Can you take Bedaquiline with Mysoline?

The primidone in Mysoline has a major potential interaction with Acute Alcohol Intoxication.

The use of barbiturates is contraindicated in patients with acute alcohol intoxication exhibiting depressed vital signs. The central nervous system depressant effects of barbiturates may be additive with those of alcohol. Severe respiratory depression and death may occur. Therapy with barbiturates should be administered cautiously in patients who might be prone to acute alcohol intake.

The primidone in Mysoline has a moderate potential interaction with Adrenal Insufficiency.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a moderate potential interaction with Adrenal Insufficiency.

Barbiturates, especially phenobarbital, secobarbital and butabarbital, may diminish the systemic effects of exogenous and endogenous corticosteroids via induction of hepatic microsomal enzymes, thereby accelerating the metabolism of corticosteroids. In addition, barbiturates may interfere with pituitary corticotropin production. Therapy with barbiturates should be administered cautiously in patients with adrenal insufficiency. Patients with borderline hypoadrenalism should be monitored closely, and patients receiving steroid supplementation may require an adjustment in dosage when barbiturates are added to or withdrawn from their medication regimen.

The primidone in Mysoline has a major potential interaction with Alcoholism.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a major potential interaction with Alcoholism.

Barbiturates have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop, particularly after prolonged use of excessive dosages. Abrupt cessation and/or a reduction in dosage may precipitate withdrawal symptoms. In patients who have developed tolerance to a barbiturate, overdosage can still produce respiratory depression and death, and cross-tolerance usually will occur with other agents in the class. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with barbiturates. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of barbiturates should be undertaken gradually using a dosage-tapering schedule.

Bedaquiline has a moderate potential interaction with Alcoholism.

The use of bedaquiline might increase hepatic-related adverse events and lead to hepatotoxicity. It is recommended to avoid alcohol and other hepatotoxic drugs while on bedaquiline. Close monitoring is recommended in alcoholic patients as they are at a greater risk of hepatic toxicity. Liver function tests should be done at baseline, monthly while on treatment, and as needed thereafter and discontinuance of therapy if evidence of new or worsening liver dysfunction occurs as indicated by the manufacturer.

The primidone in Mysoline has a major potential interaction with Asphyxia.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a major potential interaction with Asphyxia.

Barbiturates may produce severe respiratory depression, apnea, laryngospasm, bronchospasm and cough, particularly during rapid intravenous administration. In usual hypnotic dosages, the degree of respiratory depression produced is similar to that which occurs during physiologic sleep, while at higher dosages, the rate, depth and volume of respiration may be markedly decreased. However, some patients may be susceptible at commonly used dosages, including the elderly, debilitated or severely ill patients, those receiving other CNS depressants, and those with limited ventilatory reserve, chronic pulmonary insufficiency or other respiratory disorders. Therapy with barbiturates should be administered cautiously in these patients. Appropriate monitoring and individualization of dosage are particularly important, and equipment for resuscitation should be immediately available if the parenteral route is used. Barbiturates, especially injectable formulations, should generally be avoided in patients with sleep apnea, hypoxia, or severe pulmonary diseases in which dyspnea or obstruction is evident.

The primidone in Mysoline has a moderate potential interaction with Bone Marrow Depression/Low Blood Counts.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a moderate potential interaction with Bone Marrow Depression/Low Blood Counts.

Hematologic toxicity, including agranulocytosis, thrombocytopenic purpura and megaloblastic anemia, has been reported rarely during use of barbiturates. Therapy with barbiturates should be administered cautiously in patients with preexisting blood dyscrasias or bone marrow suppression. Blood counts are recommended prior to and periodically during long-term therapy, and patients should be instructed to immediately report any signs or symptoms suggestive of blood dyscrasia such as fever, sore throat, local infection, easy bruising, petechiae, bleeding, pallor, dizziness, or jaundice. Barbiturate therapy should be discontinued if blood dyscrasias occur.

The primidone in Mysoline has a major potential interaction with Depression.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a moderate potential interaction with Depression.

Barbiturates depress the central nervous system and may cause or exacerbate mental depression. Therapy with barbiturates should be administered cautiously in patients with a history of depression or suicidal tendencies. It may be prudent to refrain from dispensing large quantities of medication to these patients.

