Drug Interactions between etanercept and lidocaine

Grapefruit juice may increase the blood levels of lidocaine, which may increase the risk of side effects such as low blood pressure, slow heart rate, irregular heart rhythm, difficulty breathing and convulsions. Cigarette smoking may reduce the blood levels of lidocaine, which may make the medication less effective. It is best to avoid smoking during lidocaine therapy. Consuming cruciferous vegetables (e.G., broccoli, brussels sprouts) may also reduce the blood levels of lidocaine. Talk to a healthcare professional if you have any questions or concerns. 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.

As you stop smoking during treatment with nicotine, your dosage requirement of lidocaine may need to be changed. Talk to your doctor if you have any questions or concerns. Your doctor may be able to prescribe alternatives that do not interact, or you may need a dose adjustment or more frequent monitoring by your doctor to safely use both medications. 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.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

The use of lidocaine is contraindicated in patients with Stokes-Adam syndrome, Wolff-Parkinson White syndrome, or second- or third-degree AV block in the absence of a functional artificial pacemaker, or congenital QT prolongation.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

Etanercept is contraindicated in patients with sepsis and it should be discontinued if a patient develops a serious infection or sepsis. Etanercept therapy should not be initiated in patients with an active infection, including clinically important localized infections. Patients should be closely monitored for the development of signs and symptoms of infection during and after treatment with etanercept. A patient who develops a new infection during treatment with etanercept should be closely monitored, undergo a prompt and complete diagnostic workup appropriate for an immunocompromised patient, and appropriate antimicrobial therapy should be initiated.

Etanercept, has been associated with reactivation of hepatitis B, in some cases fatal, in patients who were previously infected with the hepatitis B virus (HBV) and had received concomitant TNF-blocking agents. Therefore, screening for viral hepatitis should be performed in accordance with published guidelines before starting therapy with etanercept. Monitor patients at risk or with evidence of current or prior HBV infection for clinical and laboratory signs of hepatitis or HBV reactivation. Prescribers should exercise caution in prescribing TNF blockers in patients previously infected with HBV Monitor patients with evidence of current or prior HBV infection for clinical and laboratory signs of hepatitis or HBV reactivation during and for several months following etanercept therapy. In patients who develop HBV reactivation, consideration should be given to stopping etanercept and initiating anti-viral therapy with appropriate supportive treatment. The safety of resuming etanercept therapy after HBV reactivation is controlled is not known. Therefore, prescribers should weigh the risks and benefits when considering resumption of therapy.

Lidocaine is rapidly and extensively metabolized by the liver. Less than 10% is eliminated unchanged in the urine. Several inactive and two active forms (MEGX and GX) have been identified. MEGX and GX exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. The pharmacokinetic disposition of lidocaine is altered by changes in hepatic function, including hepatic blood flow. Therapy with lidocaine should be administered cautiously and dosing modifications for repeated or loading and maintenance doses may be necessary. Clinical monitoring of cardiac (continuous ECG) is required and serum metabolite concentrations and monitoring hepatic function are recommended.

Lidocaine is primarily eliminated by the kidney. Less than 10% is eliminated unchanged in the urine. Two active metabolites (MEGX and GX) have been identified that exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. Serum concentrations of lidocaine and the active metabolites are increased and the half-life prolonged in patients with renal impairment. Therapy with lidocaine should be administered cautiously and dosing modified for repeated or maintenance doses in patients with compromised renal function. Clinical monitoring of cardiac function (continual ECG) is required and serum metabolite concentrations and monitoring renal function are recommended.

Seizures have occurred during lidocaine therapy and have been associated with the rapid administration of a large intravenous doses or accumulation of active metabolites with maintenance therapy. Therapy with lidocaine should be administered cautiously to patients with or predisposed to seizure disorders. Clinical monitoring of cardiac (continuous ECG) is required, and serum metabolite concentrations are recommended.

Etanercept has been associated with the reactivation of tuberculosis and new tuberculosis infections have been observed during the course of treatment, including patients who have previously received treatment for latent or active tuberculosis. Tuberculosis has developed in patients who tested negative for latent tuberculosis prior to initiation of therapy. Patients should be evaluated for tuberculosis risk factors and tested for latent infection prior to initiating etanercept and periodically during therapy. Anti-tuberculosis therapy should also be considered prior to initiation of etanercept in patients with a past history of latent or active tuberculosis in whom an adequate course of treatment cannot be confirmed, and for patients with a negative test for latent tuberculosis but having risk factors for tuberculosis infection. Tuberculosis should be strongly considered in patients who develop a new infection during etanercept treatment, especially in patients who have previously or recently traveled to countries with a high prevalence of tuberculosis, or who have had close contact with a person with active tuberculosis.

