People with severe mental illness have a considerably shorter lifespan than the general population. This excess mortality is mainly due to physical illness. Next to mental illness-related factors, unhealthy lifestyle, and disparities in health care access and utilization, psychotropic medications can contribute to the risk of physical morbidity and mortality. We systematically reviewed the effects of antipsychotics, antidepressants and mood stabilizers on physical health outcomes in people with schizophrenia, depression and bipolar disorder. Updating and expanding our prior systematic review published in this journal, we searched MEDLINE (November 2009 -November 2014, combining the MeSH terms of major physical disease categories (and/or relevant diseases within these categories) with schizophrenia, major depressive disorder and bipolar disorder, and the three major psychotropic classes which received regulatory approval for these disorders, i.e., antipsychotics, antidepressants and mood stabilizers. We gave precedence to results from (systematic) reviews and meta-analyses wherever possible. Antipsychotics, and to a more restricted degree antidepressants and mood stabilizers, are associated with an increased risk for several physical diseases, including obesity, dyslipidemia, diabetes mellitus, thyroid disorders, hyponatremia; cardiovascular, respiratory tract, gastrointestinal, haematological, musculoskeletal and renal diseases, as well as movement and seizure disorders. Higher dosages, polypharmacy, and treatment of vulnerable (e.g., old or young) individuals are associated with greater absolute (elderly) and relative (youth) risk for most of these physical diseases. To what degree medication-specific and patient-specific risk factors interact, and how adverse outcomes can be minimized, allowing patients to derive maximum benefits from these medications, requires adequate clinical attention and further research.

Since the 1970s, clinicians have increasingly become more familiar with hyperprolactinemia (HPRL) as a common adverse effect of antipsychotic medication, which remains the cornerstone of pharmacological treatment for patients with schizophrenia. Although treatment with second-generation antipsychotics (SGAs) as a group is, compared with use of the first-generation antipsychotics, associated with lower prolactin (PRL) plasma levels, the detailed effects on plasma PRL levels for each of these compounds in reports often remain incomplete or inaccurate. Moreover, at this moment, no review has been published about the effect of the newly approved antipsychotics asenapine, iloperidone and lurasidone on PRL levels. The objective of this review is to describe PRL physiology; PRL measurement; diagnosis, causes, consequences and mechanisms of HPRL; incidence figures of (new-onset) HPRL with SGAs and newly approved antipsychotics in adolescent and adult patients; and revisit lingering questions regarding this hormone. A literature search, using the MEDLINE database (1966–December 2013), was conducted to identify relevant publications to report on the state of the art of HPRL and to summarize the available evidence with respect to the propensity of the SGAs and the newly approved antipsychotics to elevate PRL levels. Our review shows that although HPRL usually is defined as a sustained level of PRL above the laboratory upper limit of normal, limit values show some degree of variability in clinical reports, making the interpretation and comparison of data across studies difficult. Moreover, many reports do not provide much or any data detailing the measurement of PRL. Although the highest rates of HPRL are consistently reported in association with amisulpride, risperidone and paliperidone, while aripiprazole and quetiapine have the most favorable profile with respect to this outcome, all SGAs can induce PRL elevations, especially at the beginning of treatment, and have the potential to cause new-onset HPRL. Considering the PRL-elevating propensity of the newly approved antipsychotics, evidence seems to indicate these agents have a PRL profile comparable to that of clozapine (asenapine and iloperidone), ziprasidone and olanzapine (lurasidone). PRL elevations with antipsychotic medication generally are dose dependant. However, antipsychotics having a high potential for PRL elevation (amisulpride, risperidone and paliperidone) can have a profound impact on PRL levels even at relatively low doses, while PRL levels with antipsychotics having a minimal effect on PRL, in most cases, can remain unchanged (quetiapine) or reduce (aripiprazole) over all dosages. Although tolerance and decreases in PRL values after long-term administration of PRL-elevating antipsychotics can occur, the elevations, in most cases, remain above the upper limit of normal. PRL profiles of antipsychotics in children and adolescents seem to be the same as in adults. The hyperprolactinemic effects of antipsychotic medication are mostly correlated with their affi...

Psychiatric disorders, and especially severe mental illness, are associated with an increased risk of severe acute respiratory syndrome coronavirus 2 infection and COVID-19-related morbidity and mortality. People with severe mental illness should therefore be prioritised in vaccine allocation strategies. Here, we discuss the risk for worse COVID-19 outcomes in this vulnerable group, the effect of severe mental illness and psychotropic medications on vaccination response, the attitudes of people with severe mental illness towards vaccination, and, the potential barriers to, and possible solutions for, an efficient vaccination programme in this population.

While preliminary data suggest the lowest weight gain potential with lurasidone and potentially relevant short-term metabolic effects for asenapine and iloperidone, data are still too sparse to comprehensively evaluate the metabolic safety of the newly approved SGAs. Therefore, there is a clear need for further controlled studies to evaluate whether these agents are less problematic regarding treatment-emergent weight gain and metabolic disturbances than other currently available antipsychotics.

ObjectiveTo assess the prevalence and moderators of low bone mass, osteopenia and osteoporosis in schizophrenia patients. MethodMajor electronic databases were searched from inception till 12/2013 for studies reporting the prevalence of low bone mass (osteopenia + osteoporosis = primary outcome), osteopenia or osteoporosis in schizophrenia patients. Two independent authors completed methodological appraisal and extracted data. A random effects meta-analysis was utilised. ResultsNineteen studies were included (n=3,038 with schizophrenia; 59.2% male; age 24.5-58.9 years). The overall prevalence of low bone mass was 51.7% (95% CI=43.1-60.3%); 40.0% (CI=34.7-45.4%) had osteopenia and 13.2% (CI=7.8-21.6%) had osteoporosis. Compared with controls, schizophrenia patients had significantly increased risk of low bone mass (OR=1.9, CI=1.30-2.77, p<0.001, n=1,872) and osteoporosis (OR=2.86, CI=1.27-6.42, p=0.01, n=1,824), but not osteopenia (OR=1.33, CI=0.934-1.90, p=0.1, n=1,862). In an exploratory regression analysis, older age (p=0.004) moderated low bone mass, whilst older age (p<0.0001) and male sex (p<0.0001) moderated osteoporosis. The subgroup analyses demonstrated high heterogeneity, but low bone mass was less prevalent in North America (35.5%, CI=26.6-45.2%) than Europe (53.6%, CI=38.0-68.5%) and Asia (58.4%, CI=48.4-67.7%), and in mixed in-/outpatients (32.9%, CI=49.6-70.1%) versus inpatients (60.3%, CI=49.6-70.1%). Conclusion 3Reduced bone mass (especially osteoporosis) is significantly more common in people with schizophrenia than controls. Summations• Low bone mass affects more than half of patients with schizophrenia and is approximately twice as common compared to age-and sex-matched controls.• Osteoporosis is over two and a half times more common in patients than in controls.• Multidisciplinary teams should routinely screen and implement appropriate interventions targeting bone health. Considerations• There was a paucity and inconsistency in the reporting of factors that may influence the prevalence of low bone mass across studies.• All of the studies included were cross-sectional; therefore directionality of the association between the variables investigated and the observed low bone mass cannot be deduced with certainty.• We could not clearly elucidate the influence of antipsychotics since there were inadequate data on specific medications.