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Drug Interactions between Glucovance and phenylbutazone

This report displays the potential drug interactions for the following 2 drugs:

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Interactions between your drugs

Moderate

glyBURIDE phenylbutazone

Applies to: Glucovance (glyburide / metformin) and phenylbutazone

MONITOR: The concomitant administration of pyrazolones may increase the hypoglycemic effects of sulfonylureas. Data have been variable. The proposed mechanisms include pyrazolone inhibition of sulfonylurea metabolism, inhibition of renal clearance and/or displacement from protein binding sites.

MANAGEMENT: Patients receiving this combination should be monitored for increased hypoglycemic effects and advised to regularly monitor their blood sugar, counseled on how to recognize and treat hypoglycemia (e.g., headache, dizziness, drowsiness, nausea, tremor, hunger, weakness, or palpitations) and to notify their physician if it occurs. The sulfonylurea dosage may require reduction in affected patients.

References

  1. Petitpierre B, Perrin L, Rudhardt M, et al. (1972) "Behaviour of chlorpropamide in renal insufficiency and under the effect of associated drug therapy." Int J Clin Pharmacol, 6, p. 120-4
  2. Shah SJ, Bhandarkar SD, Satoskar RS (1984) "Drug interaction between chlorpropamide and non-steroidal anti-flammatory drugs, ibuprofen and phenylbutazone." Int J Clin Pharmacol Ther Toxicol, 22, p. 470-2
  3. Yu T, Berger L, Gutman AB (1968) "Hypoglycemic and uricosuric properties of acetohexamide and hydroxyhexamide." Metabolism, 17, p. 309-16
  4. Field JB, Ohta M, Boyle C, Remer A (1967) "Potentiation of acetohexamide hypoglycemia by phenylbutazone." N Engl J Med, 277, p. 889-94
  5. Tannenbaum H, Anderson LG, Soeldner JS (1974) "Phenylbutazone-tolbutamide drug interaction." N Engl J Med, 290, p. 344
  6. Ober KF (1974) "Mechanism of interaction of tolbutamide and phenylbutazone in diabetic patients." Eur J Clin Pharmacol, 7, p. 291-4
  7. Slade IH, and Iosefa RN (1967) "Fatal hypoglycemic coma from the use of tolbutamide in elderly patients: report of two cases." J Am Geriatr Soc, 15, p. 948-50
  8. Pond SM, Birkett DJ, Wade DN (1977) "Mechanisms of inhibition of tolbutamide metabolism: phenylbutazone, oxyphenbutazone, sulfaphenazole." Clin Pharmacol Ther, 22, p. 573-9
  9. Christensen LK, Hansen JM, Kristensen M (1963) "Sulphaphenazole-induced hypoglycemic attacks in tolbutamide-treated diabetics." Lancet, 2, p. 1298-301
  10. Hellman B (1974) "Potentiating effects of drugs on the binding of glibenclamide to pancreatic beta cells." Metabolism, 23, p. 839-46
  11. Miners JO, Foenander T, Wanwimolruk S, Gallus AS, Birkett DJ (1982) "The effect of sulphinpyrazone on oxidative drug metabolism in man: inhibition of tolbutamide elimination." Eur J Clin Pharmacol, 22, p. 321-6
  12. Held H, Kaminski B, von Oldersausen HF (1970) "Die beeinflussung der elimination von glycodiazin durch leber- und nierenfunctionssorungen und durch eine behandlung mit phenylbutazone, phenprocumarol und doxycyclin." Diabetologia, 6, p. 386-91
  13. Mahfouz M, Abdel-Maguid R, El-Dakhakhny M (1970) "Potentiation of the hypoglycaemic action of tolbutamide by different drugs." Arzneimittelforschung, 20, p. 120-2
  14. Schultz E, Koch K, Schmidt FH (1971) "Ursachen der potenzierung der hypoglykamischen wirkung von sulfonylharnstoff-derivaten durch medikamente. II. Pharmakokinetik und metabolismus von glibenclamid (HB 419) in gegenwart von phenylbuazon." Eur J Clin Pharmacol, 4, p. 32-7
  15. Eckhardt W, Rudolph R, Sauer H, Schubert WR, Undeutsch D (1972) "Zur pharmakologischen interferenz von glibornurid mit sulfaphenazol, phenylbutazon und phenprocoumon beim menschen." Arzneimittelforschung, 22, p. 2212-9
  16. Held H, Scheible G (1981) "Interaktion von pnenylbutazon und oxyphenbutazon mit glymidin." Arzneimittelforschung, 31, p. 1036-8
  17. Cerner Multum, Inc. "UK Summary of Product Characteristics."
View all 17 references

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Moderate

glyBURIDE metFORMIN

Applies to: Glucovance (glyburide / metformin) and Glucovance (glyburide / metformin)

MONITOR: Coadministration of metformin with an insulin secretagogue (e.g., sulfonylurea, meglitinide) or insulin may potentiate the risk of hypoglycemia. Although metformin alone generally does not cause hypoglycemia under normal circumstances of use, the added therapeutic effect when combined with other antidiabetic agents may result in hypoglycemia. The risk is further increased when caloric intake is deficient or when strenuous exercise is not compensated by caloric supplementation.

