Interactions between Marax and Moexipril

The theophylline in Marax has a moderate potential interaction with Angina.

The use of theophyllines is associated with an increase in heart rate which may progress to supraventricular tachycardia or ventricular arrhythmia at high serum drug concentrations. Appearance of cardiac adverse effects is generally an indication of theophylline toxicity, although patients with a history of tachyarrhythmias may be more susceptible to the chronotropic effect of these drugs. Therapy with theophyllines should be administered cautiously in such patients. Caution is also advised in patients with hypertension, hyperthyroidism, angina pectoris, or recent myocardial infarction, since high dosages of the drugs are associated with positive inotropic as well as chronotropic effects. Clinical monitoring of serum drug concentrations is recommended to prevent toxicity.

Moexipril has a major potential interaction with Angioedema.

The use of these agents is contraindicated in patients with hereditary angioedema or a history of idiopathic angioedema. Patients with a history of angioedema unrelated to ACE inhibitors may be at increased risk of angioedema while receiving an ACE inhibitor. Patients should be advised to immediately report any signs or symptoms suggestive of angioedema (swelling of face, extremities, eyes, lips, or tongue, or difficulty swallowing or breathing) and to stop taking the medication until otherwise directed by their physician. Emergency therapy and/or measures to prevent airway obstruction are required for angioedema involving the tongue, glottis, or larynx. Treatment with ACE inhibitors should be discontinued permanently if angioedema develops in association with therapy.

The hydrOXYzine in Marax has a moderate potential interaction with Asthma.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

The ePHEDrine in Marax has a moderate potential interaction with Benign Prostatic Hyperplasia.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Moexipril has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

The ePHEDrine in Marax has a major potential interaction with Cardiovascular Conditions and Disorders.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The hydrOXYzine in Marax has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The theophylline in Marax has a major potential interaction with Cerebral Vascular Disorder.

The use of theophyllines is considered by some manufacturers to be contraindicated in patients with underlying seizure disorders unless they are receiving adequate anticonvulsant therapy. Theophyllines may cause seizures, which have generally been associated with toxic drug levels but have also been reported at therapeutic concentrations in patients with head trauma or cerebral infarct. If theophylline therapy is administered in patients with these or other risk factors for seizures, serum drug levels should be monitored closely and maintained in the low therapeutic range. Intractable seizures and death have been reported during acute theophylline toxicity.

The ePHEDrine in Marax has a major potential interaction with Cerebrovascular Insufficiency.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Moexipril has a major potential interaction with Cerebrovascular Insufficiency.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

Moexipril has a major potential interaction with Collagen Vascular Disease.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

The hydrOXYzine in Marax has a moderate potential interaction with COPD.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

The theophylline in Marax has a moderate potential interaction with Cor Pulmonale.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

Moexipril has a major potential interaction with Dehydration.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

The hydrOXYzine in Marax has a major potential interaction with Depression.

A variety of abnormal thinking and behavior changes have been reported to occur in association with the use of most anxiolytics, sedatives and hypnotics. Some of these changes include decreased inhibition, aggressiveness, agitation, and hallucinations. These drugs can cause or exacerbate mental depression and cause suicidal behavior and ideation. Therapy with these drugs should be administered cautiously in patients with a history of depression or other psychiatric disorders. Patients should be monitored for any changes in mood or behavior. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Moexipril has a major potential interaction with Diabetes Mellitus.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

The ePHEDrine in Marax has a moderate potential interaction with Diabetes Mellitus.

Ephedrine may produce slight increases in blood glucose concentrations. Therapy with ephedrine should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate. It is important that the recommended dosages of ephedrine are not exceeded.

The ePHEDrine in Marax has a moderate potential interaction with Diabetes Mellitus.

Sympathomimetic agents may cause increases in blood glucose concentrations. These effects are usually transient and slight but may be significant with dosages higher than those normally recommended. Therapy with sympathomimetic agents should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate.

Moexipril has a major potential interaction with Diarrhea.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

The theophylline in Marax has a moderate potential interaction with Fever.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

The hydrOXYzine in Marax has a moderate potential interaction with Gastrointestinal Obstruction.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, 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. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

The theophylline in Marax has a moderate potential interaction with GERD.

