Can you take Felbamate with Mirabegron?

Felbamate has a major potential interaction with Anemia.

The use of felbamate is contraindicated in patients with bone marrow suppression or a current or prior history of blood dyscrasias. A marked increase in the incidence of aplastic anemia has been associated with the use of felbamate, reportedly exceeding 100 times the incidence observed in the general population (2 to 5 per million persons per year). In the few cases that have been reported in felbamate patients, the onset of clinical manifestations of aplastic anemia ranged from 5 to 30 weeks. However, the injury to bone marrow stem cells that is believed to be ultimately responsible for the anemia may occur much earlier. Currently, it is not known whether the risk is related to dose, duration of exposure, and/or concomitant use of other antiepileptic or myelotoxic drugs. Expert hematologic consultation should be available for all patients treated with felbamate. Since aplastic anemia typically develops without premonitory clinical or laboratory signs, it should be borne in mind that routine blood testing may not be reliably used to prevent development of the syndrome. However, in some cases, it may allow the detection of hematologic changes before the condition is full-blown. Felbamate therapy should be withdrawn if evidence of bone marrow depression is observed. Patients who are discontinued from the drug may remain at risk for developing anemia for a variable and unknown period afterwards and should be monitored accordingly.

Felbamate has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

The use of felbamate is contraindicated in patients with bone marrow suppression or a current or prior history of blood dyscrasias. A marked increase in the incidence of aplastic anemia has been associated with the use of felbamate, reportedly exceeding 100 times the incidence observed in the general population (2 to 5 per million persons per year). In the few cases that have been reported in felbamate patients, the onset of clinical manifestations of aplastic anemia ranged from 5 to 30 weeks. However, the injury to bone marrow stem cells that is believed to be ultimately responsible for the anemia may occur much earlier. Currently, it is not known whether the risk is related to dose, duration of exposure, and/or concomitant use of other antiepileptic or myelotoxic drugs. Expert hematologic consultation should be available for all patients treated with felbamate. Since aplastic anemia typically develops without premonitory clinical or laboratory signs, it should be borne in mind that routine blood testing may not be reliably used to prevent development of the syndrome. However, in some cases, it may allow the detection of hematologic changes before the condition is full-blown. Felbamate therapy should be withdrawn if evidence of bone marrow depression is observed. Patients who are discontinued from the drug may remain at risk for developing anemia for a variable and unknown period afterwards and should be monitored accordingly.

Felbamate 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.

Mirabegron has a moderate potential interaction with High Blood Pressure.

Mirabegron can increase blood pressure. In clinical studies, the use of mirabegron was associated with dose-related increases in supine blood pressure. At the maximum recommended dose of 50 mg, the mean maximum increase in systolic/diastolic blood pressure was approximately 3.5/1.5 mmHg greater than placebo in healthy volunteers and approximately 0.5 to 1 mmHg greater than placebo in patients with overactive bladder. Worsening of preexisting hypertension was reported infrequently in patients receiving mirabegron. Therapy with mirabegron should be administered cautiously in patients with hypertension. Periodic blood pressure determinations are recommended. Mirabegron is not recommended for use in patients with severe, uncontrolled hypertension, defined as systolic blood pressure >=180 mm Hg and/or diastolic blood pressure >=110 mm Hg.

Felbamate has a major potential interaction with History of Blood Dyscrasias.