The primidone in Mysoline has a moderate potential interaction with Depression.

Antiepileptic drugs (AEDs) have been associated with an increased risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Pooled analyses of 199 placebo-controlled clinical studies involving the use of 11 different AEDs showed that patients receiving AEDs had approximately twice the risk of suicidal thinking or behavior compared to patients receiving placebo. AEDs should be administered cautiously in patients with depression or other psychiatric disorders; phentermine-topiramate should be avoided in patients with history of suicidal attempts or active suicidal ideation. The risk of suicidal thoughts and behavior should be carefully assessed against the risk of untreated illness, bearing in mind that epilepsy and many other conditions for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Patients, caregivers, and families should be alert to the emergence or worsening of signs and symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts or behavior. If patients have symptoms of suicidal ideation or behavior, a dosage reduction or treatment discontinuation should be considered.

The primidone in Mysoline has a major potential interaction with Dermatitis, Drug-Induced.

Skin eruptions may precede rare but potentially fatal barbiturate-induced reactions such as systemic lupus erythematosus and exfoliative dermatitis, the latter of which may be accompanied by hepatitis and jaundice. Therapy with barbiturates should be administered cautiously in patients with preexisting drug-induced dermatitis, since it may delay the recognition of a potential reaction to barbiturates. Barbiturate therapy should be withdrawn promptly at the first sign of a dermatologic adverse effect. However, cutaneous reactions may proceed to an irreversible stage even after cessation of medication due to the slow rate of metabolism and excretion of barbiturates. Patients should be advised to promptly report signs that may indicate impending development of barbiturate-related cutaneous lesions, including high fever, severe headache, stomatitis, conjunctivitis, rhinitis, urethritis, and balanitis. Rashes may be more likely to occur with phenobarbital and mephobarbital.

The primidone in Mysoline has a major potential interaction with Dermatitis, Drug-Induced.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a major potential interaction with Drug Dependence.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a major potential interaction with Drug Dependence.

Barbiturates have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop, particularly after prolonged use of excessive dosages. Abrupt cessation and/or a reduction in dosage may precipitate withdrawal symptoms. In patients who have developed tolerance to a barbiturate, overdosage can still produce respiratory depression and death, and cross-tolerance usually will occur with other agents in the class. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with barbiturates. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of barbiturates should be undertaken gradually using a dosage-tapering schedule.

Bedaquiline has a major potential interaction with Electrolyte Abnormalities.

Bedaquiline can cause QT prolongation, which may lead to an increased risk for ventricular arrhythmias, including Torsade de Pointes. Use of bedaquiline should be avoided in patients with congenital long QT syndrome, known prolongation of the QTc interval, uncompensated heart failure, or severe left ventricular hypertrophy, hypothyroidism, and in patients with electrolytes abnormalities. It is recommended to obtain an ECG before initiation of treatment, and at least 2, 12, and 24 weeks after starting treatment and to discontinue treatment if significant ventricular arrhythmia or if QTcF interval prolongation of greater than 500 ms develops.

Bedaquiline has a major potential interaction with Heart Disease.

Bedaquiline can cause QT prolongation, which may lead to an increased risk for ventricular arrhythmias, including Torsade de Pointes. Use of bedaquiline should be avoided in patients with congenital long QT syndrome, known prolongation of the QTc interval, uncompensated heart failure, or severe left ventricular hypertrophy, hypothyroidism, and in patients with electrolytes abnormalities. It is recommended to obtain an ECG before initiation of treatment, and at least 2, 12, and 24 weeks after starting treatment and to discontinue treatment if significant ventricular arrhythmia or if QTcF interval prolongation of greater than 500 ms develops.

The primidone in Mysoline has a moderate potential interaction with Hyperkinetic Syndrome of Childhood.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a moderate potential interaction with Hyperkinetic Syndrome of Childhood.

Paradoxical reactions characterized by excitability and restlessness may occur in pediatric patients with hyperactive aggressive disorders. Such patients should be monitored for signs of paradoxical stimulation during therapy with barbiturates.

The primidone in Mysoline has a major potential interaction with Liver Disease.

