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Drug Interactions between Inderal LA and rofecoxib

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

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Interactions between your drugs

Moderate

propranolol rofecoxib

Applies to: Inderal LA (propranolol) and rofecoxib

MONITOR: Nonsteroidal anti-inflammatory drugs (NSAIDs) may attenuate the antihypertensive effect of beta-blockers. The proposed mechanism is NSAID-induced inhibition of renal prostaglandin synthesis, which results in unopposed pressor activity producing hypertension. In addition, NSAIDs can cause fluid retention, which also affects blood pressure. Indomethacin and piroxicam have been reported to have greater attenuating effects than other NSAIDs, and indomethacin effects may be significant in patients with eclampsia.

MANAGEMENT: Patients receiving a beta-blocker who require prolonged (greater than 1 week) concomitant therapy with an NSAID should have blood pressure monitored more closely following initiation, discontinuation, or change of dosage of the NSAID. The interaction is not expected to occur with low doses (e.g., low-dose aspirin) or intermittent short-term administration of NSAIDs.

References (9)
  1. Salvetti A, Pedrinelli R, Alberici P, Magagna A, Abdel-Haq B (1984) "The influence of indomethacin and sulindac on some pharmacological actions of atenolol in hypertensive patients." Br J Clin Pharmacol, 17 Suppl 1, s108-11
  2. Ylitalo P, Pitkajarvi T, Pyykonen ML, Nurmi AK, Seppala E, Vapaatalo H (1985) "Inhibition of prostaglandin synthesis by indomethacin interacts with the antihypertensive effect of atenolol." Clin Pharmacol Ther, 38, p. 443-9
  3. Radack KL, Deck CC, Bloomfield SS (1987) "Ibuprofen interferes with the efficacy of antihypertensive drugs." Ann Intern Med, 107, p. 628-35
  4. Wong DG, Spence JD, Lamki L, Freeman D, McDonald JW (1986) "Effect of non-steroidal anti-inflammatory drugs on control of hypertension by beta-blockers and diuretics." Lancet, 1, p. 997-1001
  5. Durao V, Prata MM, Goncalves LM (1977) "Modification of antihypertensive effect of beta-adrenoceptor-blocking agents by inhibition of endogenous prostaglandin synthesis." Lancet, 2, p. 1005-7
  6. Abate MA, Neely JL, Layne RD, D'Allessandri R (1991) "Interaction of indomethacin and sulindac with labetalol." Br J Clin Pharmacol, 31, p. 363-6
  7. Salvetti A, Arzilli F, Pedrinelli R, Beggi P, Motolese M (1982) "Interaction between oxprenolol and indomethacin on blood pressure in essential hypertensive patients." Eur J Clin Pharmacol, 22, p. 197-201
  8. Durao V, Prata MM, Concalves LM (1977) "Modification of antihypertensive effect of B-adrenoceptor-blocking agents by inhibition of endogenous prostaglandin synthesis." Lancet, 2, p. 1005-7
  9. Hartmann D, Stief G, Lingenfelder M, Guzelhan C, Horsch AK (1995) "Study on the possible interaction between tenoxicam and atenolol in hypertensive patients." Arzneimittelforschung, 45-1, p. 494-8

Drug and food interactions

Moderate

propranolol food

Applies to: Inderal LA (propranolol)

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

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

References (2)
  1. Olanoff LS, Walle T, Cowart TD, et al. (1986) "Food effects on propranolol systemic and oral clearance: support for a blood flow hypothesis." Clin Pharmacol Ther, 40, p. 408-14
  2. Byrne AJ, McNeil JJ, Harrison PM, Louis W, Tonkin AM, McLean AJ (1984) "Stable oral availability of sustained release propranolol when co-administered with hydralazine or food: evidence implicating substrate delivery rate as a determinant of presystemic drug interactions." Br J Clin Pharmacol, 17, s45-50
Moderate

propranolol food

Applies to: Inderal LA (propranolol)

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)
  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
Moderate

propranolol food

Applies to: Inderal LA (propranolol)

MONITOR: Smoking cessation may lead to elevated plasma concentrations and enhanced pharmacologic effects of drugs that are substrates of CYP450 1A2 (and possibly CYP450 1A1) and/or certain drugs with a narrow therapeutic index (e.g., flecainide, pentazocine). One proposed mechanism is related to the loss of CYP450 1A2 and 1A1 induction by polycyclic aromatic hydrocarbons in tobacco smoke; when smoking cessation agents are initiated and smoking stops, the metabolism of certain drugs may decrease leading to increased plasma concentrations. The mechanism by which smoking cessation affects narrow therapeutic index drugs that are not known substrates of CYP450 1A2 or 1A1 is unknown. The clinical significance of this interaction is unknown as clinical data are lacking.

MANAGEMENT: Until more information is available, caution is advisable if smoking cessation agents are used concomitantly with drugs that are substrates of CYP450 1A2 or 1A1 and/or those with a narrow therapeutic range. Patients receiving smoking cessation agents may require periodic dose adjustments and closer clinical and laboratory monitoring of medications that are substrates of CYP450 1A2 or 1A1.

References (4)
  1. (2024) "Product Information. Cytisine (cytisinicline)." Consilient Health Ltd
  2. jeong sh, Newcombe D, sheridan j, Tingle M (2015) "Pharmacokinetics of cytisine, an a4 b2 nicotinic receptor partial agonist, in healthy smokers following a single dose." Drug Test Anal, 7, p. 475-82
  3. Vaughan DP, Beckett AH, Robbie DS (1976) "The influence of smoking on the intersubject variation in pentazocine elimination." Br J Clin Pharmacol, 3, p. 279-83
  4. Zevin S, Benowitz NL (1999) "Drug interactions with tobacco smoking: an update" Clin Pharmacokinet, 36, p. 425-38

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.

Further information

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