Drug Interaction Report

Gemifloxacin has a major potential interaction with Abnormal Electrocardiogram.

Quinolones have been reported to prolong the QT interval of the electrocardiogram in some patients. QT prolongation may potentiate the risk of ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsade de pointes. The risk appears to be greatest with grepafloxacin and sparfloxacin (both are no longer marketed in the U.S.), although cardiovascular morbidity and mortality attributable to QT prolongation have also been reported rarely with others like gatifloxacin, levofloxacin, ciprofloxacin, and ofloxacin. Reported cases have primarily occurred in patients with advanced age, cardiac disease, electrolyte disturbances, and/or underlying medical problems for which they were receiving concomitant medications known to prolong the QT interval. Therapy with quinolones should be avoided in patients with known QT prolongation and/or uncorrected electrolyte disorders (hypokalemia or hypomagnesemia) and in patients treated concomitantly with class IA or III antiarrhythmic agents. Cautious use with ECG monitoring is advised in patients with other proarrhythmic conditions such as clinically significant bradycardia, congestive heart failure, acute myocardial ischemia, and atrial fibrillation. As QT prolongation may be a concentration-dependent effect, it is important that the recommended dosages or infusion rates of these drugs not be exceeded, particularly in patients with renal and/or hepatic impairment.

Foscarnet has a moderate potential interaction with Anemia.

The use of foscarnet is associated with hematologic toxicities, most commonly anemia and granulocytopenia. Thrombocytopenia has been reported rarely. Therapy with foscarnet should be administered cautiously in patients with preexisting blood dyscrasias or bone marrow suppression. Routine blood counts are recommended.

Gemifloxacin has a major potential interaction with Arrhythmia.

Quinolones have been reported to prolong the QT interval of the electrocardiogram in some patients. QT prolongation may potentiate the risk of ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsade de pointes. The risk appears to be greatest with grepafloxacin and sparfloxacin (both are no longer marketed in the U.S.), although cardiovascular morbidity and mortality attributable to QT prolongation have also been reported rarely with others like gatifloxacin, levofloxacin, ciprofloxacin, and ofloxacin. Reported cases have primarily occurred in patients with advanced age, cardiac disease, electrolyte disturbances, and/or underlying medical problems for which they were receiving concomitant medications known to prolong the QT interval. Therapy with quinolones should be avoided in patients with known QT prolongation and/or uncorrected electrolyte disorders (hypokalemia or hypomagnesemia) and in patients treated concomitantly with class IA or III antiarrhythmic agents. Cautious use with ECG monitoring is advised in patients with other proarrhythmic conditions such as clinically significant bradycardia, congestive heart failure, acute myocardial ischemia, and atrial fibrillation. As QT prolongation may be a concentration-dependent effect, it is important that the recommended dosages or infusion rates of these drugs not be exceeded, particularly in patients with renal and/or hepatic impairment.

Foscarnet has a major potential interaction with Central Nervous System Disorders.

Foscarnet may cause electrolyte disturbances, including hypocalcemia, hypo- or hyperphosphatemia, hypomagnesemia, and hypokalemia. Ionized serum calcium may also demonstrate a dose-dependent (and possibly rate-dependent) decrease that may not be reflected in total serum calcium. Patients should be instructed to report symptoms of low ionized calcium such as perioral tingling, numbness in the extremities, and paresthesias. Other electrolyte-related complications include tetany, seizures, and cardiac disturbances. Therapy with foscarnet should be administered cautiously in patients with preexisting fluid and electrolyte imbalance and those with underlying cardiac or neurologic abnormalities. Serum electrolyte levels should be closely monitored and managed in all patients treated with foscarnet.

Gemifloxacin has a major potential interaction with Central Nervous System Disorders.

Quinolones may cause CNS stimulation manifested as tremors, agitation, restlessness, anxiety, confusion, hallucinations, paranoia, insomnia, toxic psychosis, and/or seizures. Benign intracranial hypertension has also been reported. Therapy with quinolones should be administered cautiously in patients with or predisposed to seizures or other CNS abnormalities. In addition, these patients should be advised to avoid the consumption of caffeine-containing products during therapy with some quinolones, most notably ciprofloxacin, enoxacin, and cinoxacin, since these agents can substantially reduce the clearance of caffeine and other methylxanthines, potentially resulting in severe CNS reactions.