Methylxanthines increase gastric acidity and may also relax lower esophageal sphincter, which can lead to gastric reflux into the esophagus. Therapy with products containing methylxanthines should be administered cautiously in patients with significant gastroesophageal reflux.

The hydrOXYzine in Marax has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, 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. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

The hydrOXYzine in Marax has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Some hypnotic drugs can have an anticholinergic effect and should be used with caution in patients with glaucoma, and trouble urinating due to retention or enlarged prostate.

The theophylline in Marax has a major potential interaction with Head Injury.

The use of theophyllines is considered by some manufacturers to be contraindicated in patients with underlying seizure disorders unless they are receiving adequate anticonvulsant therapy. Theophyllines may cause seizures, which have generally been associated with toxic drug levels but have also been reported at therapeutic concentrations in patients with head trauma or cerebral infarct. If theophylline therapy is administered in patients with these or other risk factors for seizures, serum drug levels should be monitored closely and maintained in the low therapeutic range. Intractable seizures and death have been reported during acute theophylline toxicity.

The hydrOXYzine in Marax has a major potential interaction with Heart Attack.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

The theophylline in Marax has a moderate potential interaction with Heart Attack.

The use of theophyllines is associated with an increase in heart rate which may progress to supraventricular tachycardia or ventricular arrhythmia at high serum drug concentrations. Appearance of cardiac adverse effects is generally an indication of theophylline toxicity, although patients with a history of tachyarrhythmias may be more susceptible to the chronotropic effect of these drugs. Therapy with theophyllines should be administered cautiously in such patients. Caution is also advised in patients with hypertension, hyperthyroidism, angina pectoris, or recent myocardial infarction, since high dosages of the drugs are associated with positive inotropic as well as chronotropic effects. Clinical monitoring of serum drug concentrations is recommended to prevent toxicity.

The hydrOXYzine in Marax has a major potential interaction with Heart Disease.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

The theophylline in Marax has a moderate potential interaction with Heart Failure.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

Moexipril has a major potential interaction with Hemodialysis.

Anaphylactoid reactions have been reported in patients undergoing hemodialysis with high-flux polyacrylonitrile membranes and treated concomitantly with an ACE inhibitor. The frequency and mechanism of this interaction have not been established, and it is not known whether the interaction occurs with other membrane types. Therapy with ACE inhibitors should be administered cautiously in patients requiring hemodialysis.

Moexipril has a major potential interaction with Hemodialysis.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

The theophylline in Marax has a moderate potential interaction with Hemodialysis.

Theophylline is removed by hemodialysis. Doses should either be scheduled for administration after dialysis or supplemental doses be given after dialysis.

The theophylline in Marax has a moderate potential interaction with High Blood Pressure.

The use of theophyllines is associated with an increase in heart rate which may progress to supraventricular tachycardia or ventricular arrhythmia at high serum drug concentrations. Appearance of cardiac adverse effects is generally an indication of theophylline toxicity, although patients with a history of tachyarrhythmias may be more susceptible to the chronotropic effect of these drugs. Therapy with theophyllines should be administered cautiously in such patients. Caution is also advised in patients with hypertension, hyperthyroidism, angina pectoris, or recent myocardial infarction, since high dosages of the drugs are associated with positive inotropic as well as chronotropic effects. Clinical monitoring of serum drug concentrations is recommended to prevent toxicity.

Moexipril has a major potential interaction with Hyperkalemia.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

The ePHEDrine in Marax has a major potential interaction with Hyperthyroidism.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The hydrOXYzine in Marax has a moderate potential interaction with Hyperthyroidism.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The theophylline in Marax has a moderate potential interaction with Hyperthyroidism.

The use of theophyllines is associated with an increase in heart rate which may progress to supraventricular tachycardia or ventricular arrhythmia at high serum drug concentrations. Appearance of cardiac adverse effects is generally an indication of theophylline toxicity, although patients with a history of tachyarrhythmias may be more susceptible to the chronotropic effect of these drugs. Therapy with theophyllines should be administered cautiously in such patients. Caution is also advised in patients with hypertension, hyperthyroidism, angina pectoris, or recent myocardial infarction, since high dosages of the drugs are associated with positive inotropic as well as chronotropic effects. Clinical monitoring of serum drug concentrations is recommended to prevent toxicity.

