 144, p. 2427-8
  5. Groop L, Totterman KJ, Harno K, Gordin A (1982) "Influence of beta-blocking drugs on glucose metabolism in patients with non-insulin dependent diabetes mellitus." Acta Med Scand, 211, p. 7-12
  6. Viberti GC, Keen H, Bloom SR (1980) "Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in insulin-dependent diabetics." Metabolism, 29, p. 873-9
  7. Viberti GC, Keen H, Bloom SR (1980) "Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in normal subjects." Metabolism, 29, p. 866-72
  8. Newman RJ (1976) "Comparison of propranolol, metoprolol, and acebutolol on insulin-induced hypoglycaemia." Br Med J, 2, p. 447-9
  9. Smith U (1978) "Beta blockade in diabetes." N Engl J Med, 299, p. 1467
  10. Zaman R, Kendall MJ, Biggs PI (1982) "The effect of acebutolol and propranolol on the hypoglycaemic action of glibenclamide." Br J Clin Pharmacol, 13, p. 507-12
  11. Munroe WP, Rindone JP, Kershner RM (1985) "Systemic side effects associated with the ophthalmic administratiion of timolol." Drug Intell Clin Pharm, 19, p. 85-9
  12. Ostman J (1983) "B-adrenergic blockade and diabetes mellitus." Acta Med Scand, 672, p. 69-77
  13. Deacon SP, Karunanayake A, Barnett D (1977) "Acebutolol, atenolol, and propranolol and metabolic responses to acute hypoglycaemia in diabetes." Br Med J, 12, p. 1255-7
  14. Pollare T, Lithell H, Selinus I, Berne C (1989) "Sensitivity to insulin during treatment with atenolol and metoprolol: a randomised, double blind study of effects on carbohydrate and lipoprotein metabolism in hypertensive patients." BMJ, 298, p. 1152-7
  15. Sinclair AJ, Davies IB, Warrington SJ (1990) "Betaxolol and glucose-insulin relationships: studies in normal subjects taking glibenclamide or metformin." Br J Clin Pharmacol, 30, p. 699-702
  16. (1975) "New Zealand Committee on Adverse Drug Reactions. Ninth Annual Report." N Z Dent J, 71, p. 28-32
View all 16 references

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Drug and food interactions

Moderate

metoprolol food

Applies to: Metoprolol Succinate ER (metoprolol)

ADJUST DOSING INTERVAL: The bioavailability of metoprolol may be enhanced by food.

MANAGEMENT: Patients may be instructed to take metoprolol at the same time each day, preferably with or immediately following meals.

References

  1. (2001) "Product Information. Lopressor (metoprolol)." Novartis Pharmaceuticals
  2. Darcy PF (1995) "Nutrient-drug interactions." Adverse Drug React Toxicol Rev, 14, p. 233-54

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Moderate

insulin regular food

Applies to: insulin isophane / insulin regular

GENERALLY AVOID: Alcohol may cause hypoglycemia or hyperglycemia in patients with diabetes. Hypoglycemia most frequently occurs during acute consumption of alcohol. Even modest amounts can lower blood sugar significantly, especially when the alcohol is ingested on an empty stomach or following exercise. The mechanism involves inhibition of both gluconeogenesis as well as the counter-regulatory response to hypoglycemia. Episodes of hypoglycemia may last for 8 to 12 hours after ethanol ingestion. By contrast, chronic alcohol abuse can cause impaired glucose tolerance and hyperglycemia. Moderate alcohol consumption generally does not affect blood glucose levels in patients with well controlled diabetes. A disulfiram-like reaction (e.g., flushing, headache, and nausea) to alcohol has been reported frequently with the use of chlorpropamide and very rarely with other sulfonylureas.

MANAGEMENT: Patients with diabetes should avoid consuming alcohol if their blood glucose is not well controlled, or if they have hypertriglyceridemia, neuropathy, or pancreatitis. Patients with well controlled diabetes should limit their alcohol intake to one drink daily for women and two drinks daily for men (1 drink = 5 oz wine, 12 oz beer, or 1.5 oz distilled spirits) in conjunction with their normal meal plan. Alcohol should not be consumed on an empty stomach or following exercise.

References

  1. Jerntorp P, Almer LO (1981) "Chlorpropamide-alcohol flushing in relation to macroangiopathy and peripheral neuropathy in non-insulin dependent diabetes." Acta Med Scand, 656, p. 33-6
  2. Jerntorp P, Almer LO, Holin H, et al. (1983) "Plasma chlorpropamide: a critical factor in chlorpropamide-alcohol flush." Eur J Clin Pharmacol, 24, p. 237-42
  3. Barnett AH, Spiliopoulos AJ, Pyke DA, et al. (1983) "Metabolic studies in chlorpropamide-alcohol flush positive and negative type 2 (non-insulin dependent) diabetic patients with and without retinopathy." Diabetologia, 24, p. 213-5
  4. Hartling SG, Faber OK, Wegmann ML, Wahlin-Boll E, Melander A (1987) "Interaction of ethanol and glipizide in humans." Diabetes Care, 10, p. 683-6
  5. (2002) "Product Information. Diabinese (chlorpropamide)." Pfizer U.S. Pharmaceuticals
  6. (2002) "Product Information. Glucotrol (glipizide)." Pfizer U.S. Pharmaceuticals
  7. "Product Information. Diabeta (glyburide)." Hoechst Marion-Roussel Inc, Kansas City, MO.
  8. Skillman TG, Feldman JM (1981) "The pharmacology of sulfonylureas." Am J Med, 70, p. 361-72
  9. (2002) "Position Statement: evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes related complications. American Diabetes Association." Diabetes Care, 25(Suppl 1), S50-S60
  10. Cerner Multum, Inc. "UK Summary of Product Characteristics."
View all 10 references