Etanercept has been associated with the reactivation of tuberculosis and new tuberculosis infections have been observed during the course of treatment, including patients who have previously received treatment for latent or active tuberculosis. Tuberculosis has developed in patients who tested negative for latent tuberculosis prior to initiation of therapy. Patients should be evaluated for tuberculosis risk factors and tested for latent infection prior to initiating etanercept and periodically during therapy. Anti-tuberculosis therapy should also be considered prior to initiation of etanercept in patients with a past history of latent or active tuberculosis in whom an adequate course of treatment cannot be confirmed, and for patients with a negative test for latent tuberculosis but having risk factors for tuberculosis infection. Tuberculosis should be strongly considered in patients who develop a new infection during etanercept treatment, especially in patients who have previously or recently traveled to countries with a high prevalence of tuberculosis, or who have had close contact with a person with active tuberculosis.

A study in patients with moderate to severe alcoholic hepatitis treated with etanercept or placebo, showed that the mortality rate in patients in both groups was similar at 1 month but significantly higher after 6 months on the etanercept group. Caution should be exercised when using etanercept in patients with moderate to severe alcoholic hepatitis.

Etanercept has been associated with rare cases of new onset or exacerbation of central nervous system demyelinating disorders, some presenting with mental status changes and some associated with permanent disability, and with peripheral nervous system demyelinating disorders. There have been postmarketing reports of transverse myelitis, optic neuritis, multiple sclerosis, Guillain-Barré syndromes, other peripheral demyelinating neuropathies, and new onset or exacerbation of seizure disorders with etanercept therapy. Care should exercise when considering the use of etanercept in patients with preexisting or recent-onset central or peripheral nervous system demyelinating disorders.

Rare events of pancytopenia including very rare events of aplastic anemia, some with a fatal outcome, have been reported in patients treated with etanercept. Discontinuation of etanercept therapy should be considered in patients with confirmed significant hematologic abnormalities. Caution should be exercised in patients being treated with etanercept who have a previous history of significant hematologic abnormalities. All patients should be advised to seek immediate medical attention if they develop signs and symptoms suggestive of blood dyscrasias or infection (eg, persistent fever, bruising, bleeding, pallor) while on therapy with etanercept.

Etanercept, has been associated with worsening of congestive heart failure (CHF), with and without identifiable precipitating factors. There have also been rare (< 0.1%) reports of new onset CHF, including CHF in patients without known preexisting cardiovascular disease. Care should be exercised when prescribing etanercept to patients at risk cardiovascular disease or with heart failure.

Rare events of pancytopenia including very rare events of aplastic anemia, some with a fatal outcome, have been reported in patients treated with etanercept. Discontinuation of etanercept therapy should be considered in patients with confirmed significant hematologic abnormalities. Caution should be exercised in patients being treated with etanercept who have a previous history of significant hematologic abnormalities. All patients should be advised to seek immediate medical attention if they develop signs and symptoms suggestive of blood dyscrasias or infection (eg, persistent fever, bruising, bleeding, pallor) while on therapy with etanercept.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

There have been reports of hypoglycemia following initiation of etanercept therapy in patients receiving medication for diabetes, necessitating a reduction in anti-diabetic medication in some of these patients. Care should be taken when prescribing this agent to diabetic patients.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

Rare events of pancytopenia including very rare events of aplastic anemia, some with a fatal outcome, have been reported in patients treated with etanercept. Discontinuation of etanercept therapy should be considered in patients with confirmed significant hematologic abnormalities. Caution should be exercised in patients being treated with etanercept who have a previous history of significant hematologic abnormalities. All patients should be advised to seek immediate medical attention if they develop signs and symptoms suggestive of blood dyscrasias or infection (eg, persistent fever, bruising, bleeding, pallor) while on therapy with etanercept.

Etanercept has been associated with rare cases of new onset or exacerbation of central nervous system demyelinating disorders, some presenting with mental status changes and some associated with permanent disability, and with peripheral nervous system demyelinating disorders. There have been postmarketing reports of transverse myelitis, optic neuritis, multiple sclerosis, Guillain-Barré syndromes, other peripheral demyelinating neuropathies, and new onset or exacerbation of seizure disorders with etanercept therapy. Care should exercise when considering the use of etanercept in patients with preexisting or recent-onset central or peripheral nervous system demyelinating disorders.

Etanercept has been associated with rare cases of new onset or exacerbation of central nervous system demyelinating disorders, some presenting with mental status changes and some associated with permanent disability, and with peripheral nervous system demyelinating disorders. There have been postmarketing reports of transverse myelitis, optic neuritis, multiple sclerosis, Guillain-Barré syndromes, other peripheral demyelinating neuropathies, and new onset or exacerbation of seizure disorders with etanercept therapy. Care should exercise when considering the use of etanercept in patients with preexisting or recent-onset central or peripheral nervous system demyelinating disorders.

The manufacturer of etanercept recommends that patients with a significant exposure to varicella virus should temporarily discontinue therapy and be considered for prophylactic treatment with varicella zoster immune globulin.

The use of etanercept in patients with Wegener's granulomatosis receiving immunosuppressive agents is not recommended. In a study, the addition of etanercept to standard therapy, including cyclophosphamide, to patients with Wegener's granulomatosis was associated with a higher incidence of non-cutaneous solid malignancies and was not associated with improved clinical outcomes when compared with standard therapy alone. Therefore, prescribers should weigh the risks and benefits when considering therapy in this situation.