Can you take Advil Cold and Sinus Liqui-Gels with Tramadol?

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Alcoholism.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

traMADol has a major potential interaction with Alcoholism.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

traMADol has a major potential interaction with Alcoholism.

The CNS depressant effects of tramadol may be additive with those of alcohol and may lead to profound sedation, respiratory depression, coma, and death. Therapy with tramadol should be administered cautiously (and only when alternative treatment options are inadequate) in patients who might be prone to acute alcohol intake. Dosages and durations should be limited to the minimum required and patients should be monitored for signs and symptoms of respiratory depression and sedation. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; naloxone will reverse some, but not all, symptoms caused by overdosage with tramadol, but it also increases the risk of seizures.

traMADol has a moderate potential interaction with Alcoholism.

Tramadol should not be prescribed for patients who are suicidal or addiction-prone. The use of nonnarcotic analgesics should be considered for patients who are suicidal or depressed. Tramadol should be prescribed with caution for patients with history of misuse and/or are currently taking CNS-active drugs, antidepressant drugs, alcohol in excess, and patients who suffer from emotional disturbance or depression. Patients should be advised not to exceed the recommended dose and to limit their intake of alcohol.

traMADol has a moderate potential interaction with Alcoholism.

Seizures have been reported in patients receiving tramadol within the recommended dosage range. The risk appears to increase with doses above the recommended range and with concomitant use of certain drugs (e.g., those that reduce the seizure threshold). Risk of seizure may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (e.g., head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). In tramadol overdose, naloxone administration may increase the risk of seizures.

traMADol has a major potential interaction with Altered Consciousness.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Anemia.

Anemia has been reported in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). This may be due to fluid retention, occult/gross blood loss, or an incompletely described effect on erythropoiesis. Hemoglobin or hematocrit should be monitored in patients with any signs/symptoms of anemia or blood loss, especially during long-term therapy. NSAIDs may increase risk of bleeding events; comorbid conditions (e.g., coagulation disorders; concomitant use of warfarin/other anticoagulants, antiplatelet agents, serotonin/serotonin norepinephrine reuptake inhibitors) may increase this risk, and patients with these conditions should be monitored for signs of bleeding. Therapy with NSAIDs should be administered cautiously in patients with or predisposed to anemia. Clinical monitoring of hematopoietic function may be appropriate, particularly during chronic therapy.

traMADol has a major potential interaction with Asphyxia.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Asthma.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are contraindicated in patients with history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs; severe, sometimes fatal, anaphylactic reactions to NSAIDs have been reported in such patients. A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitis complicated by nasal polyps, severe potentially fatal bronchospasm, and/or intolerance to aspirin and other NSAIDs. Since cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, therapy with any NSAID should be avoided in patients with this form of aspirin sensitivity. NSAIDs should be used with caution in patients with preexisting asthma (without known aspirin sensitivity), and these patients should be monitored for changes in the signs and symptoms of asthma.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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.

traMADol has a moderate potential interaction with Biliary Obstruction.

Tramadol may cause spasm of the sphincter of Oddi. Opioids may increase serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be monitored for worsening symptoms.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Bleeding Disorder.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Bleeding Disorder.

Anemia has been reported in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). This may be due to fluid retention, occult/gross blood loss, or an incompletely described effect on erythropoiesis. Hemoglobin or hematocrit should be monitored in patients with any signs/symptoms of anemia or blood loss, especially during long-term therapy. NSAIDs may increase risk of bleeding events; comorbid conditions (e.g., coagulation disorders; concomitant use of warfarin/other anticoagulants, antiplatelet agents, serotonin/serotonin norepinephrine reuptake inhibitors) may increase this risk, and patients with these conditions should be monitored for signs of bleeding. Therapy with NSAIDs should be administered cautiously in patients with or predisposed to anemia. Clinical monitoring of hematopoietic function may be appropriate, particularly during chronic therapy.

traMADol has a major potential interaction with Brain Tumor.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

traMADol has a major potential interaction with Cachexia.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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.