During chronic administration, primidone is slowly metabolized by the liver and excreted in the urine as phenylethylmalonamide (PEMA), phenobarbital and p-hydroxyphenobarbital, the latter two of which are pharmacologically active. The plasma clearance of primidone and its metabolites may be decreased and the half-lives prolonged in patients with impaired hepatic and/or renal function. Therapy with primidone should be administered cautiously and initiated at reduced dosages in patients with liver and/or renal disease.

Bedaquiline has a moderate potential interaction with Liver Disease.

Bedaquiline population pharmacokinetic analysis indicated that mild to moderate hepatic impairment had no significant influence on bedaquiline pharmacokinetics. Close monitoring of liver function is recommended in patients with severe hepatic impairment as the pharmacokinetics of bedaquiline is unknown in these patients.

Bedaquiline has a major potential interaction with Long QT Syndrome.

Bedaquiline causes QT prolongation. Use with drugs that prolong the QT interval may cause additive QT prolongation. Monitor ECG before initiation of treatment, and at least 2, 12, and 24 weeks after starting treatment and obtain serum potassium, calcium, and magnesium at baseline and correct if abnormal. Discontinue bedaquiline if significant ventricular arrhythmia or if QTcF interval prolongation of greater than 500 ms. develops. If syncope occurs, obtain an ECG to detect QT prolongation.

Bedaquiline has a major potential interaction with Long QT Syndrome.

Bedaquiline can cause QT prolongation, which may lead to an increased risk for ventricular arrhythmias, including Torsade de Pointes. Use of bedaquiline should be avoided in patients with congenital long QT syndrome, known prolongation of the QTc interval, uncompensated heart failure, or severe left ventricular hypertrophy, hypothyroidism, and in patients with electrolytes abnormalities. It is recommended to obtain an ECG before initiation of treatment, and at least 2, 12, and 24 weeks after starting treatment and to discontinue treatment if significant ventricular arrhythmia or if QTcF interval prolongation of greater than 500 ms develops.

The primidone in Mysoline has a moderate potential interaction with Panhypopituitarism.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a moderate potential interaction with Panhypopituitarism.

Barbiturates, especially phenobarbital, secobarbital and butabarbital, may diminish the systemic effects of exogenous and endogenous corticosteroids via induction of hepatic microsomal enzymes, thereby accelerating the metabolism of corticosteroids. In addition, barbiturates may interfere with pituitary corticotropin production. Therapy with barbiturates should be administered cautiously in patients with adrenal insufficiency. Patients with borderline hypoadrenalism should be monitored closely, and patients receiving steroid supplementation may require an adjustment in dosage when barbiturates are added to or withdrawn from their medication regimen.

The primidone in Mysoline has a major potential interaction with Porphyria.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a major potential interaction with Porphyria.

The use of barbiturates is contraindicated in patients with a history of porphyria. Barbiturates may exacerbate acute intermittent porphyria or porphyria variegata by inducing the enzymes responsible for porphyrin synthesis.

The primidone in Mysoline has a moderate potential interaction with Psychosis.

Antiepileptic drugs (AEDs) have been associated with an increased risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Pooled analyses of 199 placebo-controlled clinical studies involving the use of 11 different AEDs showed that patients receiving AEDs had approximately twice the risk of suicidal thinking or behavior compared to patients receiving placebo. AEDs should be administered cautiously in patients with depression or other psychiatric disorders; phentermine-topiramate should be avoided in patients with history of suicidal attempts or active suicidal ideation. The risk of suicidal thoughts and behavior should be carefully assessed against the risk of untreated illness, bearing in mind that epilepsy and many other conditions for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Patients, caregivers, and families should be alert to the emergence or worsening of signs and symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts or behavior. If patients have symptoms of suicidal ideation or behavior, a dosage reduction or treatment discontinuation should be considered.

The primidone in Mysoline has a major potential interaction with Pulmonary Impairment.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a major potential interaction with Pulmonary Impairment.