Foscarnet has a major potential interaction with Dehydration.

Foscarnet is nephrotoxic. Foscarnet crystals may deposit in renal tubules and capillaries, sometimes causing acute tubular necrosis and renal failure. Foscarnet may also concentrate in the urine and cause penile or vulvovaginal irritation. Adequate hydration is crucial to minimize the risk of renal damage and genital ulcerations. Generally, foscarnet should be administered by an infusion pump over 1 to 2 hours accompanied by hydration. The manufacturer recommends 750 to 1000 mL of normal saline or 5% dextrose solution prior to the first infusion of foscarnet to establish diuresis, then 500 mL (for 40 to 60 mg/kg dose of foscarnet) or 750 to 1000 mL (for 90 to 120 mg/kg dose of foscarnet) of hydration fluid concurrently with each subsequent foscarnet infusion. Patients who are dehydrated may be at increased risk for the development of nephrotoxicity and may benefit from additional hydration if tolerated.

Gemifloxacin has a moderate potential interaction with Dehydration.

Crystalluria has been reported rarely during quinolone therapy. Although it is not expected to occur under normal circumstances with usual recommended dosages, patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid to ensure an adequate urinary output. Alkalinity of the urine should be avoided, since it may also increase the risk of crystalluria. Renal function tests should be performed periodically during prolonged therapy (> 2 weeks).

Gemifloxacin has a moderate potential interaction with Diabetes Mellitus.

The use of certain quinolones has been associated with disturbances in blood glucose homeostasis possibly stemming from effects on pancreatic beta cell ATP-sensitive potassium channels that regulate insulin secretion. Hypoglycemia and, less frequently, hyperglycemia have been reported, although the latter may also occur due to infection alone. Hypoglycemia has usually occurred in patients with diabetes receiving concomitant oral hypoglycemic agents and/or insulin. Administration of ciprofloxacin, levofloxacin, norfloxacin, and especially gatifloxacin in patients treated with sulfonylureas or other oral hypoglycemic agents has resulted in severe, refractory hypoglycemia and hypoglycemic coma. Elderly patients and patients with reduced renal function are particularly susceptible. Blood glucose should be monitored more closely whenever quinolones are prescribed to patients with diabetes. Gatifloxacin has been known to cause hypoglycemic episodes generally within the first 3 days of therapy and sometimes even after the first dose, while hyperglycemia usually occurs 4 to 10 days after initiation of therapy. Patients should be counseled to recognize symptoms of hypoglycemia such as headache, dizziness, drowsiness, nausea, tremor, weakness, hunger, excessive perspiration, and palpitations. If hypo- or hyperglycemia occur during quinolone therapy, patients should initiate appropriate remedial therapy immediately, discontinue the antibiotic, and contact their physician.

Gemifloxacin has a moderate potential interaction with Diarrhea.

Crystalluria has been reported rarely during quinolone therapy. Although it is not expected to occur under normal circumstances with usual recommended dosages, patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid to ensure an adequate urinary output. Alkalinity of the urine should be avoided, since it may also increase the risk of crystalluria. Renal function tests should be performed periodically during prolonged therapy (> 2 weeks).

Foscarnet has a major potential interaction with Electrolyte Abnormalities.

Foscarnet may cause electrolyte disturbances, including hypocalcemia, hypo- or hyperphosphatemia, hypomagnesemia, and hypokalemia. Ionized serum calcium may also demonstrate a dose-dependent (and possibly rate-dependent) decrease that may not be reflected in total serum calcium. Patients should be instructed to report symptoms of low ionized calcium such as perioral tingling, numbness in the extremities, and paresthesias. Other electrolyte-related complications include tetany, seizures, and cardiac disturbances. Therapy with foscarnet should be administered cautiously in patients with preexisting fluid and electrolyte imbalance and those with underlying cardiac or neurologic abnormalities. Serum electrolyte levels should be closely monitored and managed in all patients treated with foscarnet.

