Drug Interactions between famotidine / ibuprofen and Gammaplex

MONITOR CLOSELY: Coadministration of intravenous immune globulin preparations with nephrotoxic agents may potentiate the risk of renal impairment. Many commercially available intravenous formulations of immune globulin contain sucrose as a stabilizer. Immune globulin products, particularly those that contain sucrose as a stabilizer and administered at daily doses of 350 to 400 mg/kg or greater, have been associated with renal dysfunction, acute renal failure, osmotic nephrosis, and death. Factors predisposing to acute renal failure include any degree of preexisting renal insufficiency, age greater than 65 years, diabetes mellitus, volume depletion, sepsis, paraproteinemia, and concomitant use of known nephrotoxic drugs.

MANAGEMENT: Intravenous immune globulin preparations should be administered cautiously in patients treated with other potentially nephrotoxic agents (e.g., e.g., aminoglycosides; polypeptide, glycopeptide, and polymyxin antibiotics; amphotericin B; adefovir; cidofovir; tenofovir; foscarnet; cisplatin; deferasirox; gallium nitrate; lithium; mesalamine; certain immunosuppressants; intravenous bisphosphonates; intravenous pentamidine; high intravenous dosages of methotrexate; high dosages and/or chronic use of nonsteroidal anti-inflammatory agents). The manufacturers recommend administering immune globulin infusions at the minimum concentration available and at the minimum rate of infusion feasible in such patients. Clinicians should ensure that patients are not volume depleted prior to the initiation of immune globulin therapy. Monitoring of urine output and renal function tests, including the measurement of blood urea nitrogen (BUN) and serum creatinine, is recommended prior to the initial infusion and at appropriate intervals thereafter. If renal function deteriorates, discontinuation of the product should be considered. Patients should be advised to seek medical attention if they experience symptoms that may indicate nephrotoxicity such as decreased urine output, sudden weight gain, fluid retention, edema, or shortness of breath.

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H2 antagonists may alter the disposition of nonsteroidal anti-inflammatory drugs (NSAIDs), resulting in increased or decreased plasma concentrations. Data are varied, even for the same NSAID. The mechanism may be related to inhibition of metabolism, changes in gastric pH that decrease absorption, and/or reduced urinary elimination. Statistically significant changes have been small and of limited clinical significance. Clinical monitoring of patient response and tolerance is recommended.

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