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Moderate

insulin isophane (NPH) food

Applies to: insulin isophane / insulin regular

GENERALLY AVOID: Alcohol may cause hypoglycemia or hyperglycemia in patients with diabetes. Hypoglycemia most frequently occurs during acute consumption of alcohol. Even modest amounts can lower blood sugar significantly, especially when the alcohol is ingested on an empty stomach or following exercise. The mechanism involves inhibition of both gluconeogenesis as well as the counter-regulatory response to hypoglycemia. Episodes of hypoglycemia may last for 8 to 12 hours after ethanol ingestion. By contrast, chronic alcohol abuse can cause impaired glucose tolerance and hyperglycemia. Moderate alcohol consumption generally does not affect blood glucose levels in patients with well controlled diabetes. A disulfiram-like reaction (e.g., flushing, headache, and nausea) to alcohol has been reported frequently with the use of chlorpropamide and very rarely with other sulfonylureas.

MANAGEMENT: Patients with diabetes should avoid consuming alcohol if their blood glucose is not well controlled, or if they have hypertriglyceridemia, neuropathy, or pancreatitis. Patients with well controlled diabetes should limit their alcohol intake to one drink daily for women and two drinks daily for men (1 drink = 5 oz wine, 12 oz beer, or 1.5 oz distilled spirits) in conjunction with their normal meal plan. Alcohol should not be consumed on an empty stomach or following exercise.

References

  1. Jerntorp P, Almer LO (1981) "Chlorpropamide-alcohol flushing in relation to macroangiopathy and peripheral neuropathy in non-insulin dependent diabetes." Acta Med Scand, 656, p. 33-6
  2. Jerntorp P, Almer LO, Holin H, et al. (1983) "Plasma chlorpropamide: a critical factor in chlorpropamide-alcohol flush." Eur J Clin Pharmacol, 24, p. 237-42
  3. Barnett AH, Spiliopoulos AJ, Pyke DA, et al. (1983) "Metabolic studies in chlorpropamide-alcohol flush positive and negative type 2 (non-insulin dependent) diabetic patients with and without retinopathy." Diabetologia, 24, p. 213-5
  4. Hartling SG, Faber OK, Wegmann ML, Wahlin-Boll E, Melander A (1987) "Interaction of ethanol and glipizide in humans." Diabetes Care, 10, p. 683-6
  5. (2002) "Product Information. Diabinese (chlorpropamide)." Pfizer U.S. Pharmaceuticals
  6. (2002) "Product Information. Glucotrol (glipizide)." Pfizer U.S. Pharmaceuticals
  7. "Product Information. Diabeta (glyburide)." Hoechst Marion-Roussel Inc, Kansas City, MO.
  8. Skillman TG, Feldman JM (1981) "The pharmacology of sulfonylureas." Am J Med, 70, p. 361-72
  9. (2002) "Position Statement: evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes related complications. American Diabetes Association." Diabetes Care, 25(Suppl 1), S50-S60
  10. Cerner Multum, Inc. "UK Summary of Product Characteristics."
View all 10 references

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Moderate

metoprolol food

Applies to: Metoprolol Succinate ER (metoprolol)

ADJUST DOSING INTERVAL: Concurrent administration with calcium salts may decrease the oral bioavailability of atenolol and possibly other beta-blockers. The exact mechanism of interaction is unknown. In six healthy subjects, calcium 500 mg (as lactate, carbonate, and gluconate) reduced the mean peak plasma concentration (Cmax) and area under the concentration-time curve (AUC) of atenolol (100 mg) by 51% and 32%, respectively. The elimination half-life increased by 44%. Twelve hours after the combination, beta-blocking activity (as indicated by inhibition of exercise tachycardia) was reduced compared to that with atenolol alone. However, during a 4-week treatment in six hypertensive patients, there was no difference in blood pressure values between treatments. The investigators suggest that prolongation of the elimination half-life induced by calcium coadministration may have led to atenolol cumulation during long-term dosing, which compensated for the reduced bioavailability.

MANAGEMENT: It may help to separate the administration times of beta-blockers and calcium products by at least 2 hours. Patients should be monitored for potentially diminished beta-blocking effects following the addition of calcium therapy.

References

  1. Kirch W, Schafer-Korting M, Axthelm T, Kohler H, Mutschler E (1981) "Interaction of atenolol with furosemide and calcium and aluminum salts." Clin Pharmacol Ther, 30, p. 429-35

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Therapeutic duplication warnings

No duplication warnings were found for your selected drugs.

Therapeutic duplication warnings are only returned when drugs within the same group exceed the recommended therapeutic duplication maximum.


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Drug Interaction Classification

These classifications are only a guideline. The relevance of a particular drug interaction to a specific individual is difficult to determine. Always consult your healthcare provider before starting or stopping any medication.
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.
Unknown No interaction information available.

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Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.