Drug Interactions between famotidine / ibuprofen and piroxicam

GENERALLY AVOID: The use of piroxicam in combination with another nonsteroidal anti-inflammatory drug (NSAID) may increase the risk of serious and potentially fatal gastrointestinal (GI) toxicity, including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, or intestines. These events can occur at any time during NSAID use, with or without warning symptoms, but the incidence may increase with dosage and duration of therapy. Administration of piroxicam at dosages greater than 20 mg per day carries an increased risk of GI side effects, and evidence from observational studies suggests that piroxicam may also be associated with a higher risk of serious GI toxicity relative to other NSAIDs. In clinical trials of several months to two years duration, NSAID-associated upper GI ulcers, gross bleeding, or perforation occurred in approximately 1% of patients treated for 3 to 6 months and in 2% to 4% of patients treated for one year. Patients with a prior history of peptic ulcer disease and/or GI bleeding have a greater than 10-fold increased risk of developing a GI bleed during NSAID use compared to patients without a history. Additional risk factors include advanced age (especially over 70 years), Helicobacter pylori infection, excessive alcohol use, smoking, a history of GI inflammatory conditions, advanced liver disease, coagulopathy, and poor general health status. GI toxicity aside, clinical studies have also failed to demonstrate greater therapeutic benefit from the coadministration of piroxicam with another NSAID than the use of piroxicam alone.

MANAGEMENT: Concomitant use of piroxicam with other NSAIDs, except for low-dose aspirin for cardiovascular prophylaxis, should generally be avoided. Patients treated with a NSAID should be advised to take it with food and to immediately report signs and symptoms of GI ulceration or bleeding such as severe abdominal pain, dizziness, lightheadedness, and the appearance of black, tarry stools. The lowest effective dosage should be used for the shortest possible duration. Selective use of prophylactic anti-ulcer therapy (e.g., misoprostol, proton pump inhibitors) may be considered in high-risk patients.

H2 antagonists may alter the pharmacokinetic disposition of some nonsteroidal anti-inflammatory drugs (NSAIDs), resulting in increased or decreased plasma concentrations. Data have been varied, even for the same NSAID. The mechanism may involve inhibition of metabolism, changes in gastric pH resulting in altered absorption, and/or reduced urinary elimination of the affected NSAIDs. Statistically significant changes have been small and of limited clinical significance when interactions have been observed.

H2 antagonists may alter the pharmacokinetic disposition of some nonsteroidal anti-inflammatory drugs (NSAIDs), resulting in increased or decreased plasma concentrations. Data have been varied, even for the same NSAID. The mechanism may involve inhibition of metabolism, changes in gastric pH resulting in altered absorption, and/or reduced urinary elimination of the affected NSAIDs. Statistically significant changes have been small and of limited clinical significance when interactions have been observed.