MANAGEMENT: A lower dosage of the insulin secretagogue or insulin may be required when used with metformin. Blood glucose should be closely monitored, and patients should be educated on the potential signs and symptoms of hypoglycemia (e.g., headache, dizziness, drowsiness, nervousness, confusion, tremor, hunger, weakness, perspiration, palpitation, tachycardia) and appropriate remedial actions to take if it occurs. Patients should also be advised to take precautions to avoid hypoglycemia while driving or operating hazardous machinery.

References

  1. Wiernsperger N, Rapin JR (1995) "Metformin-insulin interactions: from organ to cell." Diabetes Metab Rev, 11 Suppl, s3-12
  2. Okada S, Ishii K, Hamada H, Tanokuchi S, Ichiki K, Ota Z (1995) "Can alpha-glucosidase inhibitors reduce the insulin dosage administered to patients with non-insulin-dependent diabetes mellitus?" J Int Med Res, 23, p. 487-91

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Moderate

phenylbutazone metFORMIN

Applies to: phenylbutazone and Glucovance (glyburide / metformin)

MONITOR: Coadministration with nonsteroidal anti-inflammatory drugs (NSAIDs) may potentiate the risk of lactic acidosis associated with the use of metformin. The precise mechanism for this interaction has not been clearly delineated. Since NSAIDs have been shown to cause a deterioration in renal function, the likelihood of lactic acidosis occurring may be increased in patients with preexisting renal impairment.

MANAGEMENT: Caution and monitoring of renal function is advised if metformin is used concomitantly with NSAIDs. Dose adjustments may be considered, particularly in patients with renal impairment. Close monitoring for the development of lactic acidosis is also recommended, particularly in patients with renal impairment. Patients should contact their physician immediately if they experience potential signs and symptoms of lactic acidosis such as malaise, myalgia, respiratory distress, increasing somnolence, and nonspecific abdominal distress (especially after stabilization of metformin therapy, when gastrointestinal symptoms are uncommon). With more marked acidosis, there may also be associated hypothermia, hypotension, and resistant bradyarrhythmias. Metformin should be withdrawn promptly if lactic acidosis is suspected. Serum electrolytes, ketones, blood glucose, blood pH, lactate levels, and blood metformin levels may be useful in establishing a diagnosis. Lactic acidosis should be suspected in any diabetic patient with metabolic acidosis lacking evidence of ketoacidosis (ketonuria and ketonemia).

References

  1. Cerner Multum, Inc. "UK Summary of Product Characteristics."
  2. Cerner Multum, Inc. "Australian Product Information."

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Drug and food interactions

Major

metFORMIN food

Applies to: Glucovance (glyburide / metformin)

GENERALLY AVOID: Alcohol can potentiate the effect of metformin on lactate metabolism and increase the risk of lactic acidosis. In addition, alcohol may cause hypoglycemia or hyperglycemia in patients with diabetes. Although hypoglycemia rarely occurs during treatment with metformin alone, the risk may increase with 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.

Food may have varying effects on the absorption of metformin from immediate-release versus extended-release formulations. When a single 850 mg dose of immediate-release metformin was administered with food, mean peak plasma concentration (Cmax) and systemic exposure (AUC) decreased by 40% and 25%, respectively, and time to peak plasma concentration (Tmax) increased by 35 minutes compared to administration under fasting conditions. By contrast, administration of extended-release metformin with food increased AUC by 50% without affecting Cmax or Tmax, and both high- and low-fat meals had the same effect. These data may not be applicable to formulations that contain metformin with other oral antidiabetic agents.

MANAGEMENT: Metformin should be taken with meals, and excessive alcohol intake should be avoided during treatment. Diabetes patients in general should avoid consuming alcohol if their blood glucose is not well controlled, or if they have hypertriglyceridemia, neuropathy, or pancreatitis. Alcohol should not be consumed on an empty stomach or following exercise, as it may increase the risk of hypoglycemia. Patients should contact their physician immediately if they experience potential signs and symptoms of lactic acidosis such as malaise, myalgia, respiratory distress, increasing somnolence, and nonspecific abdominal distress (especially after stabilization of metformin therapy, when gastrointestinal symptoms are uncommon). With more marked acidosis, there may also be associated hypothermia, hypotension, and resistant bradyarrhythmias. Metformin should be withdrawn promptly if lactic acidosis is suspected. Serum electrolytes, ketones, blood glucose, blood pH, lactate levels, and blood metformin levels may be useful in establishing a diagnosis. Lactic acidosis should be suspected in any diabetic patient with metabolic acidosis lacking evidence of ketoacidosis (ketonuria and ketonemia).

References

  1. (2001) "Product Information. Glucophage (metformin)." Bristol-Myers Squibb
  2. (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

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Moderate

glyBURIDE food

Applies to: Glucovance (glyburide / metformin)

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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Therapeutic duplication warnings

No 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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