Overlooked fatal infectious diseases after long-term antipsychotic use in patients with psychiatric illness

Li, Liliang; Ye, Xing; Zhao, Ziqin; Gao, Pan; Jiang, Yan

doi:10.1016/j.schres.2017.09.033

Cited by 10 publications

(4 citation statements)

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“…Several cytokines such as interleukin 1β, interleukin 6, and C-reactive protein were higher in individuals with schizophrenia (28). Infectious disease after long-term anti-psychotic use in patients with psychiatric illness had often been over-looked (29). In our patients, the high incidences of hepatic steatosis and respiratory inflammation mirror the prevalence of MetS and inflammation in schizophrenia, and therefore may explain the premature death occurred with shorter disease duration.…”

Section: Discussionmentioning

confidence: 55%

Sudden Cardiac Death in Schizophrenia During Hospitalization: An Autopsy-Based Study

et al. 2022

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Schizophrenia is a severe mental disorder that is often comorbid with heart dysfunction and even sudden cardiac death (SCD). Clinical studies of SCD in schizophrenia have been largely reported, while there are limited autopsy studies that directly showed whole-scale information of such events. In this study, we present nine autopsy-based SCD cases in schizophrenia patients who died suddenly during hospitalization. Their medical records before and during hospitalization, and postmortem autopsy findings were summarized. These decedents had an average duration of schizophrenia for 6.83 ± 3.75 years with a male/female ratio of 4:5. They were all on intermittent antipsychotics medication before hospitalization and died within 15 days after hospitalization. Seven of the nine cases (77.8%) died of organic heart diseases such as severe coronary artery atherosclerosis (n = 4), myocarditis (n = 1), cardiomyopathy (n = 1), and pulmonary thromboembolism (n = 1). Two cases remained unexplained after systemic autopsy and toxicological examinations. Postmortem autopsy identified hepatic steatosis (n = 6) and respiratory inflammation (n = 3) as the most common associate extra-cardiac lesions. Our data provided autopsy-based data of SCD cases in schizophrenia and highlighted an intensive care of such patients during hospitalization.

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Section: Discussionmentioning

confidence: 55%

Sudden Cardiac Death in Schizophrenia During Hospitalization: An Autopsy-Based Study

et al. 2022

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“…Other severe or life‐threatening adverse cardiac effects stem from reports of myocarditis in patients treated with this drug (Ronaldson, Fitzgerald, & McNeil, ). We have also demonstrated that clozapine is the most common drug associated with antipsychotic‐induced sudden unexpected death (Li, Ye, Zhao, Gao, & Jiang, ). Health professionals have warned of the risk of potentially fatal myocarditis, cardiomyopathy, and heart failure (Kilian et al, ; La Grenade, Graham, & Trontell, ) in association with clozapine therapy.…”

Section: Introductionmentioning

confidence: 89%

Opposite effects of cannabinoid CB₁ and CB₂ receptors on antipsychotic clozapine‐induced cardiotoxicity

Dong

et al. 2019

British J Pharmacology

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Background and Purpose: Clozapine is an atypical antipsychotic drug that is very efficacious in treating psychosis, but the risk of severe cardiotoxicity limits its clinical use. The present study investigated the harmful effects of clozapine on myocardium and assessed the involvement of cannabinoid receptors in its cardiotoxicity.Experimental Approach: Clozapine alone or in combination with selective cannabinoid receptor antagonists or agonists were used to treat mice and cardiomyocytes.Key Results: Clozapine induced myocardial inflammation and infiltration 7 days after i.p. injection. Mice survival rate and myocardial infiltration, and fibrotic lesions were dose-dependently worsened by clozapine. Clozapine decreased major endocannabinoid levels in sera and cultured cardiomyocytes. Cannabinoid CB 1 receptors decreased in clozapine-treated hearts and were translocated from cytomembranes to cytoplasm and nuclei, whereas CB 2 receptors increased in clozapinetreated hearts and inversely translocated from nuclei to the cytomembrane. Selective antagonists of CB 1 receptors, rimonabant and AM281, but not its selective agonist arachidonyl-2′-chloroethylamide, ameliorated clozapine-induced myocardial inflammatory infiltration and fibrotic lesions. In contrast, selective agonists of CB 2 receptors, AM1241 and JWH-133, but not its selective antagonist AM630, blunted clozapine-mediated cardiotoxicity in mice. In cultured cardiomyocytes, clozapine increased the pro-inflammatory factor IL-1β and the concentrations of myocardial injury markers (LDH and aspartate aminotransferase); these effects were reversed by either a CB 1 antagonist or CB 2 agonist and further prevented by combined pretreatments.Conclusions and Implications: Our data provide evidence that cannabinoid CB 1 and CB 2 receptors have opposite effects and selective antagonists of CB 1 or agonists of CB 2 receptors might confer protective effects against clozapine in myocardium.

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“…Furthermore, the death rate caused by clozapine-induced acute myocarditis is approximately 25%[ 48 ]. An autopsy report also confirmed antipsychotic-induced myocarditis, which showed that in 24 sudden death cases, 11 (45.8%) died from myocarditis, and 7 (29.2%) were on clozapine medication[ 49 ].…”

Section: Pathological Changes Of Antipsychotics Cardiotoxicitymentioning

confidence: 99%

Antipsychotics cardiotoxicity: What's known and what's next

Li¹,

Tang²,

Li³

2021

WJP

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Chronic use of antipsychotic medications entails a dilemma between the benefit of alleviating psychotic symptoms and the risk of troubling, sometimes life-shortening adverse effects. Antipsychotic-induced cardiotoxicity is one of the most life-threatening adverse effects that raises widespread concerns. These cardiotoxic effects range from arrhythmia to heart failure in the clinic, with myocarditis/cardiomyopathy, ischemic injuries, and unexplained cardiac lesions as the pathological bases. Multiple mechanisms have been proposed to underlie antipsychotic cardiotoxicity. This review aims to summarize the clinical signs and pathological changes of antipsychotic cardiotoxicity and introduce recent progress in understanding the underlying mechanisms at both the subcellular organelle level and the molecular level. We also provide an up-to-date perspective on future clinical monitoring and therapeutic strategies for antipsychotic cardiotoxicity. We propose that third-generation antipsychotics or drug adjuvant therapy, such as cannabinoid receptor modulators that confer dual benefits — i.e. , alleviating cardiotoxicity and improving metabolic disorders — deserve further clinical evaluation and marketing.

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Overlooked fatal infectious diseases after long-term antipsychotic use in patients with psychiatric illness

Cited by 10 publications

References 9 publications

Sudden Cardiac Death in Schizophrenia During Hospitalization: An Autopsy-Based Study

Sudden Cardiac Death in Schizophrenia During Hospitalization: An Autopsy-Based Study

Opposite effects of cannabinoid CB₁ and CB₂ receptors on antipsychotic clozapine‐induced cardiotoxicity

Antipsychotics cardiotoxicity: What's known and what's next

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Overlooked fatal infectious diseases after long-term antipsychotic use in patients with psychiatric illness

Cited by 10 publications

References 9 publications

Sudden Cardiac Death in Schizophrenia During Hospitalization: An Autopsy-Based Study

Sudden Cardiac Death in Schizophrenia During Hospitalization: An Autopsy-Based Study

Opposite effects of cannabinoid CB1 and CB2 receptors on antipsychotic clozapine‐induced cardiotoxicity

Antipsychotics cardiotoxicity: What's known and what's next

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Product

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Opposite effects of cannabinoid CB₁ and CB₂ receptors on antipsychotic clozapine‐induced cardiotoxicity