Drug Interaction Report

Amitriptyline has a major potential interaction with Alcoholism.

Tricyclic antidepressants (TCAs), can lower the seizure threshold and trigger seizures. These drugs should be used with extreme caution in patients with a history of seizures, or other predisposing factors, such as head trauma, CNS abnormalities, and alcoholism. Daily dose restrictions might apply for specific antidepressants. Physicians are encouraged to get additional dosing recommendations on the manufacturer's prescribing information.

Amitriptyline has a moderate potential interaction with Alcoholism.

Tricyclic antidepressants can enhance the response to alcohol. In patients who may use alcohol excessively, it should be borne in mind that the potentiation may increase the danger inherent in any suicide attempt or overdosage.

Amitriptyline has a major potential interaction with Arrhythmia.

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.

Ozanimod has a moderate potential interaction with Arrhythmia.

The use of ozanimod may result in a transient decrease in heart rate and atrioventricular conduction delays upon starting treatment. It is recommended to follow an up-titration scheme to reach the maintenance dosage. Initiation of ozanimod without titration may result in greater decreases in heart rate. If treatment with ozanimod is considered, advice from a cardiologist should be sought for those individuals at risk of cardiovascular effects, particularly conduction delays.

Amitriptyline has a moderate potential interaction with Bipolar Disorder.

A major depressive episode can be the initial presentation of bipolar disorder. Patients with depressive symptoms should be adequately screened to determine if they are at risk for bipolar disorder prior to initiating treatment with a tricyclic antidepressant. This screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder, and depression. It should be noted that tricyclic antidepressants are not approved for use in treating bipolar depression.

Amitriptyline has a moderate potential interaction with Bipolar Disorder.

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.

Amitriptyline has a moderate potential interaction with Bone Marrow Depression/Low Blood Counts.

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.

Amitriptyline has a major potential interaction with Cardiovascular Conditions and Disorders.

Tricyclic antidepressants should be used with extreme caution in patients with evidence of cardiovascular disease because of the possibility of fluctuations in the blood pressure, arrhythmias, conduction defects, tachycardia, myocardial infarction and stroke. This also applies to patients who have family history of sudden death, cardiac dysrhythmias, or conduction disturbances. In some cases a gradual dose titration is recommended.

Amitriptyline has a major potential interaction with Cardiovascular Conditions and Disorders.

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.

Ozanimod has a major potential interaction with Cardiovascular Conditions and Disorders.

Ozanimod is contraindicated in patients who have had a recent myocardial infarction, those with unstable angina, stroke, transient ischemic attack, decompensated heart failure with hospitalization, or Class III/IV heart failure, a presence of Mobitz Type II 2nd degree or 3rd degree AV block, sick sinus syndrome, or sino-atrial block, unless the patient has a pacemaker, severe untreated sleep apnea or those patients being treated with monoamine oxidase inhibitor drugs.

Ozanimod has a moderate potential interaction with Cardiovascular Conditions and Disorders.

The use of ozanimod may result in a transient decrease in heart rate and atrioventricular conduction delays upon starting treatment. It is recommended to follow an up-titration scheme to reach the maintenance dosage. Initiation of ozanimod without titration may result in greater decreases in heart rate. If treatment with ozanimod is considered, advice from a cardiologist should be sought for those individuals at risk of cardiovascular effects, particularly conduction delays.

Amitriptyline has a major potential interaction with Central Nervous System Disorders.

Tricyclic antidepressants (TCAs), can lower the seizure threshold and trigger seizures. These drugs should be used with extreme caution in patients with a history of seizures, or other predisposing factors, such as head trauma, CNS abnormalities, and alcoholism. Daily dose restrictions might apply for specific antidepressants. Physicians are encouraged to get additional dosing recommendations on the manufacturer's prescribing information.

Ozanimod has a moderate potential interaction with Central Nervous System Disorders.