The use of felbamate is contraindicated in patients with bone marrow suppression or a current or prior history of blood dyscrasias. A marked increase in the incidence of aplastic anemia has been associated with the use of felbamate, reportedly exceeding 100 times the incidence observed in the general population (2 to 5 per million persons per year). In the few cases that have been reported in felbamate patients, the onset of clinical manifestations of aplastic anemia ranged from 5 to 30 weeks. However, the injury to bone marrow stem cells that is believed to be ultimately responsible for the anemia may occur much earlier. Currently, it is not known whether the risk is related to dose, duration of exposure, and/or concomitant use of other antiepileptic or myelotoxic drugs. Expert hematologic consultation should be available for all patients treated with felbamate. Since aplastic anemia typically develops without premonitory clinical or laboratory signs, it should be borne in mind that routine blood testing may not be reliably used to prevent development of the syndrome. However, in some cases, it may allow the detection of hematologic changes before the condition is full-blown. Felbamate therapy should be withdrawn if evidence of bone marrow depression is observed. Patients who are discontinued from the drug may remain at risk for developing anemia for a variable and unknown period afterwards and should be monitored accordingly.

Felbamate has a major potential interaction with Liver Disease.

The use of felbamate is contraindicated in patients with a history of hepatic impairment. A marked increase in the incidence of hepatic failure, some resulting in fatality, has been associated with the use of felbamate relative to that expected in the general population (approximately 2000 cases per year). Currently, it is not known whether the risk is related to dose, duration of exposure, and/or concomitant use of other antiepileptic or hepatotoxic drugs. All patients treated with felbamate should have serum transaminase and bilirubin levels checked prior to initiating therapy and at 1- to 2-week intervals while treatment continues. Felbamate therapy should be withdrawn if abnormal liver function tests occur.

Mirabegron has a moderate potential interaction with Liver Disease.

Mirebegron is partially metabolized by the liver through multiple pathways. Following administration of a single 100 mg dose, mean mirabegron peak plasma concentration (Cmax) and systemic exposure (AUC) increased by 9% and 19%, respectively, in volunteers with mild hepatic impairment (Child-Pugh Class A) and 175% and 65%, respectively, in volunteers with moderate hepatic impairment (Child-Pugh Class B) compared to volunteers with normal hepatic function. No dosage adjustment is necessary in patients with mild hepatic impairment. In patients with moderate hepatic impairment, the daily dosage of mirabegron should not exceed 25 mg. Mirabegron has not been studied in patients with severe hepatic impairment (Child-Pugh Class C). Mirabegron is not recommended for use in these patients.

Felbamate 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.

Felbamate has a major potential interaction with Renal Dysfunction.

Felbamate is partially eliminated by the kidney as unchanged drug (approximately 40% to 50% of absorbed dose). The plasma clearance of felbamate may be decreased and the half-life prolonged in patients with impaired renal function. Therapy with felbamate should be administered cautiously in patients with renal impairment.

Mirabegron has a moderate potential interaction with Renal Dysfunction.

Mirebegron is partially eliminated by the kidney through active tubular secretion and glomerular filtration, with renal clearance accounting for approximately 25% of the total clearance. Following administration of a single 100 mg dose, mean mirabegron peak plasma concentration (Cmax) and systemic exposure (AUC) increased by 6% and 31%, respectively, in volunteers with mild renal impairment (estimated GFR 60 to 89 mL/min/1.73 m2), 23% and 66%, respectively, in volunteers with moderate renal impairment (estimated GFR 30 to 59 mL/min/1.73 m2), and 92% and 118%, respectively, in patients with severe renal impairment (estimated GFR 15 to 29 mL/min/1.73 m2) compared to volunteers with normal renal function. No dosage adjustment is necessary in patients with mild or moderate renal impairment. In patients with severe renal impairment, the daily dosage of mirabegron should not exceed 25 mg. Mirabegron has not been studied in patients with end stage renal disease (CrCl <15 mL/min or estimated GFR <15 mL/min/1.73 m2 or requirement for hemodialysis). Mirabegron is not recommended for use in these patients.

Mirabegron has a moderate potential interaction with Urinary Retention.

Although an increased risk of urinary retention was not observed in a controlled clinical safety study in patients with bladder outlet obstruction, urinary retention has been reported in this population during postmarketing use. Therapy with mirabegron should be administered cautiously in patients with clinically significant bladder outlet obstruction and conditions predisposing to urinary retention.