Interactions between Netilmicin and Zoledronic acid

Zoledronic acid has a moderate potential interaction with Asthma.

There have been reports of bronchoconstriction in aspirin-sensitive patients receiving bisphosphonates. Use of these agents in asthmatic and in aspirin-sensitive patients should be used with caution.

Netilmicin 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.

Netilmicin 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 Therapy should be withdrawn if urinary output decreases progressively or azotemia increases.

Netilmicin 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.

Netilmicin 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.

Netilmicin 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.

Zoledronic acid has a major potential interaction with Hypocalcemia.

The use of bisphosphonates is contraindicated for the treatment of osteoporosis in patients with hypocalcemia. These agents increase bone mineral density, a process that requires an adequate supply of calcium in the body. Following the initiation of therapy, a short-term reduction in serum calcium and phosphate levels usually occurs due to inhibition of bone resorption, especially in patients with Paget's disease, in whom the pretreatment rate of bone turnover may be greatly elevated. Hypocalcemia and other disturbances of mineral metabolism, such as vitamin D deficiency, should be treated prior to initiation of therapy. Appropriate intake of calcium and vitamin D should be ensured throughout the course of treatment.

Zoledronic acid has a major potential interaction with Infection.

Osteonecrosis of the jaw (ONJ), which can occur spontaneously, is generally associated with tooth extraction and/or local infection with delayed healing, and has been reported in patients taking bisphosphonates. Known risk factors for osteonecrosis of the jaw include invasive dental procedures (e.g., tooth extraction, dental implants, boney surgery), diagnosis of cancer, concomitant therapies (e.g., chemotherapy, corticosteroids, angiogenesis inhibitors), poor oral hygiene, and co-morbid disorders (e.g., periodontal and/or other pre-existing dental disease, anemia, coagulopathy, infection, ill-fitting dentures). The manufacturers of bisphosphonates recommend discontinuation of bisphosphonate treatment for patients undergoing invasive dental procedures. Patients who develop osteonecrosis of the jaw while on bisphosphonate therapy should receive care by an oral surgeon. In these patients, extensive dental surgery to treat ONJ may exacerbate the condition. Discontinuation of bisphosphonate therapy should be considered based on individual benefit/risk assessment.

Netilmicin 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.

Netilmicin 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.

Netilmicin 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.

Zoledronic acid has a major potential interaction with Renal Dysfunction.

Zoledronic acid injection is contraindicated in patients with creatinine clearance less than 35 mL/min and in those with evidence of acute renal impairment. No dosage adjustment is required in patients with a creatinine clearance of greater than or equal to 35 mL/min. Creatinine clearance should be calculated based on actual body weight using Cockcroft-Gault formula before each zoledronic acid injection dose. Acute renal failure (ARF) has been observed in patients after a single administration. If history or physical signs suggest dehydration, zoledronic acid injection therapy should be withheld until normovolemic status has been achieved. Zoledronic acid injection should be used with caution in patients with chronic renal impairment. Consider monitoring creatinine clearance in patients at-risk for ARF who are taking concomitant medications that are primarily excreted by the kidney.

Netilmicin 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.

Zoledronic acid has a major potential interaction with Vitamin D Deficiency.

The use of bisphosphonates is contraindicated for the treatment of osteoporosis in patients with hypocalcemia. These agents increase bone mineral density, a process that requires an adequate supply of calcium in the body. Following the initiation of therapy, a short-term reduction in serum calcium and phosphate levels usually occurs due to inhibition of bone resorption, especially in patients with Paget's disease, in whom the pretreatment rate of bone turnover may be greatly elevated. Hypocalcemia and other disturbances of mineral metabolism, such as vitamin D deficiency, should be treated prior to initiation of therapy. Appropriate intake of calcium and vitamin D should be ensured throughout the course of treatment.

Netilmicin 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.