Rare cases of posterior reversible encephalopathy syndrome (PRES) have been reported in patients receiving a sphingosine 1-phosphate receptor modulator. It is recommended to promptly schedule a complete physical and neurological examination and should consider an MRI, if a patient develops any unexpected neurological or psychiatric symptoms/signs, any symptom/sign suggestive of an increase of intracranial pressure, or accelerated neurological deterioration. Delay in diagnosis and treatment may lead to permanent neurological sequelae. Exercise care when using this agent in patients with a history of ischemic stroke or cerebral hemorrhage. Treatment should be discontinued if PRES is suspected.

Amitriptyline has a major potential interaction with Cerebrovascular Insufficiency.

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.

Amitriptyline has a major potential interaction with Dehydration.

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.

Amitriptyline has a moderate potential interaction with Diabetes Mellitus.

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.

Amitriptyline has a moderate potential interaction with Diabetes Mellitus.

There have been reports of both elevation and lowering of blood sugar levels in patients receiving tricyclic antidepressants. These drugs should be used with caution in patients with hypoglycemia, hyperglycemia or diabetes. Monitoring sugar levels is recommended.

Ozanimod has a moderate potential interaction with Diabetes Mellitus.

Macular edema has been reported with the use of sphingosine 1-phosphate (S1P) receptor modulators. Care should be exercised when using these drugs in patients with a history of uveitis and patients with diabetes mellitus as these patients are at increased risk for macular edema. Before starting treatment with these agents, an ophthalmic evaluation of the fundus, including the macula, is recommended in all patients and at any time if vision change is reported during treatment. Patients with a history of uveitis and patients with diabetes mellitus should have regular follow-up examinations of the fundus, including the macula during treatment. Continuation of therapy in patients with macular edema has not been evaluated, therefore, a decision on whether or not to discontinue treatment needs to take into account the potential benefits and risks for the individual patients.

Amitriptyline has a major potential interaction with Gastrointestinal Obstruction.

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.

Amitriptyline has a moderate potential interaction with Glaucoma, Narrow Angle.

Tricyclic antidepressants as other type of antidepressants have an effect on pupil size causing dilation. This effect can potentially narrow the eye angle resulting in increased intraocular pressure and angle closure glaucoma, especially in predisposed patients. These drugs should be used with caution in patients with anatomically narrow angle or history of glaucoma. Doxepin hydrochloride capsules are contraindicated in patients with glaucoma.

Amitriptyline has a major potential interaction with Glaucoma/Intraocular Hypertension.

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.

Amitriptyline has a major potential interaction with Heart Attack.

The use of most tricyclic antidepressants is contraindicated in patients that are going through the acute recovery period after a myocardial infarction.

Ozanimod has a major potential interaction with Heart Disease.

Ozanimod is contraindicated in patients who have had a recent myocardial infarction, those with unstable angina, stroke, transient ischemic attack, decompensated heart failure with hospitalization, or Class III/IV heart failure, a presence of Mobitz Type II 2nd degree or 3rd degree AV block, sick sinus syndrome, or sino-atrial block, unless the patient has a pacemaker, severe untreated sleep apnea or those patients being treated with monoamine oxidase inhibitor drugs.

Ozanimod has a moderate potential interaction with High Blood Pressure.

The use of ozanimod may result in increased blood pressure. Care should be exercised when using this drug in hypertensive patients and those at risk for hypertension. It is recommended to monitor blood pressure during treatment and manage it according to clinical practices.

Amitriptyline has a major potential interaction with History - Cerebrovascular Disease.

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.

Amitriptyline has a major potential interaction with History - Myocardial Infarction.

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.

Amitriptyline has a major potential interaction with Hyperthyroidism.

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.

Amitriptyline has a moderate potential interaction with Hyperthyroidism.

Most tricyclic antidepressants should be administered with caution in hyperthyroid patients or those receiving thyroid medication as they may develop arrhythmias when these drugs are given.

Amitriptyline has a moderate potential interaction with Hypoglycemia.