Gemifloxacin has a major potential interaction with Electrolyte Abnormalities.

Quinolones have been reported to prolong the QT interval of the electrocardiogram in some patients. QT prolongation may potentiate the risk of ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsade de pointes. The risk appears to be greatest with grepafloxacin and sparfloxacin (both are no longer marketed in the U.S.), although cardiovascular morbidity and mortality attributable to QT prolongation have also been reported rarely with others like gatifloxacin, levofloxacin, ciprofloxacin, and ofloxacin. Reported cases have primarily occurred in patients with advanced age, cardiac disease, electrolyte disturbances, and/or underlying medical problems for which they were receiving concomitant medications known to prolong the QT interval. Therapy with quinolones should be avoided in patients with known QT prolongation and/or uncorrected electrolyte disorders (hypokalemia or hypomagnesemia) and in patients treated concomitantly with class IA or III antiarrhythmic agents. Cautious use with ECG monitoring is advised in patients with other proarrhythmic conditions such as clinically significant bradycardia, congestive heart failure, acute myocardial ischemia, and atrial fibrillation. As QT prolongation may be a concentration-dependent effect, it is important that the recommended dosages or infusion rates of these drugs not be exceeded, particularly in patients with renal and/or hepatic impairment.

Foscarnet has a major potential interaction with Heart Disease.

Foscarnet may cause electrolyte disturbances, including hypocalcemia, hypo- or hyperphosphatemia, hypomagnesemia, and hypokalemia. Ionized serum calcium may also demonstrate a dose-dependent (and possibly rate-dependent) decrease that may not be reflected in total serum calcium. Patients should be instructed to report symptoms of low ionized calcium such as perioral tingling, numbness in the extremities, and paresthesias. Other electrolyte-related complications include tetany, seizures, and cardiac disturbances. Therapy with foscarnet should be administered cautiously in patients with preexisting fluid and electrolyte imbalance and those with underlying cardiac or neurologic abnormalities. Serum electrolyte levels should be closely monitored and managed in all patients treated with foscarnet.

Gemifloxacin has a major potential interaction with Heart Failure.

Quinolones have been reported to prolong the QT interval of the electrocardiogram in some patients. QT prolongation may potentiate the risk of ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsade de pointes. The risk appears to be greatest with grepafloxacin and sparfloxacin (both are no longer marketed in the U.S.), although cardiovascular morbidity and mortality attributable to QT prolongation have also been reported rarely with others like gatifloxacin, levofloxacin, ciprofloxacin, and ofloxacin. Reported cases have primarily occurred in patients with advanced age, cardiac disease, electrolyte disturbances, and/or underlying medical problems for which they were receiving concomitant medications known to prolong the QT interval. Therapy with quinolones should be avoided in patients with known QT prolongation and/or uncorrected electrolyte disorders (hypokalemia or hypomagnesemia) and in patients treated concomitantly with class IA or III antiarrhythmic agents. Cautious use with ECG monitoring is advised in patients with other proarrhythmic conditions such as clinically significant bradycardia, congestive heart failure, acute myocardial ischemia, and atrial fibrillation. As QT prolongation may be a concentration-dependent effect, it is important that the recommended dosages or infusion rates of these drugs not be exceeded, particularly in patients with renal and/or hepatic impairment.

Foscarnet has a moderate potential interaction with History of Blood Dyscrasias.

The use of foscarnet is associated with hematologic toxicities, most commonly anemia and granulocytopenia. Thrombocytopenia has been reported rarely. Therapy with foscarnet should be administered cautiously in patients with preexisting blood dyscrasias or bone marrow suppression. Routine blood counts are recommended.

Foscarnet has a major potential interaction with Hypocalcemia.

