Can you take Avandamet with Trazodone?

The metFORMIN in Avandamet has a major potential interaction with Adrenal Insufficiency.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

The metFORMIN in Avandamet has a major potential interaction with Alcoholism.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The metFORMIN in Avandamet has a major potential interaction with Anemia.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The rosiglitazone in Avandamet has a minor potential interaction with Anemia.

Thiazolidinediones can cause slight decreases in hemoglobin and hematocrit. In clinical studies, hemoglobin levels were reduced primarily within the first 4 to 12 weeks of therapy but remained relatively constant thereafter. These changes may be related to increased plasma volume and have rarely been associated with any significant hematologic clinical effects. Nevertheless, caution may be advisable when thiazolidinediones are prescribed to patients with certain anemias.

The metFORMIN in Avandamet has a moderate potential interaction with Anemia Associated with Vitamin B12 Deficiency.

Metformin may interfere with vitamin B12 absorption from the B12-intrinsic factor complex. A decrease to subnormal levels of previously normal serum vitamin B12 levels was reported in about 7% of patients treated with metformin during clinical trials. Such decrease may be associated with anemia but appears to be rapidly reversible with metformin discontinuation or vitamin B12 supplementation. Certain patients (those with inadequate vitamin B12 or calcium intake or absorption) appear to be predisposed to developing subnormal levels of vitamin B12; caution may be warranted when metformin is administered to these patients. It is recommended to measure vitamin B12 every 2 to 3 years and hematologic parameters annually in patients on metformin. Any abnormalities should be managed.

The metFORMIN in Avandamet has a major potential interaction with Anorexia/Feeding Problems.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

traZODone has a moderate potential interaction with Arrhythmia.

Although less cardiotoxic than the tricyclic antidepressants, trazodone may be arrhythmogenic in some patients with cardiac disease. The use of trazodone has been associated with the occurrence of arrhythmias, including PVCs, ventricular couplets, ventricular tachycardia, atrial fibrillation, and heart block. Myocardial infarction has been reported. Trazodone should not be used during the acute recovery phase following myocardial infarction, and should be administered only with extreme caution in patients with hyperthyroidism and/or cardiovascular disease. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. Many of the newer antidepressants, including bupropion and the selective serotonin reuptake inhibitors (SSRIs), are considerably less or minimally cardiotoxic and may be appropriate alternatives.

The metFORMIN in Avandamet has a major potential interaction with Asphyxia.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The metFORMIN in Avandamet has a major potential interaction with Autonomic Neuropathy.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

traZODone has a moderate potential interaction with Bipolar Disorder.

Adults, young adults and children patients with depression and other psychiatric disorders may experience worsening of their symptoms and may have the emergence of suicidal thoughts and behavior. Patients should be monitored appropriately and observed closely for worsening of their symptoms, suicidality or changes in their behavior, especially during the first few months of treatment, and at times of dose changes. Discontinuing the medication should be considered if symptoms are persistently worse, or abrupt in onset. Phenylpiperazine antidepressants are not approved for use in pediatric patients.

traZODone has a moderate potential interaction with Bipolar Disorder.

All antidepressants may occasionally cause mania or hypomania, particularly in patients with bipolar disorder. Therapy with antidepressants should be administered cautiously in patients with a history of mania/hypomania.

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

Although less cardiotoxic than the tricyclic antidepressants, trazodone may be arrhythmogenic in some patients with cardiac disease. The use of trazodone has been associated with the occurrence of arrhythmias, including PVCs, ventricular couplets, ventricular tachycardia, atrial fibrillation, and heart block. Myocardial infarction has been reported. Trazodone should not be used during the acute recovery phase following myocardial infarction, and should be administered only with extreme caution in patients with hyperthyroidism and/or cardiovascular disease. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. Many of the newer antidepressants, including bupropion and the selective serotonin reuptake inhibitors (SSRIs), are considerably less or minimally cardiotoxic and may be appropriate alternatives.

traZODone has a moderate potential interaction with Cerebrovascular Insufficiency.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

The metFORMIN in Avandamet has a major potential interaction with Dehydration.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

traZODone has a moderate potential interaction with Dehydration.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

traZODone has a moderate potential interaction with Dehydration.

Treatment with trazodone may cause hyponatremia, in many cases secondary to development of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Caution should be used when treating patients at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted. Discontinuation of trazodone should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

traZODone has a moderate potential interaction with Depression.