Barbiturates may produce severe respiratory depression, apnea, laryngospasm, bronchospasm and cough, particularly during rapid intravenous administration. In usual hypnotic dosages, the degree of respiratory depression produced is similar to that which occurs during physiologic sleep, while at higher dosages, the rate, depth and volume of respiration may be markedly decreased. However, some patients may be susceptible at commonly used dosages, including the elderly, debilitated or severely ill patients, those receiving other CNS depressants, and those with limited ventilatory reserve, chronic pulmonary insufficiency or other respiratory disorders. Therapy with barbiturates should be administered cautiously in these patients. Appropriate monitoring and individualization of dosage are particularly important, and equipment for resuscitation should be immediately available if the parenteral route is used. Barbiturates, especially injectable formulations, should generally be avoided in patients with sleep apnea, hypoxia, or severe pulmonary diseases in which dyspnea or obstruction is evident.

The primidone in Mysoline has a major potential interaction with Renal Dysfunction.

During chronic administration, primidone is slowly metabolized by the liver and excreted in the urine as phenylethylmalonamide (PEMA), phenobarbital and p-hydroxyphenobarbital, the latter two of which are pharmacologically active. The plasma clearance of primidone and its metabolites may be decreased and the half-lives prolonged in patients with impaired hepatic and/or renal function. Therapy with primidone should be administered cautiously and initiated at reduced dosages in patients with liver and/or renal disease.

Bedaquiline has a moderate potential interaction with Renal Dysfunction.

No dose adjustment is required for patients with mild or moderate renal impairment. Care should be exercised when using bedaquiline in patients with severe renal impairment or end-stage renal disease requiring hemodialysis or peritoneal dialysis. It is recommended to monitor patients closely for adverse events.

The primidone in Mysoline has a major potential interaction with Respiratory Arrest.

Barbiturates may produce severe respiratory depression, apnea, laryngospasm, bronchospasm and cough, particularly during rapid intravenous administration. In usual hypnotic dosages, the degree of respiratory depression produced is similar to that which occurs during physiologic sleep, while at higher dosages, the rate, depth and volume of respiration may be markedly decreased. However, some patients may be susceptible at commonly used dosages, including the elderly, debilitated or severely ill patients, those receiving other CNS depressants, and those with limited ventilatory reserve, chronic pulmonary insufficiency or other respiratory disorders. Therapy with barbiturates should be administered cautiously in these patients. Appropriate monitoring and individualization of dosage are particularly important, and equipment for resuscitation should be immediately available if the parenteral route is used. Barbiturates, especially injectable formulations, should generally be avoided in patients with sleep apnea, hypoxia, or severe pulmonary diseases in which dyspnea or obstruction is evident.

The primidone in Mysoline has a major potential interaction with Respiratory Arrest.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

Bedaquiline has a major potential interaction with Underactive Thyroid.

Bedaquiline can cause QT prolongation, which may lead to an increased risk for ventricular arrhythmias, including Torsade de Pointes. Use of bedaquiline should be avoided in patients with congenital long QT syndrome, known prolongation of the QTc interval, uncompensated heart failure, or severe left ventricular hypertrophy, hypothyroidism, and in patients with electrolytes abnormalities. It is recommended to obtain an ECG before initiation of treatment, and at least 2, 12, and 24 weeks after starting treatment and to discontinue treatment if significant ventricular arrhythmia or if QTcF interval prolongation of greater than 500 ms develops.

Bedaquiline has a major potential interaction with Ventricular Arrhythmia.

Bedaquiline causes QT prolongation. Use with drugs that prolong the QT interval may cause additive QT prolongation. Monitor ECG before initiation of treatment, and at least 2, 12, and 24 weeks after starting treatment and obtain serum potassium, calcium, and magnesium at baseline and correct if abnormal. Discontinue bedaquiline if significant ventricular arrhythmia or if QTcF interval prolongation of greater than 500 ms. develops. If syncope occurs, obtain an ECG to detect QT prolongation.

The primidone in Mysoline has a moderate potential interaction with Vitamin D Deficiency.

Since primidone is structurally related to the barbiturate-derivative anticonvulsants and also partially metabolized to phenobarbital during chronic administration, the usual contraindications, warnings and precautions applicable to barbiturates should be observed with primidone.

The primidone in Mysoline has a moderate potential interaction with Vitamin D Deficiency.

Rickets and osteomalacia have rarely been reported following prolonged use of barbiturates, possibly due to increased metabolism of vitamin D as a result of enzyme induction by barbiturates. Long-term therapy with barbiturates should be administered cautiously in patients with vitamin D deficiency.