Can you take Aldex D with Ethacrynic acid?

Ethacrynic acid has a moderate potential interaction with Abnormal Glucose Tolerance.

Loop diuretics may cause hyperglycemia, glycosuria, and alterations in glucose tolerance tests. Rarely, precipitation of diabetes mellitus has been reported. Therapy with loop diuretics should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during therapy, and their antidiabetic regimen adjusted accordingly.

Ethacrynic acid has a major potential interaction with Anuria.

The use of loop diuretics is contraindicated in patients with anuria.

The pyrilamine in Aldex D 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 phenylephrine in Aldex D 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.

The phenylephrine in Aldex D 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 pyrilamine in Aldex D 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 phenylephrine in Aldex D 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.

Ethacrynic acid has a major potential interaction with Cirrhosis.

Loop diuretic therapy should be initiated in the hospital under strict observation in patients with liver cirrhosis and ascites. Sudden alteration of fluid and electrolyte balance may precipitate hepatic encephalopathy and coma in such patients, who are also at increased risk for the development of hypokalemia. Supplemental potassium and/or concomitant use of an aldosterone antagonist or potassium-sparing agent may help prevent hypokalemia and metabolic alkalosis. Loop diuretics should be withheld in patients with hepatic coma until the condition improves.

The pyrilamine in Aldex D 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.

Ethacrynic acid has a major potential interaction with Dehydration.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The pyrilamine in Aldex D 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.

The phenylephrine in Aldex D 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.

Ethacrynic acid has a moderate potential interaction with Diabetes Mellitus.

Loop diuretics may cause hyperglycemia, glycosuria, and alterations in glucose tolerance tests. Rarely, precipitation of diabetes mellitus has been reported. Therapy with loop diuretics should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during therapy, and their antidiabetic regimen adjusted accordingly.

Ethacrynic acid has a major potential interaction with Diarrhea.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

Ethacrynic acid has a major potential interaction with Electrolyte Abnormalities.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The pyrilamine in Aldex D 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 phenylephrine in Aldex D has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

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.

The pyrilamine in Aldex D 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 pyrilamine in Aldex D 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.

Ethacrynic acid has a moderate potential interaction with Gout.

Loop diuretics may decrease the rate of uric acid excretion. Hyperuricemia can occur but is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout or chronic renal failure. Therapy with loop diuretics should be administered cautiously in such patients.

Ethacrynic acid has a major potential interaction with Hearing Loss.

Tinnitus and hearing loss, both reversible and permanent, have been reported with the use of loop diuretics. Ototoxic effects have generally been associated with rapid intravenous or intramuscular injection, severe renal impairment, unusually high dosages (i.e. several times the usual recommended dosages), and/or concomitant use of other ototoxic agents. Therapy with loop diuretics should be administered cautiously in patients with preexisting vestibular and/or auditory impairment, since it may delay the recognition or confound the diagnosis of a drug-induced ototoxic effect. High-dose parenteral therapy should be administered as controlled infusion.

Ethacrynic acid has a major potential interaction with Hepatic Coma.

Loop diuretic therapy should be initiated in the hospital under strict observation in patients with liver cirrhosis and ascites. Sudden alteration of fluid and electrolyte balance may precipitate hepatic encephalopathy and coma in such patients, who are also at increased risk for the development of hypokalemia. Supplemental potassium and/or concomitant use of an aldosterone antagonist or potassium-sparing agent may help prevent hypokalemia and metabolic alkalosis. Loop diuretics should be withheld in patients with hepatic coma until the condition improves.

Ethacrynic acid has a major potential interaction with Hyperaldosteronism.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The phenylephrine in Aldex D 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 pyrilamine in Aldex D 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.

Ethacrynic acid has a major potential interaction with Hypocalcemia.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

Ethacrynic acid has a major potential interaction with Hypokalemia.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

Ethacrynic acid has a major potential interaction with Hyponatremia.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The pyrilamine in Aldex D 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 pyrilamine in Aldex D 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 pyrilamine in Aldex D 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.

Ethacrynic acid has a major potential interaction with Magnesium Imbalance.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

Ethacrynic acid has a major potential interaction with Malnourishment.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The phenylephrine in Aldex D 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 phenylephrine in Aldex D 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.

Ethacrynic acid has a major potential interaction with Renal Dysfunction.

Impaired effectiveness and possible delayed excretion of loop diuretics may occur in patients with severe renal dysfunction. These individuals may require high dosages that are associated with an increased risk of electrolyte abnormalities (hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia, hypocalcemia) and ototoxicity (tinnitus, hearing loss). Therapy with loop diuretics should be administered cautiously in patients with significantly impaired renal function. Prolongation of the dosing intervals may be appropriate to prevent drug accumulation. The patient should be monitored closely for the signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Excessive diuresis should be avoided as it may induce dehydration and hypovolemia, which can result in an abrupt reduction in glomerular filtration and renal blood flow. If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, or if renal function becomes progressively worse as indicated by rising BUN or serum creatinine levels, an interruption or discontinuation of therapy should be considered.

The pyrilamine in Aldex D 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.

The pyrilamine in Aldex D 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 pyrilamine in Aldex D 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.

Ethacrynic acid has a major potential interaction with Ventricular Arrhythmia.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

Ethacrynic acid has a major potential interaction with Vomiting.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.