Adults, young adults and children patients with depression and other psychiatric disorders may experience worsening of their symptoms and may have the emergence of suicidal thoughts and behavior. Patients should be monitored appropriately and observed closely for worsening of their symptoms, suicidality or changes in their behavior, especially during the first few months of treatment, and at times of dose changes. Discontinuing the medication should be considered if symptoms are persistently worse, or abrupt in onset. Phenylpiperazine antidepressants are not approved for use in pediatric patients.

The rosiglitazone in Avandamet has a major potential interaction with Diabetes, Type 1.

Thiazolidinediones exert their hypoglycemic effect only in the presence of insulin. Therefore, these agents should not be used in patients with type I diabetes or for the treatment of diabetic ketoacidosis.

The rosiglitazone in Avandamet has a moderate potential interaction with Diabetes Mellitus.

New onset or worsening diabetic macular edema with decreased visual acuity have been reported in postmarketing reports in some diabetic patients who were taking thiazolidinedione drugs. Some patients presented with blurred vision or decreased visual acuity, but some patients appear to have been diagnosed on routine ophthalmologic examination. Most patients had peripheral edema at the time macular edema was diagnosed. Some patients had improvement in their macular edema after discontinuation of their thiazolidinedione. Patients with diabetes should have regular eye exams by an ophthalmologist according to current standards of care. Additionally, any diabetic who reports any kind of visual symptom should be promptly referred to an ophthalmologist, regardless of the patient's underlying medications or other physical findings.

The metFORMIN in Avandamet has a major potential interaction with Diabetic Ketoacidosis.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The rosiglitazone in Avandamet has a major potential interaction with Diabetic Ketoacidosis.

Thiazolidinediones exert their hypoglycemic effect only in the presence of insulin. Therefore, these agents should not be used in patients with type I diabetes or for the treatment of diabetic ketoacidosis.

The rosiglitazone in Avandamet has a moderate potential interaction with Diabetic Macular Edema.

New onset or worsening diabetic macular edema with decreased visual acuity have been reported in postmarketing reports in some diabetic patients who were taking thiazolidinedione drugs. Some patients presented with blurred vision or decreased visual acuity, but some patients appear to have been diagnosed on routine ophthalmologic examination. Most patients had peripheral edema at the time macular edema was diagnosed. Some patients had improvement in their macular edema after discontinuation of their thiazolidinedione. Patients with diabetes should have regular eye exams by an ophthalmologist according to current standards of care. Additionally, any diabetic who reports any kind of visual symptom should be promptly referred to an ophthalmologist, regardless of the patient's underlying medications or other physical findings.

The metFORMIN in Avandamet has a major potential interaction with Diarrhea.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

traZODone has a moderate potential interaction with Diarrhea.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

The rosiglitazone in Avandamet has a moderate potential interaction with Fluid Retention.

Thiazolidinediones can cause dose-related edema. Therapy with thiazolidinediones should be administered cautiously in patients at risk for congestive heart failure as well as those with fluid overload or other conditions that may be adversely affected by excess fluid such as hypertension. Patients should be monitored for signs and symptoms of heart failure such as dyspnea, swelling of legs or ankles, and weight gain.

The metFORMIN in Avandamet has a moderate potential interaction with Folic Acid/Cyanocobalamin Deficiency.

Metformin may interfere with vitamin B12 absorption from the B12-intrinsic factor complex. A decrease to subnormal levels of previously normal serum vitamin B12 levels was reported in about 7% of patients treated with metformin during clinical trials. Such decrease may be associated with anemia but appears to be rapidly reversible with metformin discontinuation or vitamin B12 supplementation. Certain patients (those with inadequate vitamin B12 or calcium intake or absorption) appear to be predisposed to developing subnormal levels of vitamin B12; caution may be warranted when metformin is administered to these patients. It is recommended to measure vitamin B12 every 2 to 3 years and hematologic parameters annually in patients on metformin. Any abnormalities should be managed.

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

Some antidepressants exert mydriatic activity that can induce increased intraocular pressure and result in angle-closure (narrow-angle) glaucoma in a patient with anatomically narrow angles who does not have a patent iridectomy. Prior to initiating therapy with these agents, patients should be examined to determine whether they are susceptible to angle closure, and have a prophylactic procedure (e.g., iridectomy), if they are susceptible. The use of these drugs in patients with untreated anatomically narrow angles should be avoided.

The metFORMIN in Avandamet has a major potential interaction with Heart Attack.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The metFORMIN in Avandamet has a major potential interaction with Heart Failure.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The rosiglitazone in Avandamet has a major potential interaction with Heart Failure.

