Interactions between Cidomycin and Deferasirox

The gentamicin in Cidomycin has a major potential interaction with Botulism.

Therapy with aminoglycosides should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia. Aminoglycosides can aggravate muscle weakness because of their potential curare-like effects on the neuromuscular junction, and may cause neuromuscular blockade, respiratory failure, and prolonged respiratory paralysis on these patients. Aminoglycoside- induced neuromuscular blockade is generally self-limiting, it may rarely result in respiratory paralysis. Neomycin is thought to be the most potent neuromuscular blocking agent in the class. However, the risk is greatest with intraperitoneal or intrapleural instillation of large doses or rapid intravenous administration of parenteral aminoglycosides. If signs of respiratory paralysis occur during aminoglycoside therapy, the drug should be discontinued and mechanical respiratory assistance provided if necessary.

The gentamicin in Cidomycin has a major potential interaction with Dehydration.

Adequate hydration is crucial to minimize the risk of oto- and nephrotoxicity associated with the use of aminoglycosides. Dehydration should preferably be corrected prior to initiation of therapy. In patients who may be at risk for dehydration, such as those with severe and/or prolonged diarrhea or vomiting, fluid status should be monitored closely. If signs of renal irritation develop during therapy, hydration should be increased as indicated, accompanied by a reduction in dosage if necessary. Therapy should be withdrawn if urinary output decreases progressively or azotemia increases.

Deferasirox has a major potential interaction with Dermatitis, Drug-Induced.

Fatal cases of severe cutaneous reactions, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and erythema multiforme have occurred in patients treated with deferasirox. The risk of other skin reactions cannot be excluded. It is recommended that if SJS or TEN is suspected to interrupt therapy until the etiology of the reaction has been determined, and if SJS or TEN is confirmed to permanently discontinue treatment with deferasirox. Monitor patients for the development of these severe cutaneous reactions, discontinue deferasirox if clinically appropriate and do not reintroduce therapy. For severe cases of rash, interrupt treatment and consider reintroducing therapy after resolution of the rash at a lower dose with dose escalation as appropriate.

The gentamicin in Cidomycin has a major potential interaction with Diarrhea.

Adequate hydration is crucial to minimize the risk of oto- and nephrotoxicity associated with the use of aminoglycosides. Dehydration should preferably be corrected prior to initiation of therapy. In patients who may be at risk for dehydration, such as those with severe and/or prolonged diarrhea or vomiting, fluid status should be monitored closely. If signs of renal irritation develop during therapy, hydration should be increased as indicated, accompanied by a reduction in dosage if necessary. Therapy should be withdrawn if urinary output decreases progressively or azotemia increases.

Deferasirox has a moderate potential interaction with Esophageal Ulceration with Bleeding.

Gastrointestinal hemorrhage, ulcerations, perforations, including deaths have been documented in patients using deferasirox, especially in elderly patients who had advanced hematologic malignancies and/or low platelet counts. The risk of gastrointestinal hemorrhage may be increased when administering deferasirox in combination with drugs that have ulcerogenic or hemorrhagic potential, such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, oral bisphosphonates, or anticoagulants. It is recommended to monitor patients and discontinue therapy for suspected GI ulceration or hemorrhage. Care is recommended when using this agent in patients at risk of GI complications.

The gentamicin in Cidomycin has a major potential interaction with Hearing Loss.

Aminoglycosides can cause eighth cranial nerve damage, resulting in vestibular and/or auditory toxicities. Symptoms include dizziness, nystagmus, vertigo, ataxia, tinnitus, and varying degrees of hearing impairment. Permanent hearing loss may occur, including, rarely, total or partial irreversible bilateral deafness after the drug has been discontinued. Therapy with aminoglycosides, particularly if prolonged (> 10 days), should be administered cautiously in patients with preexisting vestibular and/or auditory impairment, since it may delay the recognition or confound the diagnosis of a drug-induced ototoxic effect. To minimize the risk of toxicity, patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other ototoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be periodically determined and dosage adjusted to maintain desired levels. Serial audiograms should be obtained in patients old enough to be tested, since loss of high- frequency perception usually precedes clinical hearing loss. The dosage should be reduced or therapy withdrawn promptly if signs and symptoms of toxicity develop.

Deferasirox has a moderate potential interaction with Hearing Loss.

