There is emerging evidence of heterogeneity within treatment-resistance schizophrenia (TRS), with some people not responding to antipsychotic treatment from illness onset and a smaller group becoming treatment-resistant after an initial response period. It has been suggested that these groups have different aetiologies. Few studies have investigated socio-demographic and clinical differences between early and late onset of TRS.

This study aims to investigate socio-demographic and clinical correlates of late-onset of TRS.

Using data from the electronic health records of the South London and Maudsley, we identified a cohort of people with TRS. Regression analyses were conducted to identify correlates of the length of treatment to TRS. Analysed predictors include gender, age, ethnicity, positive symptoms severity, problems with activities of daily living, psychiatric comorbidities, involuntary hospitalisation and treatment with long-acting injectable antipsychotics.

We observed a continuum of the length of treatment until TRS presentation. Having severe hallucinations and delusions at treatment start was associated shorter duration of treatment until the presentation of TRS.

Our findings do not support a clear cut categorisation between early and late TRS, based on length of treatment until treatment resistance onset. More severe positive symptoms predict earlier onset of treatment resistance.

DFdF, GKS, EF and IR have received research funding from Janssen and H. Lundbeck A/S. RDH and HS have received research funding from Roche, Pfizer, Janssen and Lundbeck. SES is employed on a grant held by Cardiff University from Takeda Pharmaceutical Comp

Ethnic disparities in treatment with clozapine, the antipsychotic recommended for treatment-resistant schizophrenia (TRS), have been reported. However, these investigations frequently suffer from potential residual confounding. For example, few studies have restricted the analyses to TRS samples and none has controlled for benign ethnic neutropenia.

This study investigated if service-users’ ethnicity influenced clozapine prescription in a cohort of people with TRS.

Information from the clinical records of South London and Maudsley NHS Trust was used to identify a cohort of service-users with TRS between 2007 and 2017. In this cohort, we used logistic regression to investigate any association between ethnicity and clozapine prescription while adjusting for potential confounding variables, including sociodemographic factors, psychiatric multimorbidity, substance use, benign ethnic neutropenia, and inpatient and outpatient care received.

We identified 2239 cases that met the criteria for TRS. Results show that after adjusting for confounding variables, people with Black African ethnicity had half the odds of being treated with clozapine and people with Black Caribbean or Other Black background had about two-thirds the odds of being treated with clozapine compared White British service-users. No disparities were observed regarding other ethnic groups, namely Other White background, South Asian, Other Asian, or any other ethnicity.

There was evidence of inequities in care among Black ethnic groups with TRS. Interventions targeting barriers in access to healthcare are recommended.

During the conduction of the study, DFdF, GKS, and RH received funds from the NIHR Maudsley Biomedical Research Centre. For other activities outside the submitted work, DFdF received research funding from the UK Department of Health and Social Care, Janss

Clozapine is associated with increased risk of myocarditis. However, many common side-effects of clozapine overlap with the clinical manifestations of myocarditis. As a result, there is uncertainty about which signs, symptoms and investigations are important in distinguishing myocarditis from benign adverse effects of clozapine. Clarity on this issue is important, since missing a diagnosis of myocarditis or discontinuing clozapine unnecessarily may both have devastating consequences.

To examine the clinical characteristics of clozapine-induced myocarditis and to identify which signs and symptoms distinguish true myocarditis from other clozapine adverse effects.

A retrospective analysis of the record database for 247 621 patients was performed. A natural language processing algorithm identified the instances of patients in which myocarditis was suspected. The anonymised case notes for the patients of each suspected instance were then manually examined, and those whose instances were ambiguous were referred for an independent assessment by up to three cardiologists. Patients with suspected instances were classified as having confirmed myocarditis, myocarditis ruled out or undetermined.

Of 254 instances in 228 patients with suspected myocarditis, 11.4% (n = 29 instances) were confirmed as probable myocarditis. Troponin and C-reactive protein (CRP) had excellent diagnostic value (area under the curve 0.975 and 0.896, respectively), whereas tachycardia was of little diagnostic value. All confirmed instances occurred within 42 days of clozapine initiation.

Suspicion of myocarditis can lead to unnecessary discontinuation of clozapine. The ‘critical period’ for myocarditis emergence is the first 6 weeks, and clinical signs including tachycardia are of low specificity. Elevated CRP and troponin are the best markers for the need for further evaluation.