The use of thiazolidinediones, alone or in combination with other antidiabetic agents, has been associated with fluid retention and new onset or exacerbation of heart failure. An increased risk of cardiovascular events (heart failure worsening; new or worsening edema; new or worsening dyspnea; increases in heart failure medication; myocardial infarction; angina; cardiovascular hospitalization and deaths) has been reported with rosiglitazone therapy in type II diabetic patients with New York Heart Association (NYHA) Class I or II congestive heart failure compared to placebo. Likewise, overnight hospitalization for CHF was observed in 9.9% of diabetic patients with NYHA Class II and III heart failure on pioglitazone compared to 4.7% of patients on glyburide. An increased incidence of cardiovascular adverse events including edema and cardiac failure has also been reported in patients receiving a thiazolidinedione in combination with insulin relative to insulin and placebo. Therapy with thiazolidinediones should be administered cautiously and initiated at the lowest recommended dosage in patients with congestive heart failure. Thiazolidinediones are contraindicated for the treatment of patients with NYHA Class III or IV cardiac status. Patients should be monitored for signs of worsening heart failure such as increased dyspnea, edema, and weight gain. Therapy should be discontinued if any deterioration in cardiac status occurs.

The rosiglitazone in Avandamet has a moderate potential interaction with High Blood Pressure.

Thiazolidinediones can cause dose-related edema. Therapy with thiazolidinediones should be administered cautiously in patients at risk for congestive heart failure as well as those with fluid overload or other conditions that may be adversely affected by excess fluid such as hypertension. Patients should be monitored for signs and symptoms of heart failure such as dyspnea, swelling of legs or ankles, and weight gain.

traZODone has a moderate potential interaction with History - Cerebrovascular Disease.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

The rosiglitazone in Avandamet has a major potential interaction with History - Myocardial Infarction.

Safety data from a pooled analysis of 42 randomized, controlled clinical studies suggest that patients treated with rosiglitazone may have an increased risk of myocardial infarction and/or death from heart-related causes. The overall incidence of myocardial ischemia was 1.99% in patients receiving rosiglitazone-containing therapies (n = 8,604) for at least 24 weeks, compared to 1.51% in patients receiving placebo or other antidiabetic therapies (n = 5,633) for a similar duration. The hazard ratio was 1.31 (95% CI, 1.01 to 1.70) for rosiglitazone-treated patients relative to the comparators, which represents a greater than 30% excess risk of myocardial ischemic events in the rosiglitazone group. However, other published and unpublished data from long-term clinical trials of rosiglitazone provide contradictory evidence about the potential risks. Until more data are available, caution may be advisable when rosiglitazone is prescribed to patients with underlying heart disease or a history of myocardial infarction.

traZODone has a moderate potential interaction with History - Myocardial Infarction.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

traZODone has a moderate potential interaction with Hyperthyroidism.

Although less cardiotoxic than the tricyclic antidepressants, trazodone may be arrhythmogenic in some patients with cardiac disease. The use of trazodone has been associated with the occurrence of arrhythmias, including PVCs, ventricular couplets, ventricular tachycardia, atrial fibrillation, and heart block. Myocardial infarction has been reported. Trazodone should not be used during the acute recovery phase following myocardial infarction, and should be administered only with extreme caution in patients with hyperthyroidism and/or cardiovascular disease. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. Many of the newer antidepressants, including bupropion and the selective serotonin reuptake inhibitors (SSRIs), are considerably less or minimally cardiotoxic and may be appropriate alternatives.

The metFORMIN in Avandamet has a major potential interaction with Hypoglycemia.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

traZODone has a moderate potential interaction with Hyponatremia.

Treatment with trazodone may cause hyponatremia, in many cases secondary to development of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Caution should be used when treating patients at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted. Discontinuation of trazodone should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

traZODone has a moderate potential interaction with Hypotension.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

The rosiglitazone in Avandamet has a major potential interaction with Ischemic Heart Disease.

