Biomedical subjects

Antonio Vita

Publications and source records attributed to Antonio Vita.

6 recordsLinked to original sources

PubMed2007

Aripiprazole in the treatment of schizophrenia: a consensus report produced by schizophrenia experts in Italy.

Schizophrenia is generally a chronic and disabling mental illness. Pharmacological therapy, which is used for relief of acute psychotic episodes and prevention of subsequent relapse, is essential for the effective management of schizophrenia. In order to alleviate the positive symptoms of schizophrenia, all antipsychotic agents act on the dopaminergic system. However, strong, high-affinity dopamine D(2)-receptor blockade may also be responsible for debilitating extrapyramidal symptoms (EPS) and hyperprolactinaemia. Unlike conventional antipsychotic agents, atypical antipsychotics also exert activity at other receptors, and it is generally acknowledged that, compared with conventional antipsychotics, atypical agents are associated with a broader spectrum of clinical efficacy and are better tolerated. However, other adverse effects such as weight gain and metabolic changes are cause for concern with some atypical antipsychotics. The novel atypical antipsychotic agent aripiprazole is a partial agonist at D(2) receptors that has been shown in clinical trials to be effective in treating both the positive and the negative symptoms of schizophrenia, and to be well tolerated, with a low propensity for EPS and no clinically significant weight gain, hyperprolactinaemia or corrected QT-interval prolongation. Aripiprazole thus provides clinicians with another treatment option, and in October 2005, schizophrenia experts participated in an expert consensus meeting that aimed to agree on a set of guidelines for best-practice use of aripiprazole in the acute and long-term management of schizophrenia in Italy. This report describes the outcome of the meeting. Our recommendations for dosage and administration of aripiprazole are in agreement with the manufacturer's prescribing information. Ideally, optimal dosing should be evaluated on an individual basis, taking into account patients' characteristics such as the presence or absence of agitation. Overall, in our experience, aripiprazole is generally a well accepted, well tolerated, safe and broadly effective first-line antipsychotic agent. Switching to aripiprazole from maintenance therapy with another antipsychotic also works well, provided the change is made gradually, involving tapering of the original medication.

Antipsychotic Agents↗

PubMed2005

Catechol-O-methyltransferase Val158Met polymorphism in schizophrenia: associations with cognitive and motor impairment.

Cognitive and motor deficits have been proposed as markers of abnormal neurodevelopment in schizophrenia and have been associated with genetic liability. In a multicenter study involving 106 subjects, 56 with deficit schizophrenia and 50 with nondeficit schizophrenia, we tested the hypothesis that the catechol-O-methyltransferase (COMT) Val(158)Met polymorphism is associated with cognitive and motor deficits either in schizophrenia as a whole or in its deficit subtype. The COMT Val(158)Met polymorphism shared 6.6% of the executive/attention dysfunction variance in patients with schizophrenia and 15.6% of the motor impairment variance in patients with deficit schizophrenia. These results support the hypothesis that the COMT Val(158)Met polymorphism influences executive functions in schizophrenia and the neuromotor performance in the deficit subtype only.

Adolescent↗

PubMed2005

COMT Val(158)Met and BDNF C(270)T polymorphisms in schizophrenia: a case-control study.

In a multicenter study involving 217 subjects of European ancestry [106 patients with schizophrenia and 111 healthy subjects], we tested the hypothesis that the catechol-O-methyl transferase (COMT) Val(158)Met and/or the brain-derived neurotrophic factor (BDNF) C(270)T gene polymorphisms are associated with schizophrenia. The COMT and BDNF genotype and their allele distribution did not differ between patients with schizophrenia and healthy comparison subjects. These results do not support the hypothesis that the COMT Val(158)Met or BDNF C(270)T gene polymorphisms are associated with liability to schizophrenia.

Alleles↗

PubMed2004

Tools for measuring clinical effectiveness.

