RISPERDAL(generic name: Risperidone)
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| Pharmacogenomics. 2005 Mar;6(2):139-49. Risperidone and other newer atypical antipsychotics are becoming the
mainstay for schizophrenia treatment. Recent studies suggest that the
5-hydroxytryptamine receptor 2A (5-HT2A) gene (HTR2A) T102C and G-1438A
polymorphisms may influence treatment response of risperidone or olanzapine
for schizophrenia's negative symptoms (e.g., blunted affect and social
withdrawal). In addition, the HTR6 T267C polymorphism has been linked
to risperidone response for positive symptoms (delusions and hallucinations).
The dopamine D2 receptor (DRD2) Ser311Cys polymorphism may also play a
role in determining risperidone efficacy for positive, negative and cognitive
symptoms, the DRD2 Ins-A2/Del-A1 diplotype may predict better risperidone
response, and the DRD3 Ser311Cys variant may affect general treatment
response of several atypical agents. Although investigators have started
to explore genetic effects on cognitions of schizophrenia patients receiving
antipsychotics, future larger sized pharmacogenetic studies on both psychotic
symptoms and cognitive functions are warranted. Schizophr Res. 2005 May 12; Although pharmacologic treatments are available for patients with schizophrenia,
little is known about how prescription patterns of atypical antipsychotic
agents are related to patient characteristics. In this study, we examined
the association between patient characteristics and the likelihood of
being initiated on olanzapine or risperidone, two of the most frequently
prescribed atypical agents for schizophrenia. We selected patients who
were diagnosed with schizophrenia or schizoaffective disorder based on
>/=1 inpatient or >/=2 outpatient ICD-9-CM codes (>/=7 days apart)
between 7/1/98 and 6/30/99 from the Veterans Health Administration (VA).
We classified patients into one of three types of initiation: (a) not
on olanzapine or risperidone, (b) not on any atypical agents, or (c) not
on any antipsychotic agents for 6 months, and then subsequently being
prescribed the target drugs. Using logistic regression, we examined whether
the odds ratio of being initiated on olanzapine versus risperidone are
related to patient sociodemographic and clinical characteristics. Compared
to risperidone initiators, olanzapine initiators used more drugs for psychiatric
conditions (including antiparkinsonian agents, typical antipsychotics,
and mood stabilizers) than risperidone initiators. On the other hand,
risperidone initiators had more medical comorbidities and more non-psychiatric
hospitalizations. Olanzapine and risperidone appear to be prescribed to
patients with different characteristics. Initiation of risperidone was
more common among patients who presented with more medical comorbid conditions,
whereas initiation of olanzapine was more common among patient who presented
with more mental comorbid conditions. Future research needs to determine
the reasons for those differences. Int J Neuropsychopharmacol. 2005 Mar 01;:1-12. Some reports have indicated increased rates of diabetes and increased
prevalence of glucose and lipid abnormalities during treatment with second-generation
antipsychotics, with most concern raised about clozapine and olanzapine.
Most of the findings have come from case reports, retrospective examination
of laboratory values, and analysis of health-care claims databases. This
study investigated fasting levels of glucose, lipids, and leptin in a
non-randomized, cross- sectional study of 210 patients, with schizophrenic
or schizoaffective disorder, treated with a single antipsychotic medication
- clozapine, risperidone, olanzapine, or a conventional antipsychotic.
Glucose tolerance tests (GTT), with a 75-g glucose load, were preformed
in a subset of patients. In this sample most mean fasting glucose and
lipid levels were within the normal range and were not significantly different
across the four drug treatment groups. Patients treated with clozapine
and olanzapine had higher triglyceride levels than risperidone patients.
In patients receiving a GTT, risperidone-treated patients had higher glucose
levels at 1 h than patients treated with olanzapine, and there were more
patients on risperidone who met American Diabetes Association glucose
metabolic criteria for diagnosis of diabetes. Although there were no significant
differences in age or body mass index among the four drug groups, we cannot
rule out some potential biasing factors we did not assess which could
potentially influence our results. These include unknown physician preference
in drug selection based on their beliefs about the weight-inducing or
diabetes potential of different antipsychotics, differences in visceral
fat, and differences in patients' antipsychotic drug history.
A 37-year-old man treated with valproate and lithium for bipolar affective
disorder since 1999 and with risperidone since March 2003 was admitted
to our clinic due to metabolic acidosis. Serum glucose was 647 mg/dL and
urine ketones were positive. The patient was accepted as diabetic ketoacidosis
(DKA). Risperidone, valproate, and lithium were immediately stopped, and
the patient was treated with insulin and IV fluid replacement. Serum insulin
and C-peptide levels were too low, and islet cell antibody and anti-GAD
antibody were positive. We accepted him as type 1 diabetes mellitus (DM
type 1). After the intensive treatment of diabetes, insulin requirements
decreased gradually and diabetes mellitus disappeared completely within
three months. Conclusion: Risperidone may lead to transient DM type 1
and DKA.
Atypical antipsychotics can alleviate the severity of tardive dyskinesia,
but few studies have monitored their long-term effects. The present study
investigated the effect of risperidone on pre-existing severe tardive
dyskinesia among 40 patients with chronic schizophrenia over 48 weeks.
The total Abnormal Involuntary Movement Scale (AIMS) score decreased in
35 patients (87.5%) and increased in three patients (7.5%). At the end
of the 48-week trial, the mean total AIMS score decreased significantly,
from 15.7+/-4.7 (baseline) to 10.6+/-4.4 (P<0.001), with a mean risperidone
dosage of 3.6+/-1.5 mg/day. Twenty-three patients (57.5%) were responders
with an average total AIMS score decrease of 8.0+/-2.7. Multiple logistic
regression analysis controlling for age, gender, duration of illness,
index hospitalization duration, risperidone dose, anticholinergic concomitant
use and dystonia score change revealed that a change in the parkinsonism
score was the most significant factor related to responders (odds ratio
3.476, 95% confidence interval 1.173-10.298). A significant improvement
observed in tardive dyskinesia was noted at week 8, and this improvement
persisted until week 48. The results show that the effect of risperidone
on pre-existing tardive dyskinesia may be beneficial.
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