Safety data from a pooled analysis of 42 randomized, controlled clinical studies suggest that patients treated with rosiglitazone may have an increased risk of myocardial infarction and/or death from heart-related causes. The overall incidence of myocardial ischemia was 1.99% in patients receiving rosiglitazone-containing therapies (n = 8,604) for at least 24 weeks, compared to 1.51% in patients receiving placebo or other antidiabetic therapies (n = 5,633) for a similar duration. The hazard ratio was 1.31 (95% CI, 1.01 to 1.70) for rosiglitazone-treated patients relative to the comparators, which represents a greater than 30% excess risk of myocardial ischemic events in the rosiglitazone group. However, other published and unpublished data from long-term clinical trials of rosiglitazone provide contradictory evidence about the potential risks. Until more data are available, caution may be advisable when rosiglitazone is prescribed to patients with underlying heart disease or a history of myocardial infarction.

traZODone has a moderate potential interaction with Ischemic Heart Disease.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

The metFORMIN in Avandamet has a major potential interaction with Lactic Acidosis.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The metFORMIN in Avandamet has a major potential interaction with Liver Disease.

Metformin decreases the liver uptake of lactate increasing lactate blood levels which may increase the risk of lactic acidosis, especially in at-risk patients. There have been reports of cases of metformin-associated lactic acidosis in patients with liver dysfunction. Metformin should generally be avoided in patients with evidence of hepatic disease.

The rosiglitazone in Avandamet has a moderate potential interaction with Liver Disease.

Initiation of rosiglitazone or pioglitazone therapy is not recommended in patients who exhibit clinical evidence of active liver disease or increased baseline serum transaminase levels (ALT exceeding 2.5 times upper limit of normal). Use of these agents is also not recommended in patients who have experienced jaundice during treatment with troglitazone. The use of troglitazone, another agent in the thiazolidinedione class, has been associated with clinically significant elevations in liver enzymes, reversible jaundice, and idiosyncratic hepatocellular injury including rare cases of liver failure, liver transplants, and death. Injury has occurred after both short- and long-term treatment. While these effects have not been associated with other thiazolidinediones in clinical trials, concerns exist because of their structural similarities. In addition, isolated cases of hepatitis and hepatic enzyme elevations to 3 or more times the upper limit of normal have been reported with both rosiglitazone and pioglitazone during postmarketing use. Rarely, these events have involved hepatic failure with and without fatal outcome, although causality has not been established. Until more safety data are available, patients who are prescribed thiazolidinedione therapy should have serum transaminase levels checked at baseline and periodically thereafter as clinically necessary. Mild to moderate elevations (ALT less than or equal to 2.5 times ULN) require cautious use with more frequent monitoring to determine if the elevations resolve or worsen. Patients who develop potential symptoms of hepatic injury such as unexplained nausea, vomiting, abdominal pain, fatigue, anorexia, and dark urine should have liver enzymes checked. Therapy should be withdrawn if ALT is elevated and persists above 3 times ULN or if jaundice develops.

traZODone has a moderate potential interaction with Liver Disease.

Trazodone undergoes metabolism in the liver. The metabolites, at least one of which is pharmacologically active, are excreted by the kidney. There are no data available concerning the pharmacokinetic disposition of trazodone or its metabolites in patients with renal and/or liver disease. Therapy with trazodone should be administered cautiously in patients with significantly impaired renal or hepatic function. Dosage adjustments may be necessary.

The metFORMIN in Avandamet has a major potential interaction with Malnourishment.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

traZODone has a moderate potential interaction with Mania.

All antidepressants may occasionally cause mania or hypomania, particularly in patients with bipolar disorder. Therapy with antidepressants should be administered cautiously in patients with a history of mania/hypomania.

The metFORMIN in Avandamet has a major potential interaction with Panhypopituitarism.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

The rosiglitazone in Avandamet has a moderate potential interaction with Pleural Effusion.

Thiazolidinediones can cause dose-related edema. Therapy with thiazolidinediones should be administered cautiously in patients at risk for congestive heart failure as well as those with fluid overload or other conditions that may be adversely affected by excess fluid such as hypertension. Patients should be monitored for signs and symptoms of heart failure such as dyspnea, swelling of legs or ankles, and weight gain.

The rosiglitazone in Avandamet has a moderate potential interaction with Premenopausal Anovulation.

In premenopausal, anovulatory patients with insulin resistance, treatment with thiazolidinediones may result in resumption of ovulation. Due to improved insulin sensitivity, pregnancy can occur if adequate contraception is not used.

The rosiglitazone in Avandamet has a moderate potential interaction with Pulmonary Edema.

Thiazolidinediones can cause dose-related edema. Therapy with thiazolidinediones should be administered cautiously in patients at risk for congestive heart failure as well as those with fluid overload or other conditions that may be adversely affected by excess fluid such as hypertension. Patients should be monitored for signs and symptoms of heart failure such as dyspnea, swelling of legs or ankles, and weight gain.

