Interactions between Midodrine and Nurtec ODT

Midodrine has a major potential interaction with Diabetes Mellitus.

Midodrine can cause marked elevation of supine blood pressure (BP>200 mmHg systolic) and should not be used in patients with persistent and excessive supine hypertension. Systolic elevations of this degree are most likely to be observed in patients with relatively elevated pre-treatment systolic blood pressures (mean 170 mmHg). There is no experience in patients with initial supine systolic pressure above 180 mmHg, as those patients were excluded from the clinical trials. Use of midodrine in such patients is not recommended. Additionally, care should be taken when using this agent in orthostatic hypotensive patients who are also diabetic. Supine and sitting hypertension should be evaluated at the beginning of therapy, and blood pressure (supine, sitting, and orthostatic) should be monitored regularly.

Midodrine has a major potential interaction with Heart Disease.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

Midodrine has a major potential interaction with High Blood Pressure.

Midodrine can cause marked elevation of supine blood pressure (BP>200 mmHg systolic) and should not be used in patients with persistent and excessive supine hypertension. Systolic elevations of this degree are most likely to be observed in patients with relatively elevated pre-treatment systolic blood pressures (mean 170 mmHg). There is no experience in patients with initial supine systolic pressure above 180 mmHg, as those patients were excluded from the clinical trials. Use of midodrine in such patients is not recommended. Additionally, care should be taken when using this agent in orthostatic hypotensive patients who are also diabetic. Supine and sitting hypertension should be evaluated at the beginning of therapy, and blood pressure (supine, sitting, and orthostatic) should be monitored regularly.

The rimegepant in Nurtec ODT has a major potential interaction with Liver Disease.

Rimegepant should be avoided in patients with severe hepatic impairment. A dedicated pharmacokinetic study has shown an approximately 2-fold increased exposure to a single-dose of rimegepant in patients with severe hepatic impairment (Child-Pugh class C). There were no clinically meaningful differences in rimegepant exposure with mild (Child-Pugh class A) and moderate hepatic impairment (Child-Pugh class B).

Midodrine has a moderate potential interaction with Liver Disease.

Midodrine, a prodrug, undergoes bioactivation in a variety of tissues to desglymidodrine, an alpha-1 agonist. The liver functions in the metabolism of midodrine and desglymidodrine. The pharmacokinetic disposition of midodrine has not been studied in patients with hepatic impairment. Therapy with midodrine should be administered cautiously in patients with compromised hepatic function. Clinical monitoring of hepatic function prior to initiation of therapy.

Midodrine has a major potential interaction with Pheochromocytoma.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

Midodrine has a major potential interaction with Renal Dysfunction.

The use of midodrine is contraindicated in patients with acute renal disease or urinary retention/obstruction disorder. Midodrine is primarily eliminated by the kidney as desglymidodrine (active metabolite). The serum concentration of midodrine is expected to be increased in patients with renal impairment. Desglymidodrine induces urinary retention by increasing bladder neck tone. Therapy with midodrine should be administered cautiously and initiated at 2.5 mg doses in patients with compromised renal function. Clinical monitoring of renal function prior to initiation of therapy and subsequently as appropriate and blood pressure (supine, sitting, and orthostatic) is recommended. Midodrine is removed by dialysis.

The rimegepant in Nurtec ODT has a major potential interaction with Renal Dysfunction.

Rimegepant should be avoided in patients with ESRD as it not been studied in patients with CrCl less than 15 mL/min or among patients on dialysis. No dosage adjustment is necessary for patients with mild to severe renal impairment. A single-dose pharmacokinetic study showed exposure to rimegepant in patients with mild or severe renal impairment was not clinically meaningful different compared to normal subjects, however, exposure in subjects with moderate renal impairment was approximately 40% higher. In healthy male subjects, 78% of a radiolabeled dose was excreted in the feces and 24% in the urine.

Midodrine has a major potential interaction with Thyrotoxicosis.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

Midodrine has a major potential interaction with Urinary Retention.

The use of midodrine is contraindicated in patients with acute renal disease or urinary retention/obstruction disorder. Midodrine is primarily eliminated by the kidney as desglymidodrine (active metabolite). The serum concentration of midodrine is expected to be increased in patients with renal impairment. Desglymidodrine induces urinary retention by increasing bladder neck tone. Therapy with midodrine should be administered cautiously and initiated at 2.5 mg doses in patients with compromised renal function. Clinical monitoring of renal function prior to initiation of therapy and subsequently as appropriate and blood pressure (supine, sitting, and orthostatic) is recommended. Midodrine is removed by dialysis.