Efficacy studies fail to consider the multiple aspects of schizophrenia that determine the overall clinical effectiveness of treatment. We address this shortcoming by proposing definitions of six schizophrenia outcome domains which we believe contribute to clinical effectiveness: symptoms of disease, tolerability, everyday functioning, subjective well-being, family/career burden, and treatment adherence. Numerous specialised rating scales are in widespread use; however, these only assess specific aspects of schizophrenia within individual domains and are of limited use for measuring clinical effectiveness. New rating instruments that measure treatment outcomes across all six domains of schizophrenia need to be developed. One such scale is the revised Global Outcome Assessment of Life in Schizophrenia (GOALS) scale. We propose that further development of this scale should include validation in long-term studies, incorporation of the patient perspective of treatment within assessments, and education of clinicians on how to score this scale. If this approach to evaluating treatment outcomes is adopted, clinicians will be better placed to differentiate therapeutic interventions on the basis of clinical effectiveness.

Humans↗

PubMed2002

A genome-wide scan for linkage to chromosomal regions in 382 sibling pairs with schizophrenia or schizoaffective disorder.

OBJECTIVE: Some genome-wide scans and association studies for schizophrenia susceptibility genes have yielded significant positive findings, but there is disagreement between studies on their locations, and no mutation has yet been found in any gene. Since schizophrenia is a complex disorder, a study with sufficient power to detect a locus with a small or moderate gene effect is necessary. METHOD: In a genome-wide scan of 382 sibling pairs with a diagnosis of schizophrenia or schizoaffective disorder, 396 highly polymorphic markers spaced approximately 10 centimorgans apart throughout the genome were genotyped in all individuals. Multipoint nonparametric linkage analysis was performed to evaluate regions of the genome demonstrating increased allele sharing, as measured by a lod score. RESULTS: Two regions with multipoint maximum lod scores suggesting linkage were found. The highest lod scores occurred on chromosome 10p15-p13 (peak lod score of 3.60 at marker D10S189) and the centromeric region of chromosome 2 (peak lod score of 2.99 at marker D2S139). In addition, a maximum lod score of 2.00 was observed with marker D22S283 on chromosome 22q12, which showed evidence of an imprinting effect, whereby an excess sharing of maternal, but not paternal, alleles was present. No evidence of linkage was obtained at several locations identified in previous studies, including chromosomes 1q, 4p, 5p-q, 6p, 8p, 13q, 15p, and 18p. CONCLUSIONS: The findings of this large genome-wide scan emphasize the weakness and fragility of linkage reports on schizophrenia. No linkage appears to be consistently replicable across large studies. Thus, it has to be questioned whether the genetic contribution to this disorder is detectable by these strategies and the possibility raised that it may be epigenetic, i.e., related to gene expression rather than sequence variation. Nevertheless, the positive findings on chromosome 2, 10, and 22 should be pursued further.

Chromosome Mapping↗

PubMed2002

Historical, psychopathological, neurological, and neuropsychological aspects of deficit schizophrenia: a multicenter study.

OBJECTIVE: This multicenter study aimed to verify whether the historical and psychopathological characteristics of a large group of patients with deficit schizophrenia were consistent with those reported in previous studies. The authors also tested the hypothesis that neurological and neuropsychological indices sensitive to frontoparietal dysfunction, but not those sensitive to temporal lobe dysfunction, are more impaired in patients with deficit schizophrenia than in those with non-deficit schizophrenia. METHOD: For each patient with deficit schizophrenia enrolled in the study, a matched subject with non-deficit schizophrenia was recruited. Historical, psychopathological, neurological, and neuropsychological evaluations were carried out for all patients. RESULTS: Patients with deficit schizophrenia, compared with patients with non-deficit schizophrenia, had a similar severity of positive symptoms and disorganization and less hostility. They had poorer premorbid adjustment during childhood and early adolescence and exhibited more impairment in general cognitive abilities. The deficit state was associated with impairment in sequencing of complex motor acts, which suggests frontoparietal dysfunction. CONCLUSIONS: Previous reports of differences in historical, psychopathological, and neuropsychological characteristics between patients with deficit schizophrenia and those with non-deficit schizophrenia were mostly supported by the present findings. Neurological findings suggest that frontoparietal functioning is more impaired in patients with deficit schizophrenia. Deficit schizophrenia might represent a neurodevelopmental subtype of schizophrenia in which significant behavioral and cognitive impairment since childhood compromises the development of basic capacities relevant to subsequent cognitive and social functioning.

Adolescent↗