Foscarnet may cause electrolyte disturbances, including hypocalcemia, hypo- or hyperphosphatemia, hypomagnesemia, and hypokalemia. Ionized serum calcium may also demonstrate a dose-dependent (and possibly rate-dependent) decrease that may not be reflected in total serum calcium. Patients should be instructed to report symptoms of low ionized calcium such as perioral tingling, numbness in the extremities, and paresthesias. Other electrolyte-related complications include tetany, seizures, and cardiac disturbances. Therapy with foscarnet should be administered cautiously in patients with preexisting fluid and electrolyte imbalance and those with underlying cardiac or neurologic abnormalities. Serum electrolyte levels should be closely monitored and managed in all patients treated with foscarnet.

Foscarnet has a major potential interaction with Hypokalemia.

Foscarnet may cause electrolyte disturbances, including hypocalcemia, hypo- or hyperphosphatemia, hypomagnesemia, and hypokalemia. Ionized serum calcium may also demonstrate a dose-dependent (and possibly rate-dependent) decrease that may not be reflected in total serum calcium. Patients should be instructed to report symptoms of low ionized calcium such as perioral tingling, numbness in the extremities, and paresthesias. Other electrolyte-related complications include tetany, seizures, and cardiac disturbances. Therapy with foscarnet should be administered cautiously in patients with preexisting fluid and electrolyte imbalance and those with underlying cardiac or neurologic abnormalities. Serum electrolyte levels should be closely monitored and managed in all patients treated with foscarnet.

Gemifloxacin has a major potential interaction with Hypokalemia.

Quinolones have been reported to prolong the QT interval of the electrocardiogram in some patients. QT prolongation may potentiate the risk of ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsade de pointes. The risk appears to be greatest with grepafloxacin and sparfloxacin (both are no longer marketed in the U.S.), although cardiovascular morbidity and mortality attributable to QT prolongation have also been reported rarely with others like gatifloxacin, levofloxacin, ciprofloxacin, and ofloxacin. Reported cases have primarily occurred in patients with advanced age, cardiac disease, electrolyte disturbances, and/or underlying medical problems for which they were receiving concomitant medications known to prolong the QT interval. Therapy with quinolones should be avoided in patients with known QT prolongation and/or uncorrected electrolyte disorders (hypokalemia or hypomagnesemia) and in patients treated concomitantly with class IA or III antiarrhythmic agents. Cautious use with ECG monitoring is advised in patients with other proarrhythmic conditions such as clinically significant bradycardia, congestive heart failure, acute myocardial ischemia, and atrial fibrillation. As QT prolongation may be a concentration-dependent effect, it is important that the recommended dosages or infusion rates of these drugs not be exceeded, particularly in patients with renal and/or hepatic impairment.

Gemifloxacin has a major potential interaction with Ischemic Heart Disease.

Quinolones have been reported to prolong the QT interval of the electrocardiogram in some patients. QT prolongation may potentiate the risk of ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsade de pointes. The risk appears to be greatest with grepafloxacin and sparfloxacin (both are no longer marketed in the U.S.), although cardiovascular morbidity and mortality attributable to QT prolongation have also been reported rarely with others like gatifloxacin, levofloxacin, ciprofloxacin, and ofloxacin. Reported cases have primarily occurred in patients with advanced age, cardiac disease, electrolyte disturbances, and/or underlying medical problems for which they were receiving concomitant medications known to prolong the QT interval. Therapy with quinolones should be avoided in patients with known QT prolongation and/or uncorrected electrolyte disorders (hypokalemia or hypomagnesemia) and in patients treated concomitantly with class IA or III antiarrhythmic agents. Cautious use with ECG monitoring is advised in patients with other proarrhythmic conditions such as clinically significant bradycardia, congestive heart failure, acute myocardial ischemia, and atrial fibrillation. As QT prolongation may be a concentration-dependent effect, it is important that the recommended dosages or infusion rates of these drugs not be exceeded, particularly in patients with renal and/or hepatic impairment.

Foscarnet has a major potential interaction with Magnesium Imbalance.

