Drug Interactions between Alka-Seltzer Original and dexamethasone / ketorolac / moxifloxacin

CONTRAINDICATED: The use of ketorolac in combination with other nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk of serious adverse effects such as renal failure and gastrointestinal toxicity including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, or intestines.

MANAGEMENT: Concurrent use of ketorolac with other NSAIDs or aspirin is considered contraindicated.

MONITOR CLOSELY: Concomitant administration of corticosteroids may potentiate the risk of tendinitis and tendon rupture associated with fluoroquinolone treatment. The mechanism is unknown. Tendinitis and tendon rupture have most frequently involved the Achilles tendon, although cases involving the rotator cuff (the shoulder), the hand, the biceps, and the thumb have also been reported. Some have required surgical repair or resulted in prolonged disability. Tendon rupture can occur during or up to several months after completion of fluoroquinolone therapy.

MANAGEMENT: Caution is recommended if fluoroquinolones are prescribed in combination with corticosteroids, particularly in patients with other concomitant risk factors (e.g., age over 60 years; recipient of kidney, heart, and/or lung transplant). Patients should be advised to stop taking the fluoroquinolone, avoid exercise and use of the affected area, and promptly contact their physician if they experience pain, swelling, or inflammation of a tendon. In general, fluoroquinolones should only be used to treat conditions that are proven or strongly suspected to be caused by bacteria and only if the benefits outweigh the risks.

MONITOR: Coadministration with corticosteroids may decrease the serum concentrations and therapeutic effects of salicylates. Likewise, serum salicylate levels may increase following withdrawal of corticosteroid therapy, potentially resulting in salicylate toxicity. This interaction has been reported in patients receiving intra-articular as well as oral corticosteroids. One or more mechanisms may be involved, including an increase in the renal clearance and/or an induction of hepatic metabolism of salicylates caused by corticosteroids. Pharmacologically, the potential for increased gastrointestinal (GI) toxicity, including inflammation, bleeding, ulceration and perforation, should be considered due to additive ulcerogenic effects of these agents (especially aspirin) on the GI mucosa.

MANAGEMENT: Patients treated concomitantly with a corticosteroid may require higher dosages of salicylates or salicylate-like drugs. Pharmacologic response to these agents should be monitored more closely whenever a corticosteroid is added to or withdrawn from therapy in patients stabilized on their existing salicylate regimen, and the salicylate dosage adjusted as necessary. During concomitant therapy, patients should be advised to take the medications with food and to immediately report signs and symptoms of GI ulceration and bleeding such as severe abdominal pain, dizziness, lightheadedness, and the appearance of black, tarry stools. The selective use of prophylactic anti-ulcer therapy (e.g., antacids, H2-antagonists) may be appropriate, particularly in patients with a prior history of peptic ulcer disease or GI bleeding and in elderly and debilitated patients.

MONITOR: Agents that cause urinary alkalinization can reduce serum salicylate concentrations in patients receiving anti-inflammatory dosages of aspirin or other salicylates. The mechanism involves reduction in salicylate renal tubular reabsorption due to increased urinary pH, resulting in increased renal salicylate clearance especially above urine pH of 7. This interaction is sometimes exploited in the treatment of salicylate toxicity.

MANAGEMENT: Patients treated chronically with urinary alkalinizers and large doses of salicylates (i.e. 3 g/day or more) should be monitored for potentially diminished or inadequate analgesic and anti-inflammatory effects, and the salicylate dosage adjusted if necessary.

MONITOR: Coadministration with nonsteroidal anti-inflammatory drugs (NSAIDs) may potentiate the risk of central nervous system toxicity sometimes associated with fluoroquinolone use. The interaction has been reported most often with enoxacin. It may occur with other fluoroquinolones as well, but is poorly documented. The exact mechanism of interaction is unknown. Some investigators suggest that the piperazine ring of fluoroquinolones may inhibit the binding of gamma-aminobutyric acid (GABA) to brain receptors and that NSAIDs may synergistically add to this effect. Patients with a history of seizures may be at greater risk.

MANAGEMENT: Clinical monitoring for signs of CNS stimulation such as tremors, involuntary muscle movements, hallucinations, or seizures is recommended if fluoroquinolone antibiotics are prescribed in combination with NSAIDs.

MONITOR: The combined use of corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the potential for serious gastrointestinal (GI) toxicity, including inflammation, bleeding, ulceration, and perforation. In a large, case-control study of elderly patients, those who used corticosteroids and NSAIDs concurrently had an estimated relative risk (RR) for peptic ulcer disease and GI hemorrhage of 14.6 compared to those who used neither. Corticosteroid use was associated with a doubling of the risk (estimated RR = 2.0), but the risk was confined to those who also used NSAIDs. It is possible that both categories of agents are ulcerogenic and have additive effects on the GI mucosa during coadministration. Some investigators have also suggested that the primary effect of corticosteroids in this interaction is to delay healing of erosions caused by NSAIDs rather than cause de novo ulcerations.

MANAGEMENT: Caution is advised if corticosteroids and NSAIDs are used together, especially in patients with a prior history of peptic ulcer disease or GI bleeding and in elderly and debilitated patients. During concomitant therapy, patients should be advised to take the medications with food and to immediately report signs and symptoms of GI ulceration and bleeding such as severe abdominal pain, dizziness, lightheadedness, and the appearance of black, tarry stools. The selective use of prophylactic anti-ulcer therapy (e.g., antacids, H2-antagonists) may be considered.

MONITOR: Coadministration with nonsteroidal anti-inflammatory drugs (NSAIDs) may potentiate the risk of central nervous system toxicity sometimes associated with fluoroquinolone use. The interaction has been reported most often with enoxacin. It may occur with other fluoroquinolones as well, but is poorly documented. The exact mechanism of interaction is unknown. Some investigators suggest that the piperazine ring of fluoroquinolones may inhibit the binding of gamma-aminobutyric acid (GABA) to brain receptors and that NSAIDs may synergistically add to this effect. Patients with a history of seizures may be at greater risk.

MANAGEMENT: Clinical monitoring for signs of CNS stimulation such as tremors, involuntary muscle movements, hallucinations, or seizures is recommended if fluoroquinolone antibiotics are prescribed in combination with NSAIDs.

GENERALLY AVOID: Urinary alkalinizers such as citrates may decrease the solubility of fluoroquinolones in the urine and increase the risk of crystalluria.

MANAGEMENT: Concomitant use should generally be avoided. Patients receiving this combination should be monitored for signs of renal toxicity and crystalluria.

GENERALLY AVOID: Urinary alkalinizers such as citrates may decrease the solubility of fluoroquinolones in the urine and increase the risk of crystalluria.

MANAGEMENT: Concomitant use should generally be avoided. Patients receiving this combination should be monitored for signs of renal toxicity and crystalluria.

Antacids and agents with acid-neutralizing effects may impair the oral absorption of dexamethasone, prednisolone, prednisone, and other orally administered corticosteroids, although data from published studies are somewhat conflicting. The mechanism of interaction and clinical significance are unknown. No particular intervention is necessary during concomitant therapy with these agents, but clinicians should be aware of the potential for interaction.