Auditory disturbances (high-frequency hearing loss, decreased hearing), and ocular disturbances (lens opacities, cataracts, elevations in intraocular pressure, and retinal disorders) have been reported in patients using deferasirox. It is recommended to perform auditory and ophthalmic testing (including slit lamp examinations and dilated fundoscopy) before starting therapy with deferasirox and thereafter as clinically indicated. If disturbances are noted, consider dose reduction or interruption if appropriate.

The gentamicin in Cidomycin has a major potential interaction with Hypocalcemia.

Therapy with aminoglycosides should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia. Aminoglycosides can aggravate muscle weakness because of their potential curare-like effects on the neuromuscular junction, and may cause neuromuscular blockade, respiratory failure, and prolonged respiratory paralysis on these patients. Aminoglycoside- induced neuromuscular blockade is generally self-limiting, it may rarely result in respiratory paralysis. Neomycin is thought to be the most potent neuromuscular blocking agent in the class. However, the risk is greatest with intraperitoneal or intrapleural instillation of large doses or rapid intravenous administration of parenteral aminoglycosides. If signs of respiratory paralysis occur during aminoglycoside therapy, the drug should be discontinued and mechanical respiratory assistance provided if necessary.

Deferasirox has a major potential interaction with Immunodeficiency.

The use of deferasirox is contraindicated in patients with platelet counts below 50 x 109/L. Cytopenias, worsening anemia, and thrombocytopenia, including fatal events, have been reported in patients treated with deferasirox. Preexisting hematologic disorders may increase this risk. It is recommended to monitor blood counts in all patients and to interrupt treatment in patients who develop cytopenias until the cause of the cytopenia has been determined.

Deferasirox has a major potential interaction with Liver Disease.

The use of deferasirox should be avoided in patients with severe hepatic impairment. The starting dose of deferasirox should be reduced by 50% in patients with moderate hepatic impairment. It is recommended to measure serum transaminases and bilirubin in all patients prior to initiating treatment, every 2 weeks during the first month, and at least monthly or more frequently as clinically appropriate. Closely monitor patients with mild or moderate hepatic impairment for efficacy and adverse reactions that may require dose titration.

The gentamicin in Cidomycin has a major potential interaction with Myoneural Disorder.

Therapy with aminoglycosides should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia. Aminoglycosides can aggravate muscle weakness because of their potential curare-like effects on the neuromuscular junction, and may cause neuromuscular blockade, respiratory failure, and prolonged respiratory paralysis on these patients. Aminoglycoside- induced neuromuscular blockade is generally self-limiting, it may rarely result in respiratory paralysis. Neomycin is thought to be the most potent neuromuscular blocking agent in the class. However, the risk is greatest with intraperitoneal or intrapleural instillation of large doses or rapid intravenous administration of parenteral aminoglycosides. If signs of respiratory paralysis occur during aminoglycoside therapy, the drug should be discontinued and mechanical respiratory assistance provided if necessary.

The gentamicin in Cidomycin has a major potential interaction with Parkinsonism.

Therapy with aminoglycosides should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia. Aminoglycosides can aggravate muscle weakness because of their potential curare-like effects on the neuromuscular junction, and may cause neuromuscular blockade, respiratory failure, and prolonged respiratory paralysis on these patients. Aminoglycoside- induced neuromuscular blockade is generally self-limiting, it may rarely result in respiratory paralysis. Neomycin is thought to be the most potent neuromuscular blocking agent in the class. However, the risk is greatest with intraperitoneal or intrapleural instillation of large doses or rapid intravenous administration of parenteral aminoglycosides. If signs of respiratory paralysis occur during aminoglycoside therapy, the drug should be discontinued and mechanical respiratory assistance provided if necessary.

The gentamicin in Cidomycin has a major potential interaction with Renal Dysfunction.

