Can you take Flibanserin 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.

Flibanserin has a major potential interaction with Alcoholism.

The use of flibanserin is contraindicated along with the ingestion of alcohol, as it increases the risk of hypotension and syncope. It is important to assess the likelihood of the patient abstaining from alcohol, taking into account the current and past drinking behavior.

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.

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.

Flibanserin has a major potential interaction with Hypotension.

The use of flibanserin can cause hypotension and syncope. The benefits and risks of therapy should be considered in patients with preexisting conditions that predispose to hypotension. Flibanserin should be used with caution in these patients.

Flibanserin has a major potential interaction with Liver Disease.

Flibanserin may accumulate in patients with hepatic impairment. Therapy with flibanserin is contraindicated in patients with compromised hepatic function.

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.

Flibanserin has a major potential interaction with Syncope.

The use of flibanserin can cause hypotension and syncope. The benefits and risks of therapy should be considered in patients with preexisting conditions that predispose to hypotension. Flibanserin should be used with caution in these patients.