The metFORMIN in Avandamet has a major potential interaction with Renal Dysfunction.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

The metFORMIN in Avandamet has a major potential interaction with Renal Dysfunction.

The use of metformin is contraindicated in patients with severe renal dysfunction (estimated GFR [eGFR] less than 30 mL/min/1.73 m2). Metformin is substantially excreted by the kidney; the risk of metformin accumulation and lactic acidosis increases with the degree of renal dysfunction. Before starting metformin, an eGFR should be obtained. Initiation of metformin is not recommended in patients with eGFR between 30 and 45 mL/min/1.73 m2. An eGFR should be obtained at least annually in all patients; in those at risk of developing renal dysfunction (e.g., older adult patients), renal function should be assessed more frequently. In patients whose eGFR falls below 45 mL/min/1.73 m2, the benefit/risk of continuing therapy should be assessed. Postmarketing cases of metformin-associated lactic acidosis primarily occurred with significant renal dysfunction; metformin plasma levels generally exceeded 5 mcg/mL.

traZODone has a moderate potential interaction with Renal Dysfunction.

Trazodone undergoes metabolism in the liver. The metabolites, at least one of which is pharmacologically active, are excreted by the kidney. There are no data available concerning the pharmacokinetic disposition of trazodone or its metabolites in patients with renal and/or liver disease. Therapy with trazodone should be administered cautiously in patients with significantly impaired renal or hepatic function. Dosage adjustments may be necessary.

traZODone has a moderate potential interaction with Seizures.

The use of most antidepressants is associated with a risk of seizures. There have been only rare reports of convulsions, including grand mal seizures, following the administration of nefazodone or trazodone. Although a causal relationship has not been established, therapy with these agents should be administered cautiously in patients with a history of seizures.

The metFORMIN in Avandamet has a major potential interaction with Shock.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

traZODone has a moderate potential interaction with SIADH.

Treatment with trazodone may cause hyponatremia, in many cases secondary to development of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Caution should be used when treating patients at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted. Discontinuation of trazodone should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

The metFORMIN in Avandamet has a major potential interaction with Vomiting.

Metformin is contraindicated in patients with acute or chronic metabolic acidosis (including diabetic ketoacidosis) with or without coma. Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Risk factors include renal dysfunction, age 65 years and older, hypoxic states, excessive alcohol intake, and liver dysfunction. Lactic acidosis has been associated with metformin accumulation in plasma at levels generally exceeding 5 mcg/mL. The risk of metformin-associated lactic acidosis increases with the patient's age because patients 65 years and older have a greater likelihood of having hepatic, renal, or cardiac impairment. Renal function should be assessed more frequently in older adult patients. Several postmarketing cases of metformin-associated lactic acidosis occurred in the setting of acute congestive heart failure, especially when accompanied by hypoperfusion and hypoxemia; cardiovascular collapse (shock), acute myocardial infarction, sepsis, and other conditions associated with hypoxemia (e.g., severe anemia, asphyxia) have been associated with lactic acidosis and may cause prerenal azotemia. When such an event occurs, metformin should be discontinued. Dehydration (e.g., severe diarrhea or vomiting) may increase the risk for volume depletion, hypotension, and renal impairment; such patients may be at increased risk for lactic acidosis. Alcohol potentiates the effect of metformin on lactate metabolism; patients should be advised against excessive alcohol intake while receiving metformin. All patients treated with metformin should have renal function monitored regularly (at least annually or more frequently if necessary). If metformin-associated lactic acidosis is suspected, general supportive measures should be instituted promptly in a hospital setting, as well as immediate discontinuation of metformin. If lactic acidosis is diagnosed or strongly suspected, prompt hemodialysis is recommended to correct the acidosis and remove accumulated metformin. Patients and their families should be educated about the symptoms of lactic acidosis and, if these symptoms occur, they should be instructed to discontinue metformin and contact their health care provider.

traZODone has a moderate potential interaction with Vomiting.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

The rosiglitazone in Avandamet has a moderate potential interaction with Weight Loss.

Thiazolidinediones can cause dose-related weight gain, which may be undesirable in obese patients attempting to lose weight. The mechanism of weight gain is unclear but probably involves a combination of fluid retention and fat accumulation. In postmarketing experience with rosiglitazone, there have been reports of unusually rapid increases in weight, greater than those generally observed in clinical trials. Patients who experience such increases should be assessed for fluid retention and volume-related events such as excessive edema and congestive heart failure.