Aminoglycosides are potentially oto- and nephrotoxic. Eighth cranial nerve damage may manifest as vestibular and/or auditory toxicities, including dizziness, nystagmus, vertigo, ataxia, tinnitus, and varying degrees of hearing impairment. Nephrotoxicity is usually evidenced by tubular necrosis; increases in BUN, nonprotein nitrogen, and serum creatinine concentration; decreases in urine specific gravity and creatinine clearance; proteinuria; and cells or casts in the urine. Rarely, renal electrolyte wasting may occur, resulting in hypocalcemia, hypomagnesemia, and hypokalemia that may be associated with paresthesia, tetany, confusion, and positive Chvostek and Trousseau signs. Although aminoglycoside- induced nephrotoxicity is generally reversible following discontinuation of the drug, death from uremia has occurred rarely. Therapy with aminoglycosides should be administered cautiously at reduced dosages in patients with renal impairment, since they may be at increased risk for oto- and nephrotoxicity due to drug accumulation. To minimize the risk of toxicity, patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other neuro- and nephrotoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be periodically determined and dosage adjusted to maintain desired levels. Renal and eighth cranial nerve function should be closely monitored, and the dosage reduced or therapy withdrawn if toxicity develops.

Deferasirox has a major potential interaction with Renal Dysfunction.

The use of deferasirox is contraindicated in patients with serum creatinine greater than two times the age-appropriate upper limit of normal or creatinine clearance less than 40 mL/min. The starting dose of deferasirox should be reduced by 50% in patients with creatine clearance 40 to 60 mL/min. It is recommended to measure serum creatine and calculate clearance in duplicate prior to initiating treatment in all patients and monitor renal function at least monthly or more frequently as clinically appropriate. Consider dose reduction, interruption, or discontinuation of deferasirox based on increases in serum creatinine.

Deferasirox has a major potential interaction with Thrombocytopenia.

The use of deferasirox is contraindicated in patients with platelet counts below 50 x 109/L. Cytopenias, worsening anemia, and thrombocytopenia, including fatal events, have been reported in patients treated with deferasirox. Preexisting hematologic disorders may increase this risk. It is recommended to monitor blood counts in all patients and to interrupt treatment in patients who develop cytopenias until the cause of the cytopenia has been determined.

Deferasirox has a moderate potential interaction with Thrombocytopenia.

Gastrointestinal hemorrhage, ulcerations, perforations, including deaths have been documented in patients using deferasirox, especially in elderly patients who had advanced hematologic malignancies and/or low platelet counts. The risk of gastrointestinal hemorrhage may be increased when administering deferasirox in combination with drugs that have ulcerogenic or hemorrhagic potential, such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, oral bisphosphonates, or anticoagulants. It is recommended to monitor patients and discontinue therapy for suspected GI ulceration or hemorrhage. Care is recommended when using this agent in patients at risk of GI complications.

The gentamicin in Cidomycin has a major potential interaction with Tinnitus.

Aminoglycosides can cause eighth cranial nerve damage, resulting in vestibular and/or auditory toxicities. Symptoms include dizziness, nystagmus, vertigo, ataxia, tinnitus, and varying degrees of hearing impairment. Permanent hearing loss may occur, including, rarely, total or partial irreversible bilateral deafness after the drug has been discontinued. Therapy with aminoglycosides, particularly if prolonged (> 10 days), should be administered cautiously in patients with preexisting vestibular and/or auditory impairment, since it may delay the recognition or confound the diagnosis of a drug-induced ototoxic effect. To minimize the risk of toxicity, patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other ototoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be periodically determined and dosage adjusted to maintain desired levels. Serial audiograms should be obtained in patients old enough to be tested, since loss of high- frequency perception usually precedes clinical hearing loss. The dosage should be reduced or therapy withdrawn promptly if signs and symptoms of toxicity develop.

Deferasirox has a moderate potential interaction with Visual Defect/Disturbance.

Auditory disturbances (high-frequency hearing loss, decreased hearing), and ocular disturbances (lens opacities, cataracts, elevations in intraocular pressure, and retinal disorders) have been reported in patients using deferasirox. It is recommended to perform auditory and ophthalmic testing (including slit lamp examinations and dilated fundoscopy) before starting therapy with deferasirox and thereafter as clinically indicated. If disturbances are noted, consider dose reduction or interruption if appropriate.

The gentamicin in Cidomycin has a major potential interaction with Vomiting.

Adequate hydration is crucial to minimize the risk of oto- and nephrotoxicity associated with the use of aminoglycosides. Dehydration should preferably be corrected prior to initiation of therapy. In patients who may be at risk for dehydration, such as those with severe and/or prolonged diarrhea or vomiting, fluid status should be monitored closely. If signs of renal irritation develop during therapy, hydration should be increased as indicated, accompanied by a reduction in dosage if necessary. Therapy should be withdrawn if urinary output decreases progressively or azotemia increases.