Pasireotide Disease Interactions

The use of pasireotide causes elevations in ALT or AST. No dose adjustment is required in patients with mild hepatic impairment, but is required for patients with moderate hepatic impairment. The use of pasireotide should be avoided in patients with severe hepatic impairment. Regular monitoring of liver function test is recommended and interruption of treatment should be considered if abnormal values exceeding 5 times ULN or rising values are obtained during the course of therapy.

The use of pasireotide is associated with QT prolongation. Pasireotide should be used with caution in patients who are at significant risk of developing QT prolongation. It is recommended to correct levels of hypokalemia and hypomagnesemia prior to starting therapy with this agent. Assess ECG at the beginning of therapy and monitor during therapy. Care should be taken in predisposed patients.

Treatment with somatostatin analogs may suppress the pituitary hormones other than GH/IGF-1. It is recommended to monitor pituitary function prior to initiation of therapy and periodically during treatment, as clinically appropriate. Patients should be monitored for and instructed on the signs and symptoms of adrenal insufficiency during therapy. If adrenal insufficiency is suspected it should be confirmed and treated per standard of care with exogenous glucocorticoids at replacement doses.

Bradycardia has been reported with the use of somatostatin analogs. It is recommended to carefully monitor patients with cardiac disorders for the development of bradycardia. Dose adjustments of beta-blockers, calcium channel blockers, or correction of electrolyte disturbances may be necessary. Care should be taken when initiating treatment with these agents in patients with bradycardia.

Somatostatin analogs may reduce gallbladder motility and lead to gallstones formation. It is recommended to assess the gallbladder prior to starting therapy and periodically thereafter.

Elevations in blood glucose levels have been reported with the use of somatostatin analogs. Cushing's disease patients with poor glycemic control may be at a higher risk of developing severe hyperglycemia and associated complications, e.g., ketoacidosis. It is recommended to assess the glycemic status of hemoglobin A1C prior to starting treatment with these agents. Self-monitoring of blood glucose and/or FPG assessments should be done every week for the first two to three months and periodically thereafter, as clinically appropriate, as well as over the first two to four weeks after any dose increase. If uncontrolled hyperglycemia persists, despite appropriate medical management, the dose of these agents should be reduced or discontinued.