There have been reports of both elevation and lowering of blood sugar levels in patients receiving tricyclic antidepressants. These drugs should be used with caution in patients with hypoglycemia, hyperglycemia or diabetes. Monitoring sugar levels is recommended.

Amitriptyline has a major potential interaction with Hypotension.

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.

Ozanimod has a moderate potential interaction with Infection.

Ozanimod may increase the risk of infections and some serious infections with opportunistic pathogens including viruses have been reported. Because of reversible sequestration of lymphocytes in lymphoid tissues, this drug causes a mean reduction in peripheral blood lymphocyte count to approximately 45% of baseline values. Prior to treatment, a recent CBC (i.e., within 6 months or after discontinuation of prior therapy), including lymphocyte count must be available. It is recommended to delay treatment initiation in patients with an active infection until complete resolution. Consider withholding or discontinuing treatment if a patient develops a serious infection, and reassess the benefits and risks prior to reinitiating therapy.

Amitriptyline has a moderate potential interaction with Liver Disease.

In general, tricyclic antidepressants should be used with caution in patients with liver or renal disease, as these drugs are metabolized and excreted through the liver and kidneys. Dose selection, especially in the elderly patients that might have liver or renal dysfunction, should usually be limited to the smallest effective total daily dose. Some tricyclic antidepressants such as clomipramine and nortriptyline have occasionally been associated with elevations in SGOT (AST) and SGPT (ALT), and other hepatic adverse events such as jaundice. Although serious liver injury has only been reported rarely, therapy with these drugs should be administered cautiously in patients with preexisting liver disease and periodic monitoring of liver enzyme levels is recommended.

Amitriptyline has a moderate potential interaction with Liver Disease.

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.

Ozanimod has a moderate potential interaction with Liver Disease.

The use of ozanimod may result in elevations of aminotransferases. The use of ozanimod in patients with hepatic impairment is not recommended. While on treatment with this drug, if a patient develop symptoms suggestive of hepatic dysfunction, such as unexplained nausea, vomiting, abdominal pain, fatigue, anorexia, or jaundice and/or dark urine, should have hepatic enzymes checked, and ozanimod should be discontinued if significant liver injury is confirmed.

Ozanimod has a moderate potential interaction with Macular Edema.

Macular edema has been reported with the use of sphingosine 1-phosphate (S1P) receptor modulators. Care should be exercised when using these drugs in patients with a history of uveitis and patients with diabetes mellitus as these patients are at increased risk for macular edema. Before starting treatment with these agents, an ophthalmic evaluation of the fundus, including the macula, is recommended in all patients and at any time if vision change is reported during treatment. Patients with a history of uveitis and patients with diabetes mellitus should have regular follow-up examinations of the fundus, including the macula during treatment. Continuation of therapy in patients with macular edema has not been evaluated, therefore, a decision on whether or not to discontinue treatment needs to take into account the potential benefits and risks for the individual patients.

Amitriptyline has a moderate potential interaction with Mania.

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.

Ozanimod has a moderate potential interaction with Multiple Sclerosis.

Rare cases of severe exacerbation of multiple sclerosis (MS), including disease rebound, have been reported after discontinuation of sphingosine 1-phosphate receptor modulator in MS treated patients. The possibility of severe exacerbation of disease should be considered after stopping treatment with these agents. Patients should be observed for a severe increase in disability upon discontinuation and appropriate treatment should be instituted, as required.

Amitriptyline has a moderate potential interaction with Neutropenia.

The use of some tricyclic antidepressants has been associated with neutropenia (ANC < 500/mm3) and agranulocytosis (ANC < 500/mm3). Leukocyte and differential blood counts should be performed in patients that develop fever and sore throat during treatment. Therapy should be discontinued if there is evidence of pathologic neutrophil depression.

Amitriptyline has a major potential interaction with Pheochromocytoma.

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.

Ozanimod has a moderate potential interaction with Pulmonary Impairment.

