Suicide is a major cause of death among patients with schizophrenia. Research indicates that at least 5–13% of schizophrenic patients die by suicide, and it is likely that the higher end of range is the most accurate estimate. There is almost total agreement that the schizophrenic patient who is more likely to commit suicide is young, male, white and never married, with good premorbid function, post-psychotic depression and a history of substance abuse and suicide attempts. Hopelessness, social isolation, hospitalization, deteriorating health after a high level of premorbid functioning, recent loss or rejection, limited external support, and family stress or instability are risk factors for suicide in patients with schizophrenia. Suicidal schizophrenics usually fear further mental deterioration, and they experience either excessive treatment dependence or loss of faith in treatment. Awareness of illness has been reported as a major issue among suicidal schizophrenic patients, yet some researchers argue that insight into the illness does not increase suicide risk. Protective factors play also an important role in assessing suicide risk and should also be carefully evaluated. The neurobiological perspective offers a new approach for understanding self-destructive behavior among patients with schizophrenia and may improve the accuracy of screening schizophrenics for suicide. Although, there is general consensus on the risk factors, accurate knowledge as well as early recognition of patients at risk is still lacking in everyday clinical practice. Better knowledge may help clinicians and caretakers to implement preventive measures.This review paper is the results of a joint effort between researchers in the field of suicide in schizophrenia. Each expert provided a brief essay on one specific aspect of the problem. This is the first attempt to present a consensus report as well as the development of a set of guidelines for reducing suicide risk among schizophenia patients.

Clozapine is, in most countries, underutilized and the initiation of clozapine is often delayed. The purpose of this study is to investigate the reasons for the delay and the underutilization of clozapine. One hundred psychiatrists were interviewed by phone. The interview was a structured interview with questions regarding attitude to, knowledge of and experiences with clozapine. Forty-eight (48%) psychiatrists had treatment responsibility of fewer than five patients treated with clozapine and 31 of the interviewed psychiatrists (31%) had started clozapine within the last 3 months. Seven psychiatrists (7%) had never prescribed clozapine despite the fact that they had been working more than five years in general psychiatry. Sixty-four psychiatrists (64%) would rather combine two antipsychotics than use clozapine. Sixty-six psychiatrists (66%) believed that patients treated with clozapine were less satisfied with their treatment when compared with those treated with other atypical antipsychotics. Many psychiatrists are reluctant to use clozapine and this might be due to less experience and knowledge of clozapine. A reason for the low awareness of clozapine's properties might be that clozapine is now a generic drug, and therefore, the marketing and education in using the drug is sparse.

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Clozapine is a particularly effective antipsychotic medication but its use is curtailed by the risk of clozapine-induced agranulocytosis/granulocytopenia (CIAG), a severe adverse drug reaction occurring in up to 1% of treated individuals. Identifying genetic risk factors for CIAG could enable safer and more widespread use of clozapine. Here we perform the largest and most comprehensive genetic study of CIAG to date by interrogating 163 cases using genome-wide genotyping and whole-exome sequencing. We find that two loci in the major histocompatibility complex are independently associated with CIAG: a single amino acid in HLA-DQB1 (126Q) (P=4.7×10−14, odds ratio, OR=0.19, 95% CI 0.12–0.29) and an amino acid change in the extracellular binding pocket of HLA-B (158T) (P=6.4×10−10, OR=3.3, 95% CI 2.3–4.9). These associations dovetail with the roles of these genes in immunogenetic phenotypes and adverse drug responses for other medications, and provide insight into the pathophysiology of CIAG.