Moexipril has a major potential interaction with Hyponatremia.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

The hydrOXYzine in Marax has a moderate potential interaction with Hypotension.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The theophylline in Marax has a moderate potential interaction with Influenza.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

Moexipril has a major potential interaction with Ischemic Heart Disease.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

The hydrOXYzine in Marax has a moderate potential interaction with Liver Disease.

In general, anxiolytics, sedatives and hypnotics are extensively metabolized by the liver. Their plasma clearance may be decreased and their half-life prolonged in patients with impaired hepatic function. Therapy with these drugs should be administered cautiously in patients with liver disease (some are not recommended in severe liver impairment), and the dosage should be adjusted accordingly. Laboratory testing is recommended prior and during treatment.

The theophylline in Marax has a moderate potential interaction with Liver Disease.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

The hydrOXYzine in Marax has a moderate potential interaction with Liver Disease.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

The hydrOXYzine in Marax has a moderate potential interaction with Liver Disease.

Some anxiolytics, sedatives and hypnotics are extensively metabolized by the liver, and excreted in the urine. Patients with impaired renal and/or hepatic function may be at greater risk for adverse effects, including central nervous system and respiratory depression, due to drug and metabolite accumulation. Therapy with these drugs should be administered cautiously in such patients, with careful dose selection usually starting at the low end of the dosing range.

Moexipril has a moderate potential interaction with Liver Disease.

Rarely, elevations of liver enzymes and/or serum bilirubin have occurred with the use of ACE inhibitors. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.

The hydrOXYzine in Marax has a major potential interaction with Long QT Syndrome.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

The theophylline in Marax has a moderate potential interaction with Panhypopituitarism.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

The theophylline in Marax has a major potential interaction with Peptic Ulcer.

Methylxanthines are known to stimulate peptic acid secretion. Therapy with products containing methylxanthines should be administered with extreme caution in patients with active peptic ulcer disease. Some manufacturers consider their use to be contraindicated under such circumstance.

The ePHEDrine in Marax has a major potential interaction with Pheochromocytoma.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The theophylline in Marax has a moderate potential interaction with Post MI Syndrome.

The use of theophyllines is associated with an increase in heart rate which may progress to supraventricular tachycardia or ventricular arrhythmia at high serum drug concentrations. Appearance of cardiac adverse effects is generally an indication of theophylline toxicity, although patients with a history of tachyarrhythmias may be more susceptible to the chronotropic effect of these drugs. Therapy with theophyllines should be administered cautiously in such patients. Caution is also advised in patients with hypertension, hyperthyroidism, angina pectoris, or recent myocardial infarction, since high dosages of the drugs are associated with positive inotropic as well as chronotropic effects. Clinical monitoring of serum drug concentrations is recommended to prevent toxicity.

The ePHEDrine in Marax has a moderate potential interaction with Prostate Tumor, Benign.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

The theophylline in Marax has a moderate potential interaction with Pulmonary Edema.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

The theophylline in Marax has a major potential interaction with Renal Dysfunction.

The metabolites of theophylline, which are generally undetectable in patients with normal renal function, may accumulate in patients with renal impairment and contribute to the toxicity of theophylline. In addition, the plasma protein binding of theophylline may be significantly decreased in renal impairment, resulting in elevated free drug concentrations and further increasing the risk of toxicity. Therapy with theophyllines should be administered cautiously in patients with impaired renal function. Dosage adjustments and more intensive monitoring of serum theophylline concentrations may be required.

Moexipril has a major potential interaction with Renal Dysfunction.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

Moexipril has a major potential interaction with Renal Dysfunction.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

The hydrOXYzine in Marax has a moderate potential interaction with Renal Dysfunction.

Some anxiolytics, sedatives and hypnotics are extensively metabolized by the liver, and excreted in the urine. Patients with impaired renal and/or hepatic function may be at greater risk for adverse effects, including central nervous system and respiratory depression, due to drug and metabolite accumulation. Therapy with these drugs should be administered cautiously in such patients, with careful dose selection usually starting at the low end of the dosing range.

