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antipsychotics/nécrose
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Antipsychotics-induced ischaemic colitis and gastrointestinal necrosis: a review of the French pharmacovigilance database.
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OBJECTIVE
First- and second-generation antipsychotics commonly cause mild gastrointestinal hypomotility. Intestinal necrosis may be a consequence of such gastrointestinal perturbations.
METHODS
We reviewed all the observations of ischaemic colitis and gastrointestinal necrosis notified to the French
Focal parietal necrosis of the sigmoid due to atypical neuroleptics: a case report.
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We present the case of a 26-year-old man with schizoid personality disorder who suffered from a very focal and transparietal necrosis of the sigmoid after an overdose of atypical neuroleptics. This is a singular, rather unknown and potentially lethal side effect of these drugs. The physiopathology
A pilot study investigating tumor necrosis factor-α as a potential intervening variable of atypical antipsychotic-associated metabolic syndrome in bipolar disorder.
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BACKGROUND
Strong associations exist between tumor necrosis factor-α (TNF-α) and metabolic syndrome (MetS). Although TNF-α is associated with bipolar depression (BD), its role in atypical antipsychotic (AAP)-associated MetS in BD is unclear. Here, we investigate the potential intervening role of
Neuroleptics normalize increased release of interleukin- 1 beta and tumor necrosis factor-alpha from monocytes in schizophrenia.
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Some recent reports show that schizophrenia is accompanied by changes in lymphocyte activity. This study investigated the activity of monocytes by determining their release of interleukin- 1 beta (IL- 1 beta) and tumor necrosis factor-alpha (TNF-alpha). Monocytes were immunomagnetically isolated
Family and case-control association study of the tumor necrosis factor-alpha (TNF-alpha) gene with schizophrenia and response to antipsychotic medication.
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BACKGROUND
Dysregulation of the immune system has been suggested to play a role in the etiology of schizophrenia (SCZ). In this context, the tumor necrosis factor-alpha (TNF-alpha) is considered an interesting candidate for genetic studies as overproduction of TNF-alpha, which may be genetically
Fatal hepatic necrosis associated with trazodone and neuroleptic drugs.
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Antipsychotic agent thioridazine sensitizes renal carcinoma Caki cells to TRAIL-induced apoptosis through reactive oxygen species-mediated inhibition of Akt signaling and downregulation of Mcl-1 and c-FLIP(L).
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Thioridazine has been known as an antipsychotic agent, but it also has anticancer activity. However, the effect of thioridazine on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitization has not yet been studied. Here, we investigated the ability of thioridazine to sensitize
Small-intestinal necrosis due to non-occlusive mesenteric ischemia with diabetic ketoacidosis after quetiapine treatment.
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We report a 66-year-old male who developed diabetic ketoacidosis (DKA) and necrosis of the small intestine due to non-occlusive mesenteric ischemia (NOMI), 3 months after starting quetiapine treatment. He was transferred to our hospital and diagnosed as diabetic for the first time, associated with
Activation of the immune-inflammatory response system and the compensatory immune-regulatory system in antipsychotic naive first episode psychosis.
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Psychotic disorders are accompanied by activation of the immune inflammatory response system (IRS). The compensatory immune-regulatory system (CIRS) is a regulatory immune response that is induced by the IRS but exerts negative feedback through increased levels of anti-inflammatory cytokines such as
Dysregulation of adipocytokines related to second-generation antipsychotics in normal fasting glucose patients with schizophrenia.
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OBJECTIVE
The underlying mechanism for second-generation antipsychotic (SGA)-related glucose-lipid metabolic dysfunction is not fully understood. Recent studies have suggested a possible impact of SGAs on endocrine regulation, especially on adipocytokines. We examined the effect of each SGA on
Pharmacogenetics of antipsychotic-induced weight gain.
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BACKGROUND
Antipsychotic medications have been associated with considerable weight gain. The degree of inter-individual variability and known genetic contributions to obesity suggest a combination of genetic and environmental factors. In the absence of established mechanisms and valid predictors for
Are leptin and cytokines involved in body weight gain during treatment with antipsychotic drugs?
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OBJECTIVE
To critically review published literature on the causal association between leptin, cytokines, and excessive body weight gain (BWG) induced by antipsychotic drugs (APs).
METHODS
We completed a Medline search using the words leptin, cytokines, antipsychotic drugs, neuroleptics, psychotropic
Genetic dissection of atypical antipsychotic-induced weight gain: novel preliminary data on the pharmacogenetic puzzle.
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Atypical antipsychotics such as clozapine represent a significant improvement over typical antipsychotics in the treatment of schizophrenia, particularly regarding extrapyramidal symptoms. Despite their benefits, use is limited by the occurrence of adverse reactions such as sedation and weight gain.
Hypothalamic pathology in the neuroleptic malignant syndrome.
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The pathogenesis of the neuroleptic malignant syndrome is currently unclear, and no specific morphological abnormalities in the CNS of victims of neuroleptic malignant syndrome have been described. The authors report a case of neuroleptic malignant syndrome with recent foci of necrosis in the
[Hemostatic evaluation of a patient with haloperidol-induced neuroleptic malignant syndrome associated with disseminated intravascular coagulation].
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A 94-year-old man who had been admitted to our hospital for the treatment of senile dementia and restless behavior exhibited consciousness disturbances, acute respiratory failure, high fever, and thrombocytopenia the day after receiving haloperidol as prescribed by a psychiatrist. On the fourth day
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