Seroquel (quetiapine) Disease Interactions
There are 14 disease interactions with Seroquel (quetiapine):
- Acute Alcohol Intoxication
- Cardiovascular Disease
- Cns Depression
- Tardive Dyskinesia
- Breast Cancer
- Liver Disease
- Seizure Disorders
- Alt Elevations
The use of neuroleptic agents is contraindicated in patients with acute alcohol intoxication exhibiting depressed vital signs. The central nervous system depressant effects of neuroleptic agents may be additive with those of alcohol. Severe respiratory depression and respiratory arrest may occur. Therapy with neuroleptic agents should be administered cautiously in patients who might be prone to acute alcohol intake.
Neuroleptic agents may cause hypotension (including orthostatic hypotension), reflex tachycardia, increased pulse rate, syncope and dizziness, particularly during initiation of therapy or rapid escalation of dosage. Tolerance to the hypotensive effects often develops after a few doses to a few weeks. Rarely, fatal cardiac arrest has occurred secondary to severe hypotension. Other reported adverse cardiovascular effects include hypertension, edema, arrhythmias, thrombophlebitis, myocarditis, angina, myocardial infarction, congestive heart failure, and ECG abnormalities such as PR and QT interval prolongation, diffuse T-wave flattening, and ST segment depression. Therapy with neuroleptic agents should be administered cautiously in patients with severe cardiovascular disease, pheochromocytoma, a predisposition to hypotension, or conditions that could be exacerbated by hypotension such as a history of myocardial infarction, angina, or ischemic stroke. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. If parenteral therapy is given, patients should be in a supine position during administration and for at least 30 to 60 minutes afterwards. Patients who experience orthostatic hypotension should be cautioned not to rise too abruptly. Occasionally, when severe, hypotension may require treatment with vasoconstrictive agents such as norepinephrine or phenylephrine. Epinephrine should not be used, however, since neuroleptic agents can reverse its vasopressor effects and cause a further lowering of blood pressure.
The use of neuroleptic agents is contraindicated in comatose patients and patients with severe central nervous system depression. Neuroleptic agents may potentiate the CNS and respiratory depression in these patients.
The central dopaminergic blocking effects of neuroleptic agents may precipitate or aggravate a potentially fatal symptom complex known as neuroleptic malignant syndrome (NMS). NMS is observed most frequently when high-potency agents like haloperidol are administered intramuscularly, but may occur with any neuroleptic agent given for any length of time. Clinical manifestations of NMS include hyperpyrexia, muscle rigidity, altered mental status and autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis and cardiac arrhythmias). Additional signs may include elevated creatine phosphokinase, myoglobinuria, and acute renal failure. Neuroleptic agents should not be given to patients with active NMS and should be immediately discontinued if currently being administered in such patients. In patients with a history of NMS, introduction or reintroduction of neuroleptic agents should be carefully considered, since NMS may recur.
Neuroleptic agents may precipitate symptoms of tardive dyskinesia (TD), a syndrome consisting of rhythmic involuntary movements variously involving the tongue, face, mouth, lips, jaw, and/or trunk and extremities, following chronic use of at least several months but often years. Elderly patients, particularly women, are most susceptible. Both the risk of developing the syndrome and the likelihood that it will become irreversible increase with the duration and total cumulative dose of neuroleptic therapy administered. However, patients may infrequently develop symptoms after relatively brief treatment periods at low dosages. If TD occurs during neuroleptic therapy, prompt withdrawal of the offending agent or at least a lowering of the dosage should be considered. TD symptoms may become more severe after drug discontinuation or a dosage reduction, but may gradually improve over months to years. In patients with preexisting drug-induced TD, initiating or increasing the dosage of neuroleptic therapy may temporarily mask the symptoms of TD but could eventually worsen the condition. The newer, atypical neuroleptic agents (e.g., risperidone, quetiapine, olanzapine) tend to be associated with a substantially reduced risk of inducing TD and are considered the drugs of choice in patients being treated for psychosis.
The chronic use of neuroleptic agents can cause persistent elevations in prolactin levels. Based on in vitro data, approximately one-third of human breast cancers are thought to be prolactin-dependent. The clinical significance of this observation with respect to long-term neuroleptic therapy is unknown. Chronic administration of neuroleptic drugs has been associated with mammary tumorigenesis in rodent studies but not in human clinical or epidemiologic studies. Until further data are available, therapy with neuroleptic agents should be administered cautiously in patients with a previously detected breast cancer.