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

Seizures have been reported in patients receiving tramadol within the recommended dosage range. The risk appears to increase with doses above the recommended range and with concomitant use of certain drugs (e.g., those that reduce the seizure threshold). Risk of seizure may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (e.g., head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). In tramadol overdose, naloxone administration may increase the risk of seizures.

traMADol has a major potential interaction with Cerebral Vascular Disorder.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Cerebrovascular Insufficiency.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Coagulation Defects and Disorders.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Colonic Ulceration.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

traMADol has a major potential interaction with Cor Pulmonale.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Dehydration.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

traMADol has a moderate potential interaction with Dehydration.

Tramadol may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating tramadol. In patients with circulatory shock, tramadol may cause vasodilation that can further reduce cardiac output and blood pressure; tramadol should be avoided in patients with circulatory shock.

traMADol has a major potential interaction with Depression.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

traMADol has a moderate potential interaction with Depression.

Tramadol should not be prescribed for patients who are suicidal or addiction-prone. The use of nonnarcotic analgesics should be considered for patients who are suicidal or depressed. Tramadol should be prescribed with caution for patients with history of misuse and/or are currently taking CNS-active drugs, antidepressant drugs, alcohol in excess, and patients who suffer from emotional disturbance or depression. Patients should be advised not to exceed the recommended dose and to limit their intake of alcohol.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Dermatitis, Drug-Induced.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious skin adverse reactions (e.g., Stevens-Johnson syndrome, toxic epidermal necrolysis, and exfoliative dermatitis), which can be fatal. NSAIDs can also cause fixed drug eruption, and may present as generalized bullous fixed drug eruption, which can be life-threatening. These serious events may occur without warning. Patients should be advised to discontinue the NSAID and seek medical attention promptly at the first sign of skin rash or any other sign of hypersensitivity. NSAIDs are contraindicated in patients with previous serious skin reactions to these drugs.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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.

traMADol has a moderate potential interaction with Diabetes Mellitus.

Cases of tramadol-associated hypoglycemia have been reported, some resulting in hospitalization. In most cases, patients had predisposing risk factors (e.g., diabetes); caution is recommended in these patients. If hypoglycemia is suspected, blood glucose levels should be monitored and discontinuation of therapy should be considered as appropriate.

traMADol has a major potential interaction with Drug Dependence.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

traMADol has a moderate potential interaction with Drug Dependence.

Seizures have been reported in patients receiving tramadol within the recommended dosage range. The risk appears to increase with doses above the recommended range and with concomitant use of certain drugs (e.g., those that reduce the seizure threshold). Risk of seizure may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (e.g., head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). In tramadol overdose, naloxone administration may increase the risk of seizures.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Fluid Retention.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

traMADol has a moderate potential interaction with Gallbladder Disease.

Tramadol may cause spasm of the sphincter of Oddi. Opioids may increase serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be monitored for worsening symptoms.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Gastritis/Duodenitis.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Gastrointestinal Hemorrhage.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

traMADol has a major potential interaction with Gastrointestinal Obstruction.

Opioid analgesics are contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Gastrointestinal Obstruction.

The extended-release formulation of pseudoephedrine (Sudafed 24 Hour) contains a non-deformable material. There have been rare reports of obstructive symptoms in patients with known strictures following the ingestion of similar sustained-release products. Therapy with the extended-release formulation of pseudoephedrine should be administered cautiously in patients with preexisting severe gastrointestinal narrowing or obstruction, whether pathologic or iatrogenic.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Gastrointestinal Perforation.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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.

traMADol has a major potential interaction with Head Injury.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

traMADol has a moderate potential interaction with Head Injury.

Opioids may obscure the clinical course in a patient with a head injury. The use of tramadol should be avoided in patients with impaired consciousness or coma.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Heart Failure.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Heart Failure.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with High Blood Pressure.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with History, Peptic Ulcer.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with History - Cerebrovascular Disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with History - Myocardial Infarction.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Hyperkalemia.

Increases in serum potassium concentration (including hyperkalemia) have been reported with use of nonsteroidal anti-inflammatory drugs (NSAIDs), even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state. Caution is advised in patients with hyperkalemia.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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 ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Hyponatremia.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

traMADol has a moderate potential interaction with Hypotension.

Tramadol may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating tramadol. In patients with circulatory shock, tramadol may cause vasodilation that can further reduce cardiac output and blood pressure; tramadol should be avoided in patients with circulatory shock.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Intestinal Anastomoses.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Ischemic Heart Disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Liver Disease.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Liver Disease.

Therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) should be administered cautiously in patients with preexisting liver disease. Periodic monitoring of liver function is recommended during prolonged therapy. NSAIDs are also highly protein-bound and some are extensively metabolized by the liver. Metabolic activity and/or plasma protein binding may be altered in patients with hepatic impairment. A dosage reduction may be required in some cases.

traMADol has a moderate potential interaction with Liver Disease.

Tramadol is converted by the liver to several metabolites, one of which (referred to as M1) is pharmacologically active and a more potent analgesic than tramadol itself. The metabolism of both tramadol and M1 has been shown to decrease in patients with advanced cirrhosis of the liver, resulting in increased exposure to tramadol as well as substantially prolonged elimination half-lives for both tramadol and M1. Therapy with tramadol should be administered cautiously in patients with liver dysfunction. In patients with severe liver dysfunction, dosage reduction is recommended with the immediate-release formulations, while the extended-release formulations should not be used.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Noninfectious Colitis.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

traMADol has a moderate potential interaction with Pancreatitis.

Tramadol may cause spasm of the sphincter of Oddi. Opioids may increase serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be monitored for worsening symptoms.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Peptic Ulcer.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Phenylketonuria.

Chewable products frequently may contain aspartame, which is metabolized in the gastrointestinal tract to phenylalanine. Sudafed (brand of pseudoephedrine) chewable 15 mg tablets provide the equivalent of 0.78 mg of phenylalanine per each tablet. The aspartame/phenylalanine content should be considered when this and similar products are used in patients who must restrict their intake of phenylalanine (i.e. phenylketonurics).

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Phenylketonuria.

Chewable products frequently may contain aspartame, which is metabolized in the gastrointestinal tract to phenylalanine. Motrin (brand of ibuprofen) chewable 50 mg and 100 mg tablets provide the equivalent of 3 mg and 6 mg of phenylalanine each, respectively. The aspartame/phenylalanine content should be considered when these and similar products are used in patients who must restrict their intake of phenylalanine (i.e. phenylketonurics).

The pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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 pseudoephedrine in Advil Cold and Sinus Liqui-Gels 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.

traMADol has a moderate potential interaction with Pseudotumor Cerebri.

Opioids may obscure the clinical course in a patient with a head injury. The use of tramadol should be avoided in patients with impaired consciousness or coma.

traMADol has a major potential interaction with Psychiatric Disorders.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

traMADol has a moderate potential interaction with Psychosis.

Tramadol should not be prescribed for patients who are suicidal or addiction-prone. The use of nonnarcotic analgesics should be considered for patients who are suicidal or depressed. Tramadol should be prescribed with caution for patients with history of misuse and/or are currently taking CNS-active drugs, antidepressant drugs, alcohol in excess, and patients who suffer from emotional disturbance or depression. Patients should be advised not to exceed the recommended dose and to limit their intake of alcohol.

traMADol has a major potential interaction with Pulmonary Impairment.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Renal Dysfunction.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Renal Dysfunction.

Increases in serum potassium concentration (including hyperkalemia) have been reported with use of nonsteroidal anti-inflammatory drugs (NSAIDs), even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state. Caution is advised in patients with hyperkalemia.

traMADol has a moderate potential interaction with Renal Dysfunction.

Tramadol and its metabolites, one of which (referred to as M1) is pharmacologically active and a more potent analgesic than tramadol itself, are primarily excreted in the urine. The rate and extent of excretion of both tramadol and M1 have been shown to decrease in patients with impaired renal function. Therapy with tramadol should be administered cautiously in such patients. In patients with CrCl less than 30 mL/min, dosage reduction is recommended with the immediate-release formulations, while the extended-release formulations should not be used.

traMADol has a major potential interaction with Respiratory Arrest.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

traMADol has a moderate potential interaction with Shock.

Tramadol may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating tramadol. In patients with circulatory shock, tramadol may cause vasodilation that can further reduce cardiac output and blood pressure; tramadol should be avoided in patients with circulatory shock.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a major potential interaction with Smoking.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Thrombocytopathy.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Thrombocytopenia.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

The ibuprofen in Advil Cold and Sinus Liqui-Gels has a moderate potential interaction with Vitamin K Deficiency.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.