Interactions between Norvasc and Olaparib

The amLODIPine in Norvasc has a major potential interaction with Aortic Stenosis.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

The amLODIPine in Norvasc has a major potential interaction with Cardiogenic Shock.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

The amLODIPine in Norvasc has a moderate potential interaction with Heart Attack.

Calcium channel blockers (CCBs) may have varying degrees of negative inotropic effect. Congestive heart failure (CHF), worsening of CHF, and pulmonary edema have occurred in some patients treated with a CCB, primarily verapamil. Some CCBs have also caused mild to moderate peripheral edema due to localized vasodilation of dependent arterioles and small blood vessels, which can be confused with the effects of increasing left ventricular dysfunction. Although some CCBs have been used in the treatment of CHF, therapy with CCBs should be administered cautiously in patients with severe left ventricular dysfunction (e.g., ejection fraction < 30%) or moderate to severe symptoms of cardiac failure and in patients with any degree of ventricular dysfunction if they are receiving a beta-adrenergic blocker. Likewise, caution is advised in patients with acute myocardial infarction and pulmonary congestion documented by X-ray on admission, since associated heart failure may be acutely worsened by administration of a CCB.

The amLODIPine in Norvasc has a moderate potential interaction with Heart Failure.

Calcium channel blockers (CCBs) may have varying degrees of negative inotropic effect. Congestive heart failure (CHF), worsening of CHF, and pulmonary edema have occurred in some patients treated with a CCB, primarily verapamil. Some CCBs have also caused mild to moderate peripheral edema due to localized vasodilation of dependent arterioles and small blood vessels, which can be confused with the effects of increasing left ventricular dysfunction. Although some CCBs have been used in the treatment of CHF, therapy with CCBs should be administered cautiously in patients with severe left ventricular dysfunction (e.g., ejection fraction < 30%) or moderate to severe symptoms of cardiac failure and in patients with any degree of ventricular dysfunction if they are receiving a beta-adrenergic blocker. Likewise, caution is advised in patients with acute myocardial infarction and pulmonary congestion documented by X-ray on admission, since associated heart failure may be acutely worsened by administration of a CCB.

The amLODIPine in Norvasc has a major potential interaction with Hypotension.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

The amLODIPine in Norvasc has a major potential interaction with Ischemic Heart Disease.

Increased frequency, duration, and/or severity of angina, as well as acute myocardial infarction, have rarely developed during initiation or dosage increase of calcium channel blockers (CCBs), particularly in patients with severe obstructive coronary artery disease and those treated with immediate-release formulations. The mechanism of this effect is not established. Therapy with CCBs should be administered cautiously in patients with significant coronary artery disease.

The amLODIPine in Norvasc has a major potential interaction with Liver Disease.

Calcium channel blockers (CCBs) are extensively metabolized by the liver. The half-lives of CCBs may be prolonged substantially in patients with severe hepatic impairment, with the potential for significant drug accumulation. In addition, the use of some CCBs has been associated with elevations in serum transaminases, both with and without concomitant elevations in alkaline phosphatase and bilirubin. While these effects may be transient and reversible, some patients have developed cholestasis or hepatocellular injury. Therapy with CCBs should be administered cautiously and often at reduced dosages in patients with significantly impaired hepatic function. Periodic monitoring of liver function is advised.

Olaparib has a moderate potential interaction with Liver Disease.

Olaparib primarily undergoes hepatic metabolism via CYP450 3A4 and CYP450 3A5; the majority of metabolism is through oxidation with some metabolites undergoing subsequent glucuronide or sulfate conjugation. No dose adjustment is needed in patients with mild hepatic impairment. It is recommended to use caution when using olaparib in patients with moderate or severe hepatic impairment as there are no data available. Close monitoring is recommended.

Olaparib has a moderate potential interaction with Myelodysplastic Diseases.

Olaparib might cause Myelodysplastic Syndrome/Acute Myeloid Leukemia (MDS/AML), sometimes with fatal outcomes. Care should be exercised when using olaparib in patients with a history of previous cancer or bone marrow dysplasia. Do not start olaparib until patients have recovered from hematological toxicity caused by previous chemotherapy (<= Grade 1). It is recommended to monitor patients for hematological toxicities at baseline and monthly thereafter for clinically significant changes during treatment. Interrupt olaparib for prolonged hematological toxicities and monitor blood counts weekly until recovery and discontinue treatment if MDS/AML is confirmed.

Olaparib has a moderate potential interaction with Pulmonary Impairment.

Pneumonitis, including fatal cases, occurred in <1% of patients treated with olaparib. It is recommended to interrupt treatment if patients present new or worsening respiratory symptoms such as dyspnea, cough and fever, or a radiological abnormality. Assess for the source of symptoms and if pneumonitis is confirmed, olaparib should be discontinued and the patient treated appropriately.

Olaparib has a moderate potential interaction with Renal Dysfunction.

In a olaparib renal impairment trial, the mean AUC increased by 24%, and the Cmax increased by 15%, in patients with mild renal impairment. In patients with moderate renal impairment, the AUC increased by 44% and the Cmax by 26%. No dose adjustment is needed in patients with mild renal impairment. The dose of olaparib in patients with moderate renal impairment should be adjusted according to the prescribing information. It is recommended to monitor for toxicity all patient with renal impairment. The pharmacokinetics of olaparib have not been evaluated in patients with severe renal impairment or end-stage renal disease.