Can you take Felbamate with Toremifene?

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 Felbamate therapy should be withdrawn if evidence of bone marrow depression is observed.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.

Toremifene has a moderate potential interaction with Endometrial Dysplasia.

Endometrial cancer, endometrial hyperplasia, hypertrophy, and uterine polyps have been reported in some patients treated with toremifene. Long-term use of toremifene has not been established in patients with preexisting endometrial hyperplasia. All patients should have baseline and annual gynecological examinations. In particular, patients at high risk of endometrial cancer should be closely monitored.

Toremifene has a major potential interaction with Heart Failure.

Toremifene has shown to prolong the QTc interval in a dose and concentration related manner, which can result in Torsade de Pointes (ventricular tachycardia), syncope, seizure, and/or death. Toremifene should not be prescribed to patients with congenital or acquired QT prolongation, uncorrected hypokalemia or uncorrected hypomagnesemia. Caution is advised in patients with congestive heart failure, and patients taking other drugs that can prolong the QT interval.

Toremifene has a moderate potential interaction with History, Thrombotic/Thromboembolic Disorder.

Thromboembolic events such as thrombophlebitis and pulmonary embolism have been noted during toremifene therapy. Patients with an active or past history of thromboembolic events should generally not be administered toremifene.

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.

Toremifene has a major potential interaction with Hypokalemia.

Toremifene has shown to prolong the QTc interval in a dose and concentration related manner, which can result in Torsade de Pointes (ventricular tachycardia), syncope, seizure, and/or death. Toremifene should not be prescribed to patients with congenital or acquired QT prolongation, uncorrected hypokalemia or uncorrected hypomagnesemia. Caution is advised in patients with congestive heart failure, and patients taking other drugs that can prolong the QT interval.

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.

Toremifene has a moderate potential interaction with Liver Disease.

Hepatotoxicity, hepatitis, and non-alcoholic fatty liver disease have been reported in clinical trials and postmarketing with toremifene. Liver function tests should be performed periodically. Caution is advised in patients with any hepatic impairment.

Toremifene has a major potential interaction with Long QT Syndrome.

Toremifene has shown to prolong the QTc interval in a dose and concentration related manner, which can result in Torsade de Pointes (ventricular tachycardia), syncope, seizure, and/or death. Toremifene should not be prescribed to patients with congenital or acquired QT prolongation, uncorrected hypokalemia or uncorrected hypomagnesemia. Caution is advised in patients with congestive heart failure, and patients taking other drugs that can prolong the QT interval.

Toremifene has a major potential interaction with Magnesium Imbalance.

Toremifene has shown to prolong the QTc interval in a dose and concentration related manner, which can result in Torsade de Pointes (ventricular tachycardia), syncope, seizure, and/or death. Toremifene should not be prescribed to patients with congenital or acquired QT prolongation, uncorrected hypokalemia or uncorrected hypomagnesemia. Caution is advised in patients with congestive heart failure, and patients taking other drugs that can prolong the QT interval.

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.

Toremifene has a moderate potential interaction with Thrombotic/Thromboembolic Disorder.

Thromboembolic events such as thrombophlebitis and pulmonary embolism have been noted during toremifene therapy. Patients with an active or past history of thromboembolic events should generally not be administered toremifene.