Foscarnet may cause electrolyte disturbances, including hypocalcemia, hypo- or hyperphosphatemia, hypomagnesemia, and hypokalemia. Ionized serum calcium may also demonstrate a dose-dependent (and possibly rate-dependent) decrease that may not be reflected in total serum calcium. Patients should be instructed to report symptoms of low ionized calcium such as perioral tingling, numbness in the extremities, and paresthesias. Other electrolyte-related complications include tetany, seizures, and cardiac disturbances. Therapy with foscarnet should be administered cautiously in patients with preexisting fluid and electrolyte imbalance and those with underlying cardiac or neurologic abnormalities. Serum electrolyte levels should be closely monitored and managed in all patients treated with foscarnet.

Gemifloxacin has a major potential interaction with Magnesium Imbalance.

Quinolones have been reported to prolong the QT interval of the electrocardiogram in some patients. QT prolongation may potentiate the risk of ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsade de pointes. The risk appears to be greatest with grepafloxacin and sparfloxacin (both are no longer marketed in the U.S.), although cardiovascular morbidity and mortality attributable to QT prolongation have also been reported rarely with others like gatifloxacin, levofloxacin, ciprofloxacin, and ofloxacin. Reported cases have primarily occurred in patients with advanced age, cardiac disease, electrolyte disturbances, and/or underlying medical problems for which they were receiving concomitant medications known to prolong the QT interval. Therapy with quinolones should be avoided in patients with known QT prolongation and/or uncorrected electrolyte disorders (hypokalemia or hypomagnesemia) and in patients treated concomitantly with class IA or III antiarrhythmic agents. Cautious use with ECG monitoring is advised in patients with other proarrhythmic conditions such as clinically significant bradycardia, congestive heart failure, acute myocardial ischemia, and atrial fibrillation. As QT prolongation may be a concentration-dependent effect, it is important that the recommended dosages or infusion rates of these drugs not be exceeded, particularly in patients with renal and/or hepatic impairment.

Gemifloxacin has a major potential interaction with Myasthenia Gravis.

Fluoroquinolones have neuromuscular blocking activity and may exacerbate muscle weakness in persons with myasthenia gravis. Postmarketing serious adverse events, including deaths and requirement for ventilatory support, have been associated with fluoroquinolones use in persons with myasthenia gravis. Fluoroquinolones should be avoided in patients with history of myasthenia gravis.

Foscarnet has a moderate potential interaction with Neutropenia.

The use of foscarnet is associated with hematologic toxicities, most commonly anemia and granulocytopenia. Thrombocytopenia has been reported rarely. Therapy with foscarnet should be administered cautiously in patients with preexisting blood dyscrasias or bone marrow suppression. Routine blood counts are recommended.

Gemifloxacin has a major potential interaction with Noninfectious Colitis.

Clostridioides difficile-associated diarrhea (CDAD), formerly pseudomembranous colitis, has been reported with almost all antibacterial drugs and may range from mild diarrhea to fatal colitis. The most common culprits include clindamycin and lincomycin. Antibacterial therapy alters the normal flora of the colon, leading to overgrowth of C difficile, whose toxins A and B contribute to CDAD development. Morbidity and mortality are increased with hypertoxin-producing strains of C difficile; these infections can be resistant to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea after antibacterial use. Since CDAD has been reported to occur more than 2 months after antibacterial use, careful medical history is necessary. Therapy with broad-spectrum antibacterials and other agents with significant antibacterial activity should be administered cautiously in patients with history of gastrointestinal disease, particularly colitis; pseudomembranous colitis (generally characterized by severe, persistent diarrhea and severe abdominal cramps, and sometimes associated with the passage of blood and mucus), if it occurs, may be more severe in these patients and may be associated with flares in underlying disease activity. Antibacterial drugs not directed against C difficile may need to be stopped if CDAD is suspected or confirmed. Appropriate fluid and electrolyte management, protein supplementation, antibacterial treatment of C difficile, and surgical evaluation should be started as clinically indicated.

Gemifloxacin has a major potential interaction with Organ Transplant.

Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.

Gemifloxacin has a major potential interaction with Peripheral Neuropathy.

The use of quinolones has been associated with an increased risk of peripheral neuropathy. Monitor closely and discontinue their use in patients experiencing symptoms of peripheral neuropathy. It is recommended to avoid these agents in patients who have previously experienced peripheral neuropathy.

