half life of geodon im

Patients with severe neutropenia (absolute neutrophil count <1000/mm3) should discontinue Geodon and have their WBC followed until recovery.During clinical trials, seizures occurred in 0.4% of patients treated with ziprasidone.

While you are on Geodon, check with your doctor before starting any new prescription or over-the-counter medications, including natural/herbal remedies.Because these problems could mean you're having a heart rhythm abnormality, contact your doctor Common side effects of Geodon include the following and should also be discussed with your doctor if they occur:If you develop any side effects that concern you, talk with your doctor.

Some neonates recovered within hours or days without specific treatment; others required prolonged hospitalization.Published data from observational studies, birth registries, and case reports on the use of atypical antipsychotics during pregnancy do not report a clear association with antipsychotics and major birth defects.

We recently met with a new psychiatrist who mentioned a very long half-life for Geodon and that the reason he has not relapsed, is likely because he still …

In the ziprasidone-treated patients, neither case suggested a role of ziprasidone. Severe cutaneous adverse reactions are sometimes fatal. My son was taking Geodon for 2 years following a diagnosis of Schizoaffective Disorder - Depressed type. In clinical trials with oral ziprasidone, the electrocardiograms of 2/2988 (0.06%) patients who received GEODON and 1/440 (0.23%) patients who received placebo revealed QTc intervals exceeding the potentially clinically relevant threshold of 500 msec. The multiple-dose pharmacokinetics of ziprasidone are dose-proportional within the proposed clinical dose range, and ziprasidone accumulation is predictable with multiple dosing. Patients' scores on the BARS at baseline were mostly 5 (signs of overt activity [physical or verbal], calms down with instructions) and as determined by investigators, exhibited a degree of agitation that warranted intramuscular therapy. Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever, and primary central nervous system (CNS) pathology.The management of NMS should include: (1) immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy; (2) intensive symptomatic treatment and medical monitoring; and (3) treatment of any concomitant serious medical problems for which specific treatments are available. The premarketing experience for ziprasidone did not reveal an excess risk of mortality for ziprasidone compared to other antipsychotic drugs or placebo, but the extent of exposure was limited, especially for the drugs used as active controls and placebo.

Ziprasidone was significantly more effective than placebo in reduction of the MRS total score and the CGI-S score. Nevertheless, the presence of multiple factors that might increase the pharmacodynamic response to ziprasidone, or cause poorer tolerance or orthostasis, should lead to consideration of a lower starting dose, slower titration, and careful monitoring during the initial dosing period for some elderly patients.Ziprasidone intramuscular has not been systematically evaluated in elderly patients (65 years and over).Because ziprasidone is highly metabolized, with less than 1% of the drug excreted unchanged, renal impairment alone is unlikely to have a major impact on the pharmacokinetics of ziprasidone. In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought.

Ziprasidone dosed adjunctively to valproate in a maintenance trial of bipolar patients did not affect mean therapeutic valproate levels.Population pharmacokinetic analysis of schizophrenic patients enrolled in controlled clinical trials has not revealed evidence of any clinically significant pharmacokinetic interactions with benztropine, propranolol, or lorazepam.The absolute bioavailability of a 20 mg dose under fed conditions is approximately 60%.

Chemically, ziprasidone hydrochloride monohydrate is 5-[2-[4-(1,2- benzisothiazol-3-yl)-1-piperazinyl]ethyl]-6-chloro-1,3-dihydro-2H-indol-2-one, monohydrochloride, monohydrate.

Less than one-third of ziprasidone metabolic clearance is mediated by cytochrome P450 catalyzed oxidation.Ziprasidone should not be used with any drug that prolongs the QT interval [see Given the primary CNS effects of ziprasidone, caution should be used when it is taken in combination with other centrally acting drugs.Because of its potential for inducing hypotension, ziprasidone may enhance the effects of certain Ziprasidone may antagonize the effects of levodopa and Carbamazepine is an inducer of CYP3A4; administration of 200 mg twice daily for 21 days resulted in a decrease of approximately 35% in the AUC of ziprasidone. The relationship of QT prolongation to torsade de pointes is clearest for larger increases (20 msec and greater) but it is possible that smaller QT/QTc prolongations may also increase risk, or increase it in susceptible individuals Although torsade de pointes has not been observed in association with the use of ziprasidone in premarketing studies and experience is too limited to rule out an increased risk, there have been rare post-marketing reports (in the presence of multiple confounding factors) A study evaluating the QT/QTc prolonging effect of intramuscular ziprasidone, with intramuscular haloperidol as a control, was conducted in patient volunteers.

... Neuroleptic malignant syndrome is a rare, life threatening adverse effect of antipsychotics which occurs in <1% of patients. There were trends toward dose response within the range of 20 mg to 80 mg twice daily, but results were not consistent. In the double-blind randomized phase, patients continued treatment with lithium or valproic acid and were randomized to receive either ziprasidone (administered twice daily totaling 80 mg to 160 mg per day) or placebo. It is greater than 99% bound to plasma proteins, binding primarily to Ziprasidone is extensively metabolized after oral administration with only a small amount excreted in the urine (<1%) or feces (<4%) as unchanged drug.