Asendin (amoxapine) Disease Interactions

There are 10 disease interactions with Asendin (amoxapine):

Nms Tardive Dyskinesia Anticholinergic Effects Cardiovascular Disease Pheochromocytoma

Seizure Disorders Bone Marrow Suppression Diabetes Renal/Liver Disease Schizophrenia/Bipolar Disorder

Although not a neuroleptic agent, amoxapine has substantive neuroleptic activity due to its dopaminergic receptor-blocking effects and may precipitate or aggravate a potentially fatal symptom complex known as Neuroleptic Malignant Syndrome (NMS). Clinical manifestations of NMS include hyperpyrexia, muscle rigidity, involuntary movements, altered mental status and autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis and cardiac arrhythmias). Amoxapine therapy should not be initiated in patients with active NMS and should be immediately discontinued if currently being administered in such patients. In patients with a history of NMS, introduction or reintroduction of amoxapine therapy should be carefully considered, since NMS may recur.

Although not a neuroleptic agent, amoxapine has substantive neuroleptic activity due to its postsynaptic dopamine-blocking effects and may precipitate or aggravate symptoms of tardive dyskinesia (TD) following chronic use. Neuroleptic-induced TD may or may not be reversible depending, at least partially, on the duration and total cumulative dose of neuroleptic therapy administered. The use of amoxapine should preferably be avoided in patients with TD. If amoxapine is given to these patients and worsening of TD occurs, prompt withdrawal of therapy will provide better chances of improving the condition.

Tricyclic and tetracyclic antidepressants (TCAs) have anticholinergic activity, to which elderly patients are particularly sensitive. Tertiary amines such as amitriptyline and trimipramine tend to exhibit greater anticholinergic effects than other agents in the class. Therapy with TCAs should be administered cautiously in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. In patients with angle-closure glaucoma, even average doses can precipitate an attack. Glaucoma should be treated and under control prior to initiation of therapy with TCAs, and intraocular pressure monitored during therapy.

Tricyclic and tetracyclic antidepressants (TCAs) may cause orthostatic hypotension, reflex tachycardia, syncope, and dizziness, particularly during initiation of therapy or rapid escalation of dosage. Imipramine appears to have the greatest propensity to induce these effects, while secondary amines such as nortriptyline may do so less frequently. Tolerance to the hypotensive effects often develops after a few doses to a few weeks. Rarely, collapse and sudden death have occurred secondary to severe hypotension. Other reported adverse cardiovascular effects include tachycardia, arrhythmias, heart block, hypertension, thrombosis, thrombophlebitis, myocardial infarction, strokes, congestive heart failure, and ECG abnormalities such as PR and QT interval prolongation. Therapy with TCAs should be avoided during the acute recovery phase following myocardial infarction, and should be administered only with extreme caution in patients with hyperthyroidism, a history of cardiovascular or cerebrovascular disease, or a predisposition to hypotension. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. Many of the newer antidepressants, including bupropion and the selective serotonin reuptake inhibitors (SSRIs), are considerably less or minimally cardiotoxic and may be appropriate alternatives.

Tricyclic and tetracyclic antidepressants (TCAs) may potentiate the effects of circulating catecholamines. Enhanced sympathetic activity can provoke hypertensive crises in patients with pheochromocytoma or other tumors of the adrenal medulla, such as some neuroblastomas. Therapy with TCAs should be administered cautiously in patients with these tumors.

Tricyclic antidepressants (TCAs) can lower the seizure threshold and trigger seizures in a dose-dependent manner. The risk appears to be greater with amoxapine and the tertiary amines (amitriptyline, doxepin, imipramine, trimipramine) than with the secondary amines (desipramine, nortriptyline, protriptyline). An incidence of up to 0.6% has been reported in patients treated with imipramine dosages > 200 mg/day. However, the incidence is generally much lower when smaller doses are used in patients without a predisposition to seizures. Therapy with TCAs should be administered cautiously in patients with a history of seizures or other predisposing factors, such as head trauma, CNS abnormalities, and alcoholism. High dosages should be avoided if possible.

The use of tricyclic and tetracyclic antidepressants (TCAs) has rarely been associated with bone marrow suppression. Leukopenia, agranulocytosis, thrombocytopenia, anemia, eosinophilia, purpura, and pancytopenia have been reported with some TCAs. Patients with preexisting bone marrow suppression or blood dyscrasias receiving TCAs should be monitored closely during therapy for further decreases in blood counts.

Both elevation and lowering of blood sugar levels have been reported with the use of some tricyclic antidepressants (TCAs). Rarely, these effects have also occurred with maprotiline, a tetracyclic antidepressant. Patients with diabetes should be monitored for worsening control of blood glucose when treated with these agents, particularly during dosage escalation or whenever dosage has been altered.

Tricyclic and tetracyclic antidepressants (TCAs) are known to undergo metabolism in the liver. Some of the metabolites, such as those of imipramine, clomipramine and desipramine, may be pharmacologically active. Many of the metabolites are also excreted by the kidney. There are very limited data concerning the use of TCAs in patients with renal and/or liver disease. Therapy with TCAs should be administered cautiously in patients with significantly impaired renal or hepatic function. Dosage adjustments may be necessary.

Tricyclic antidepressants (TCAs) may aggravate symptoms of psychosis in schizophrenic patients, particularly those with paranoid symptomatology. Depressed patients, usually those with bipolar disorder, may experience a switch from depression to mania or hypomania. These occurrences have also been reported rarely with the tetracyclic antidepressant, maprotiline. Therapy with these agents should be administered cautiously in patients with schizophrenia, bipolar disorder, or a history of mania.

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