Foscarnet has a major potential interaction with Phosphate Imbalance.

Foscarnet may cause electrolyte disturbances, including hypocalcemia, hypo- or hyperphosphatemia, hypomagnesemia, and hypokalemia. Ionized serum calcium may also demonstrate a dose-dependent (and possibly rate-dependent) decrease that may not be reflected in total serum calcium. Patients should be instructed to report symptoms of low ionized calcium such as perioral tingling, numbness in the extremities, and paresthesias. Other electrolyte-related complications include tetany, seizures, and cardiac disturbances. Therapy with foscarnet should be administered cautiously in patients with preexisting fluid and electrolyte imbalance and those with underlying cardiac or neurologic abnormalities. Serum electrolyte levels should be closely monitored and managed in all patients treated with foscarnet.

Foscarnet has a major potential interaction with Renal Dysfunction.

Foscarnet is eliminated primarily by the kidney. Patients with renal impairment may be at greater risk for dose-limiting nephrotoxicity and other adverse effects of foscarnet due to decreased drug clearance. Renal function should be closely monitored in all patients receiving therapy with foscarnet, and the dosage adjusted based on serum creatinine. Hydration is recommended to reduce the risk of nephrotoxicity. The manufacturer recommends 750 to 1000 mL of normal saline or 5% dextrose solution prior to the first infusion of foscarnet to establish diuresis, then 500 mL (for 40 to 60 mg/kg dose of foscarnet) or 750 to 1000 mL (for 90 to 120 mg/kg dose of foscarnet) of hydration fluid concurrently with each subsequent foscarnet infusion. Foscarnet should be used with caution in patients with abnormal renal function because reduced plasma clearance of foscarnet will result in elevated plasma levels. Foscarnet dosing must be individualized according to the patient's renal function status. The use of foscarnet is not recommended in patients with severe renal impairment indicated by a CrCl < 0.4 mL/min/kg and in those patients undergoing hemodialysis because dosage guidelines have not been established.

Gemifloxacin has a major potential interaction with Renal Dysfunction.

Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.

Gemifloxacin has a moderate potential interaction with Renal Dysfunction.

Quinolones (except trovafloxacin, moxifloxacin, and nalidixic acid) and their metabolites are eliminated by the kidney. Patients with renal impairment may be at greater risk for adverse effects from quinolones, including nephrotoxicity, due to decreased drug clearance. Dosage adjustments may be necessary and modifications should be based on the degree of renal impairment and severity of infection in accordance with the individual product package labeling. Renal function tests should be performed periodically during therapy.

Gemifloxacin has a major potential interaction with Rheumatoid Arthritis.

Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.

Gemifloxacin has a major potential interaction with Tendonitis.

Tendonitis and ruptures of the shoulder, hand, and Achilles tendons have been reported in patients receiving quinolones, both during and after treatment. Avoid the use of these agents in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture. Therapy with quinolones should be administered cautiously in patients with patients with kidney, heart, and lung transplant, since it may delay the recognition or confound the diagnosis of a quinolone-induced musculoskeletal effect. Factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. It is recommended to discontinue these agents if, at any time during therapy, pain, inflammation or rupture of a tendon develops and institute appropriate treatment.

Foscarnet has a moderate potential interaction with Thrombocytopenia.

The use of foscarnet is associated with hematologic toxicities, most commonly anemia and granulocytopenia. Thrombocytopenia has been reported rarely. Therapy with foscarnet should be administered cautiously in patients with preexisting blood dyscrasias or bone marrow suppression. Routine blood counts are recommended.

Gemifloxacin has a moderate potential interaction with Vomiting.

Crystalluria has been reported rarely during quinolone therapy. Although it is not expected to occur under normal circumstances with usual recommended dosages, patients who are dehydrated (e.g., due to severe diarrhea or vomiting) may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluid to ensure an adequate urinary output. Alkalinity of the urine should be avoided, since it may also increase the risk of crystalluria. Renal function tests should be performed periodically during prolonged therapy (> 2 weeks).