The use of ozanimod may result in a dose-dependent reduction in absolute forced expiratory volume over 1 second (FEV1) and may manifest as early as 3 months after treatment initiation. Care should be exercised when using this drug in patients with respiratory complications. It is recommended to perform spirometric evaluation of respiratory function during therapy if clinically appropriate.

Amitriptyline has a moderate potential interaction with Renal Dysfunction.

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.

Amitriptyline has a moderate potential interaction with Renal Dysfunction.

In general, tricyclic antidepressants should be used with caution in patients with liver or renal disease, as these drugs are metabolized and excreted through the liver and kidneys. Dose selection, especially in the elderly patients that might have liver or renal dysfunction, should usually be limited to the smallest effective total daily dose. Some tricyclic antidepressants such as clomipramine and nortriptyline have occasionally been associated with elevations in SGOT (AST) and SGPT (ALT), and other hepatic adverse events such as jaundice. Although serious liver injury has only been reported rarely, therapy with these drugs should be administered cautiously in patients with preexisting liver disease and periodic monitoring of liver enzyme levels is recommended.

Amitriptyline has a moderate potential interaction with Schizophrenia.

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.

Amitriptyline has a moderate potential interaction with Schizophrenia.

Some tricyclic antidepressants have shown to cause activation or exacerbation of psychosis in schizophrenic patients. A dosage reduction might be required.

Ozanimod has a major potential interaction with Sleep Apnea.

Ozanimod is contraindicated in patients who have had a recent myocardial infarction, those with unstable angina, stroke, transient ischemic attack, decompensated heart failure with hospitalization, or Class III/IV heart failure, a presence of Mobitz Type II 2nd degree or 3rd degree AV block, sick sinus syndrome, or sino-atrial block, unless the patient has a pacemaker, severe untreated sleep apnea or those patients being treated with monoamine oxidase inhibitor drugs.

Amitriptyline has a moderate potential interaction with Tardive Dyskinesia.

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. As with other drugs that possess anticholinergic activity, TCAs may aggravate tardive dyskinesia or induce previously suppressed symptoms. Patients with tardive dyskinesia requiring therapy with TCAs should be monitored for exacerbation of the condition.

Amitriptyline has a major potential interaction with Urinary Retention.

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.

Amitriptyline has a moderate potential interaction with Urinary Retention.

Due to their anticholinergic properties, tricyclic antidepressants should be administered with caution in patients with history of urinary retention. Particularly doxepin hydrochloride capsules are contraindicated in patients with tendency to urinary retention.

Ozanimod has a moderate potential interaction with Uveitis.

Macular edema has been reported with the use of sphingosine 1-phosphate (S1P) receptor modulators. Care should be exercised when using these drugs in patients with a history of uveitis and patients with diabetes mellitus as these patients are at increased risk for macular edema. Before starting treatment with these agents, an ophthalmic evaluation of the fundus, including the macula, is recommended in all patients and at any time if vision change is reported during treatment. Patients with a history of uveitis and patients with diabetes mellitus should have regular follow-up examinations of the fundus, including the macula during treatment. Continuation of therapy in patients with macular edema has not been evaluated, therefore, a decision on whether or not to discontinue treatment needs to take into account the potential benefits and risks for the individual patients.

Ozanimod has a moderate potential interaction with Vaccination.

Vaccinations may be less effective if administered during ozanimod treatment. Patients without a clinical confirmed history of chickenpox or without documentation of a full course of vaccination against VZV should be tested for antibodies to VZV before initiating treatment. It is recommended to obtain a full course of vaccination for antibody-negative patients with varicella vaccine prior to starting treatment with ozanimod and to postpone treatment for 4 weeks to allow the full effect of vaccination. If live attenuated vaccine immunizations are required, administer at least 1 month prior to initiation of ozanimod. Avoid the use of live attenuated vaccines during and for 3 months after treatment with ozanimod.