Neuroleptic agents may cause hypotension (including orthostatic hypotension) and associated reflex tachycardia, syncope or dizziness, particularly during initiation of therapy or rapid escalation of dosage. Tolerance to the hypotensive effects often develops after a few doses to a few months. Rarely, fatal cardiac arrest has occurred secondary to severe hypotension. Therapy with neuroleptic agents should be administered cautiously in patients with conditions that would predispose them to hypotension, such as hypovolemia or dehydration (e.g., due to severe diarrhea or vomiting). In addition, neuroleptic agents can interfere with the body's ability to regulate core body temperature, occasionally producing hyperthermia during strenuous exercise, exposure to hot weather, and concomitant treatment with anticholinergic medications. Patients who are dehydrated may be particularly susceptible.
Most neuroleptic agents are extensively metabolized by the liver. The plasma concentrations of these agents may be increased and the half-lives prolonged in patients with impaired hepatic function. Therapy with neuroleptic agents should be administered cautiously in patients with significant liver disease. Lower initial dosages and slower titration may be appropriate.
The use of neuroleptic agents is associated with pseudo-parkinsonian symptoms such as akinesia, bradykinesia, tremors, pill-rolling motion, cogwheel rigidity, and postural abnormalities including stooped posture and shuffling gait. The onset is usually 1 to 2 weeks following initiation of therapy or an increase in dosage. Older neuroleptic agents such as haloperidol are more likely to induce these effects, and their use may be contraindicated in patients with Parkinson's disease or parkinsonian symptoms.
Neuroleptic agents can lower the seizure threshold and induce seizures, particularly when dosages are high or increased rapidly and during the initiation of therapy. Clozapine appears to have the greatest epileptogenic potential, while most of the other newer, atypical neuroleptic agents (e.g., risperidone, quetiapine, olanzapine), as well as haloperidol and molindone, have the least. Therapy with neuroleptic agents should be administered cautiously in patients with a history of seizures or other factors predisposing to seizures such as abnormal EEG, preexisting CNS pathology, or head trauma. Adequate anticonvulsant therapy should be maintained during administration of neuroleptic agents. Clozapine should not be used in patients with uncontrolled epilepsy.
The use of quetiapine may be associated with transient, asymptomatic elevations in serum transaminase. During a series of 3- to 6-week clinical trials, 6% of patients exposed to quetiapine experienced ALT (SGPT) elevations greater than three times the upper limit of normal, compared to 1% in the placebo group. Liver enzymes tended to increase within the first 3 weeks of therapy and return to baseline with continued treatment. Therapy with quetiapine should be administered cautiously in patients with signs and symptoms of hepatic impairment. Periodic assessment of serum transaminases should be performed in patients with significant hepatic disease.
Prolonged use of quetiapine was associated with the development of cataracts in dogs. Lens changes have also been observed in humans during chronic treatment with quetiapine, but a causal relationship has not been established. Long-term therapy with quetiapine should be administered cautiously in patients with a history of cataracts. Examination of the lens by slit lamp exam or other appropriately sensitive methods is recommended at initiation of treatment or shortly thereafter and at 6-month intervals during chronic treatment.
According to the manufacturer, patients treated with quetiapine in 3- to 6-week placebo-controlled trials had increases in cholesterol and triglyceride of 11% and 17%, respectively, compared to slight decreases in the placebo group. Patients with preexisting hyperlipidemia may require closer monitoring during quetiapine therapy, and adjustments made accordingly in their lipid-lowering regimen.
During clinical trials, the use of quetiapine was associated with a dose-related decrease in total and free thyroxine (T4) levels that reached approximately 20% at the higher end of the therapeutic dose range and peaked within the first 2 to 4 weeks of treatment. Generally, the changes were of no clinical significance and were reversible following discontinuation of quetiapine regardless of the duration of treatment. TBG levels were not altered in any patient, while TSH increased in 0.4% (10/2386) of patients, some of whom required thyroid replacement therapy. Therapy with quetiapine should be administered cautiously in patients with thyroid disease. Closer monitoring of thyroid function may be appropriate following initiation or cessation of quetiapine.
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Seroquel (quetiapine) drug Interactions
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Seroquel (quetiapine) alcohol/food Interactions
There are 2 alcohol/food interactions with Seroquel (quetiapine)
Drug Interaction Classification
The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.
|Major||Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.|
|Moderate||Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.|
|Minor||Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.|
Do not stop taking any medications without consulting your healthcare provider.
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