Drug Interactions between chloroquine and levofloxacin

You may want to limit your consumption of grapefruit or grapefruit juice during treatment with chloroquine. Grapefruit juice can significantly increase the blood levels and effects of chloroquine, which may result in an irregular heart rate or other conduction disturbances. Hydroxychloroquine should also be taken with food or milk to reduce the incidence of stomach upset. Talk to your doctor if you have any questions or concerns. You should seek immediate medical attention if you develop sudden dizziness, lightheadedness, fainting, shortness of breath, or heart palpitations during treatment with chloroquine. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

When levoFLOXacin as the oral solution is given with enteral (tube) feedings, levoFLOXacin may not work as well. You could interrupt the feeding for 1 hour before and 2 hours after the levoFLOXacin dose. However, this still may not entirely avoid the interaction and may not always be feasible. LevoFLOXacin oral tablets may be taken without regard to food. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

The use of aminoquinolines in patients with porphyria may exacerbate the condition. Aminoquinolines should not be used in these patients unless the potential benefits are anticipated to outweigh the risks.

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.

The use of 4-aminoquinolines is generally considered contraindicated in the presence of retinal or visual field changes, whether attributable to 4-aminoquinoline compounds or to any other etiology. However, in the treatment of acute attacks of malaria caused by susceptible strains of plasmodia, these agents may be considered if potential benefits are anticipated to outweigh the risks. 4-aminoquinolines are oculotoxic and can cause dose-related, irreversible retinal damage and vision loss during and up to several years after long-term or high-dose therapy (e.g., in the treatment of systemic lupus erythematosus or rheumatoid arthritis). Ophthalmologic monitoring, including visual acuity, expert slit-lamp, funduscopic, and visual field tests, is recommended at baseline and every three months during prolonged use. Therapy should be discontinued immediately if abnormalities develop in visual acuity, visual field, or retinal macular areas (e.g., pigmentary changes, loss of foveal reflex), or if the patient experiences visual symptoms such as light flashes and streaks that are not fully explainable by difficulties of accommodation or corneal opacities. Other common symptoms that may indicate retinopathy include nyctalopia, photophobia, blurred distance vision, difficulty reading or seeing (e.g., words or letters disappearing or parts of objects missing; misty vision; fog before the eyes), and missing or blacked out areas in the central or peripheral visual field. Retinal changes and visual disturbances may progress even after cessation of therapy. However, in a number of patients, early retinopathy (macular pigmentation sometimes with central field defects) diminished or regressed completely after therapy was discontinued. Paracentral scotoma to red targets, sometimes termed premaculopathy, is indicative of early retinal dysfunction and is usually reversible with cessation of therapy.

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.

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.

Aminoquinolines may concentrate in the liver. Isolated cases of abnormal liver function and fulminant hepatic failure have been reported. Therapy with aminoquinolines should be administered cautiously in patients with hepatic disease or alcoholism and in patients receiving other hepatotoxic drugs. Periodic evaluation of hepatic function should be performed during prolonged therapy.

The use of 4-aminoquinolines such as hydroxychloroquine and chloroquine prolong the QT interval. Ventricular arrhythmias and torsades de pointes have been reported in patients taking these agents. Care should be exercised in patients with a prolonged QT interval at baseline or at increased risk for arrythmia. A baseline electrocardiogram should be obtained to assess for QT interval prolongation and other abnormalities. It is recommended to use appropriate diagnostic tools such as ECG to monitor patients during therapy.

Adverse hematologic effects including neutropenia, agranulocytosis, aplastic anemia, and thrombocytopenia have been rarely associated with 4-aminoquinolines. Therapy with 4-aminoquinolines should be administered cautiously in patients with preexisting bone marrow suppression. A complete blood count should be performed periodically in patients on prolonged therapy. If any severe blood disorder appears which is not attributable to the disease under treatment, discontinuance of the drug should be considered.

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).

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.

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).

Hemolysis and acute renal failure have been reported during use of aminoquinolines in patients with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. Therapy with aminoquinolines should be administered cautiously in these patients. Blood cell counts and hemoglobin determinations should be performed regularly. Aminoquinoline therapy should be discontinued immediately if signs suggestive of hemolytic anemia occur, such as marked darkening of the urine or sudden decrease in hemoglobin concentration or erythrocytic count.

The use of 4-aminoquinolines has been associated rarely with ototoxicity. Nerve-type deafness, which is usually irreversible, has occurred during long-term, high-dose therapy. Deafness may not be apparent until several weeks after 4-aminoquinoline therapy. Tinnitus and reduced hearing have been reported in patients with preexisting auditory damage. Therapy with 4-aminoquinolines should be administered cautiously in such patients. If new auditory defects develop or if hearing loss becomes worse, therapy should be immediately discontinued and the patient closely monitored.

The following quinolones are known to be partially removed by hemodialysis and should be administered after dialysis: ciprofloxacin, enoxacin, gatifloxacin, levofloxacin, lomefloxacin, and ofloxacin.

Aminoquinolines may concentrate in the liver. Isolated cases of abnormal liver function and fulminant hepatic failure have been reported. Therapy with aminoquinolines should be administered cautiously in patients with hepatic disease or alcoholism and in patients receiving other hepatotoxic drugs. Periodic evaluation of hepatic function should be performed during prolonged therapy.

Certain aminoquinolines such as chloroquine, and hydroxychloroquine should be used with caution in patients with myasthenia gravis (MG). These agents may exacerbate or trigger new onset of symptoms in patients with previously diagnosed MG. It is recommended to advise patients with MG about this possible side effect.

The use of aminoquinolines in patients with psoriasis may precipitate a severe attack of psoriasis. Aminoquinolines should not be used in these patients unless the potential benefits are anticipated to outweigh the risks.

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.

4-aminoquinolines may cause epileptic seizures in susceptible individuals. Patients with epilepsy or an otherwise low seizure threshold may be at greater risk. Therapy with 4-aminoquinolines, particularly chloroquine, should be administered cautiously in patients with epilepsy.

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).