The hydrOXYzine in Marax has a moderate potential interaction with Renal Dysfunction.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Moexipril has a moderate potential interaction with Renal Dysfunction.

With the exception of fosinopril, ACE inhibitors (and/or their active metabolites in some cases) are primarily eliminated by the kidney and may accumulate in patients with renal impairment. ACE inhibitors can also worsen renal function in some patients by blocking the effect of angiotensin II-mediated efferent arteriolar vasoconstriction, thereby decreasing glomerular filtration. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting renal dysfunction, particularly those with renovascular disease. Patients with moderate to severe renal impairment usually require lower or less frequent doses and smaller increments in dose. In addition, a dosage reduction or discontinuation of any concomitantly administered diuretics may be helpful. Fosinopril probably does not require dosage adjustments unless hepatic function is also significantly impaired.

In patients with bilateral renal artery stenosis or renal artery stenosis in a solitary kidney, ACE inhibitors may reduce renal perfusion to a critically low level. Renal function should be monitored closely for the first few weeks of therapy.

The theophylline in Marax has a major potential interaction with Seizures.

The use of theophyllines is considered by some manufacturers to be contraindicated in patients with underlying seizure disorders unless they are receiving adequate anticonvulsant therapy. Theophyllines may cause seizures, which have generally been associated with toxic drug levels but have also been reported at therapeutic concentrations in patients with head trauma or cerebral infarct. If theophylline therapy is administered in patients with these or other risk factors for seizures, serum drug levels should be monitored closely and maintained in the low therapeutic range. Intractable seizures and death have been reported during acute theophylline toxicity.

The theophylline in Marax has a moderate potential interaction with Shock.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

The theophylline in Marax has a moderate potential interaction with Tachyarrhythmia.

The use of theophyllines is associated with an increase in heart rate which may progress to supraventricular tachycardia or ventricular arrhythmia at high serum drug concentrations. Appearance of cardiac adverse effects is generally an indication of theophylline toxicity, although patients with a history of tachyarrhythmias may be more susceptible to the chronotropic effect of these drugs. Therapy with theophyllines should be administered cautiously in such patients. Caution is also advised in patients with hypertension, hyperthyroidism, angina pectoris, or recent myocardial infarction, since high dosages of the drugs are associated with positive inotropic as well as chronotropic effects. Clinical monitoring of serum drug concentrations is recommended to prevent toxicity.

The theophylline in Marax has a moderate potential interaction with Underactive Thyroid.

Certain conditions have been identified as causes of reduced theophylline clearance. They include age (neonates and infants < 1 year as well as elderly patients > 60 years) and the following concurrent diseases: acute pulmonary edema; decompensated heart failure; cor pulmonale; fever (>= 102 degrees for 24 hours or more, or lesser temperature elevations for longer periods); influenza; untreated or uncontrolled hypothyroidism; liver disease, cirrhosis or acute hepatitis; reduced renal function in infants < 3 months of age; sepsis with multi-organ failure; and shock. Therapy with theophyllines should be administered cautiously in patients presenting with one or more of these risk factors, and the dosage should be appropriately reduced to prevent toxicity. More intensive monitoring of serum theophylline concentrations may be required. Toxicity is most likely to occur when levels exceed 20 mcg/mL. Severe cases, sometimes without previous warning, have led to cardiac arrhythmias, intractable seizures, and death.

The hydrOXYzine in Marax has a moderate potential interaction with Urinary Retention.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, 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. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

The hydrOXYzine in Marax has a moderate potential interaction with Urinary Retention.

Some hypnotic drugs can have an anticholinergic effect and should be used with caution in patients with glaucoma, and trouble urinating due to retention or enlarged prostate.

The ePHEDrine in Marax has a moderate potential interaction with Urinary Tract Obstruction.

Sympathomimetic agents such as ephedrine have the potential for producing clinically significant systemic effects, particularly during prolonged or indiscriminate use. In patients with prostate enlargement, urinary difficulty may develop or worsen due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with ephedrine should be administered cautiously in patients with difficulty for urination due to hypertrophy or neoplasm of the prostate. It is important that the recommended dosages are not exceeded.

The hydrOXYzine in Marax has a major potential interaction with Ventricular Arrhythmia.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

Moexipril has a major potential interaction with Vomiting.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.