Drug Interactions between chlorpheniramine / guaifenesin / phenylephrine and oxcarbazepine

Alcohol can increase the nervous system side effects of chlorpheniramine such as dizziness, drowsiness, and difficulty concentrating. Some people may also experience impairment in thinking and judgment. You should avoid or limit the use of alcohol while being treated with chlorpheniramine. Do not use more than the recommended dose of chlorpheniramine, and avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. Talk to your doctor or pharmacist if you have any questions or concerns.

Alcohol can increase the nervous system side effects of OXcarbazepine such as dizziness, drowsiness, and difficulty concentrating. Some people may also experience impairment in thinking and judgment. You should avoid or limit the use of alcohol while being treated with OXcarbazepine. Do not use more than the recommended dose of OXcarbazepine, and avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. Talk to your doctor or pharmacist if you have any questions or concerns.

Both phenylephrine and caffeine can increase blood pressure and heart rate, and combining them may enhance these effects. Talk to your doctor before using these medications, especially if you have a history of high blood pressure or heart disease. You may need a dose adjustment or more frequent monitoring by your doctor to safely use both medications. Contact your doctor if your condition changes or you experience increased side effects. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

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.

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.

Antiepileptic drugs can increase depression and suicidal thoughts or behaviors in patients receiving these drugs for any indication. Patients should be monitored for the emergence or worsening of depression, suicidal thoughts and unusual changes in mood or behavior. Caregivers and family should be alert for the emergence or worsening of symptoms. Behaviors of concern should be reported immediately to the healthcare providers.

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.

Most anticonvulsants are primarily metabolized by the liver. Metabolic activity may be decreased in patients with liver disease, resulting in elevated drug levels and increased risk of toxicity. Therapy with anticonvulsants should be administered cautiously in patients with mild and moderate liver impairment. Therapy with these drugs is mostly not recommended in patients with severe liver impairment. Caution is also advised when treating patients with a history of liver disease, since the use of some anticonvulsants has been associated with hepatotoxicity. Baseline and periodic evaluation of liver function is recommended. Therapy should be discontinued and not readministered if evidence of liver damage is observed and felt to be drug-related.

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.

Most anticonvulsants are primarily excreted by the kidney. The plasma clearance may be decreased and the half-life prolonged in patients with impaired renal function. Therapy with anticonvulsants should be administered cautiously in patients with significant renal dysfunction. In most cases it is recommended to adjust the dosage in patients with CrCl <50 mL/min to half the usual starting dose and then increase slowly to achieve the desired clinical response. The renal function should be monitored regularly in patients receiving therapy.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Aromatic antiepileptic drugs such as phenytoin, carbamazepine, and oxcarbazepine, inhibit voltage- gated sodium channels and reduce membrane excitability in neurons and muscle and can be associated with cardiovascular effects. Individual agents have demonstrated AV heart block, including second and third-degree block following treatment. This occurred generally, but not solely in patients with underlying EKG abnormalities or risk factors for conduction abnormalities. Therapy with these agents should be considered and administered cautiously in patients with a history of cardiovascular disease and conduction abnormalities.

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.

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.

Rare events of pancytopenia, leukopenia, and agranulocytosis have been reported in patients treated with oxcarbazepine during postmarketing observations. Discontinuation of the drug should be considered if any evidence of these hematologic events develop. Therapy with oxcarbazepine should be administered with caution in patients with preexisting blood dyscrasias and/or bone marrow depression. Complete blood counts, including platelets and possibly reticulocytes and serum iron, should be performed prior to initiating therapy and regularly during therapy.

Aromatic antiepileptic drugs such as phenytoin, carbamazepine, and oxcarbazepine, inhibit voltage- gated sodium channels and reduce membrane excitability in neurons and muscle and can be associated with cardiovascular effects. Individual agents have demonstrated AV heart block, including second and third-degree block following treatment. This occurred generally, but not solely in patients with underlying EKG abnormalities or risk factors for conduction abnormalities. Therapy with these agents should be considered and administered cautiously in patients with a history of cardiovascular disease and conduction abnormalities.

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.

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.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Antiepileptic drugs (AEDs) have been associated with an increased risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Pooled analyses of 199 placebo-controlled clinical studies involving the use of 11 different AEDs showed that patients receiving AEDs had approximately twice the risk of suicidal thinking or behavior compared to patients receiving placebo. AEDs should be administered cautiously in patients with depression or other psychiatric disorders; phentermine-topiramate should be avoided in patients with history of suicidal attempts or active suicidal ideation. The risk of suicidal thoughts and behavior should be carefully assessed against the risk of untreated illness, bearing in mind that epilepsy and many other conditions for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Patients, caregivers, and families should be alert to the emergence or worsening of signs and symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts or behavior. If patients have symptoms of suicidal ideation or behavior, a dosage reduction or treatment discontinuation should be considered.

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.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

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.

Sympathomimetic agents can induce transient mydriasis via stimulation of alpha-1 adrenergic receptors. In patients with anatomically narrow angles or narrow-angle glaucoma, pupillary dilation can provoke an acute attack. In patients with other forms of glaucoma, mydriasis may occasionally increase intraocular pressure. Therapy with sympathomimetic agents should be administered cautiously in patients with or predisposed to glaucoma, particularly narrow-angle glaucoma.

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.

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.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

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.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

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.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

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.

Antiepileptic drugs (AEDs) have been associated with an increased risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Pooled analyses of 199 placebo-controlled clinical studies involving the use of 11 different AEDs showed that patients receiving AEDs had approximately twice the risk of suicidal thinking or behavior compared to patients receiving placebo. AEDs should be administered cautiously in patients with depression or other psychiatric disorders; phentermine-topiramate should be avoided in patients with history of suicidal attempts or active suicidal ideation. The risk of suicidal thoughts and behavior should be carefully assessed against the risk of untreated illness, bearing in mind that epilepsy and many other conditions for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior. Patients, caregivers, and families should be alert to the emergence or worsening of signs and symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts or behavior. If patients have symptoms of suicidal ideation or behavior, a dosage reduction or treatment discontinuation should be considered.

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.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Some anticonvulsants can cause clinically significant hyponatremia (Na < 125 mmol/L). Therapy with these drugs should be administered cautiously in patients with conditions predisposing to hyponatremia, such as SIADH, use of diuretics or drugs associated with inappropriate antidiuretic hormone secretion, adrenal insufficiency, hypothyroidism, primary polydipsia, and edema (e.g., due to liver cirrhosis, congestive heart failure, or nephrotic syndrome). Serum sodium levels should be monitored during maintenance therapy, and patients should be monitored for signs and symptoms possibly indicating hyponatremia such as nausea, malaise, headache, lethargy, confusion, obtundation, and increase in seizure frequency or severity. If hyponatremia occurs, conservative measures such as fluid restriction, a reduction in dosage, or discontinuation of therapy will usually suffice.

Decreased values for thyroid function tests, especially T4 have been observed with the administration of oxcarbazepine. This should be taken into account in patients with thyroid disorders.

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.