Can you take Felbamate with Tipranavir?

Tipranavir has a moderate potential interaction with Abnormal Glucose Tolerance.

New onset diabetes mellitus, exacerbation of preexisting diabetes mellitus, hyperglycemia, and some cases of diabetic ketoacidosis have been reported during postmarketing surveillance in HIV-infected patients treated with protease inhibitors. Some patients required either initiation or dosage adjustments of insulin or oral hypoglycemic agents for treatment of these events. In some cases, hyperglycemia persisted despite discontinuation of protease inhibitor therapy. A causal relationship has not been established between protease inhibitor therapy and these events. Monitoring patients for hyperglycemia, new onset diabetes mellitus, or exacerbation of diabetes mellitus should be considered during protease inhibitor therapy.

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 Felbamate therapy should be withdrawn if evidence of bone marrow depression is observed.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

Tipranavir has a moderate potential interaction with Coagulation Defects and Disorders.

There have been reports of increased bleeding, including spontaneous skin hematomas and hemarthrosis, in patients with hemophilia type A and B treated with protease inhibitors; however, a causal relationship has not been established. In some patients, additional factor VIII was given. In more than half of the reported cases, protease inhibitor therapy was continued or reintroduced. Patients with hemophilia or other coagulation defects should be monitored closely for bleeding during protease inhibitor therapy.

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.

Tipranavir has a moderate potential interaction with Diabetes Mellitus.

New onset diabetes mellitus, exacerbation of preexisting diabetes mellitus, hyperglycemia, and some cases of diabetic ketoacidosis have been reported during postmarketing surveillance in HIV-infected patients treated with protease inhibitors. Some patients required either initiation or dosage adjustments of insulin or oral hypoglycemic agents for treatment of these events. In some cases, hyperglycemia persisted despite discontinuation of protease inhibitor therapy. A causal relationship has not been established between protease inhibitor therapy and these events. Monitoring patients for hyperglycemia, new onset diabetes mellitus, or exacerbation of diabetes mellitus should be considered during protease inhibitor therapy.

Tipranavir has a moderate potential interaction with High Cholesterol.

Treatment with ritonavir alone or in combination with other protease inhibitors (e.g., lopinavir, saquinavir, tipranavir, fosamprenavir) has resulted in substantial increases in the concentration of total cholesterol and triglycerides. These effects have also been reported with other protease inhibitors but may be the most dramatic with ritonavir. The clinical significance of these elevations is unclear. Marked elevation in triglyceride levels is a risk factor for development of pancreatitis. Triglyceride and cholesterol testing is recommended before starting ritonavir (with or without other protease inhibitors) and periodically during therapy. Lipid disorders should be managed as clinically appropriate.

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.

Tipranavir has a major potential interaction with Liver Disease.

The use of tipranavir is contraindicated in patients with moderate to severe (Child-Pugh Class B and C) hepatic impairment. Tipranavir is primarily metabolized by the liver and may accumulate substantially in such patients. In addition, tipranavir coadministered with ritonavir 200 mg has been associated with reports of clinical hepatitis and hepatic decompensation, including some fatalities. Most cases occurred in patients with advanced HIV disease taking multiple concomitant medications, thus a causal relationship to tipranavir/ritonavir could not be established. Nevertheless, extra caution is recommended if tipranavir and ritonavir are prescribed to patients with chronic hepatitis B or C coinfection or elevations in liver transaminases, as these patients have an approximately 2.5- fold increased risk of developing further transaminase elevations or hepatic decompensation. In clinical studies, Grade 3 and 4 increases in hepatic transaminases were observed in 6% of healthy volunteers and HIV subjects. Liver function tests should be performed prior to initiating therapy and frequently throughout the duration of treatment. Patients should be advised to promptly discontinue tipranavir/ritonavir therapy and seek medical attention if they experience signs or symptoms suggestive of hepatotoxicity such as fever, rash, anorexia, nausea, vomiting, fatigue, right upper quadrant pain, dark urine, and jaundice.

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.