Loxitane (loxapine) Disease Interactions

There are 12 disease interactions with Loxitane (loxapine):

Seizure Disorders Acute Alcohol Intoxication Cardiovascular Disease Cns Depression Nms Tardive Dyskinesia

Anticholinergic Effects Breast Cancer Dehydration Liver Disease Parkinsonism Seizure Disorders

Loxapine can lower the seizure threshold and trigger seizures in a dose-dependent manner. According to the product labeling, seizures have been reported in patients receiving loxapine at antipsychotic dosages and may occur in epileptic patients even with maintenance of routine anticonvulsant treatment. However, most published reports of seizures attributed to dibenzoxazepine use occurred with amoxapine, often in cases of overdose but also in patients receiving therapeutic dosages. Nevertheless, due to their structural similarities, therapy with loxapine should be administered cautiously in patients with a history of seizures or other predisposing factors, such as head trauma, CNS abnormalities, and alcoholism. High dosages should be avoided if possible.

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.

Most neuroleptic agents have anticholinergic activity, to which elderly patients are particularly sensitive. Clozapine and low-potency agents such as chlorpromazine and thioridazine tend to exhibit the greatest degree of anticholinergic effects in the class, while haloperidol as well as the newer, atypical agents like quetiapine, risperidone and ziprasidone have generally been associated with very low frequencies of anticholinergic adverse effects. Therapy with neuroleptic agents should be administered cautiously in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders.

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.

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