Bipolar disorder is now known to be associated not only with highly prevalent co-occurring psychiatric and substance use disorders but also with medical comorbidities, such as cardiovascular diseases, diabetes mellitus, obesity and thyroid dysfunction. Inflammatory disturbances repeatedly observed in bipolar disorder, can explain some of the comorbidity between bipolar disorder and medical disorder. This revised perspective of bipolar disorders should promote the development of therapeutic tools. Immuno-inflammatory dysfunction may well represent a significant component of the underlying pathophysiology of the disorder. We therefore propose to review the immuno-inflammatory hypothesis in bipolar disorder considering the co-occurence with autoimmune diseases, immunological and inflammatory markers, as well as immuno-genetic markers which could lead to personalized treatments.

Clinical trials should carefully consider the impact of exclusion criteria on the generalizability of their results and explain the rationale for their use. For SAD treatment trials to adequately inform clinical practice, the eligibility rate must be increased through a general relaxation of overly stringent eligibility criteria.

BackgroundImmune dysfunction could play a significant role in the pathogenesis of bipolar disorder (BD) and schizophrenia (SZ), conditions with an underlying pro-inflammatory state. Studies on humoral immune responses (which reflects antibody mediated fight against pathogens) in schizophrenia and bipolar disorder are sparse and often providing contradictory results. The aim of this study was to assess humoral immunity in a group of stable bipolar disorder and schizophrenia patients compared to controls by determining total Immunoglobulins and IgG subclasses and to assess their association with latent Toxoplasma gondii and/or CMV infection.Methods334 subjects (124 BD, 75 SZ and 135 Healthy Controls [HC]) were included and tested for humoral immunity by determining the total immunoglobulins (IgG,A and M) and IgG subclasses (IgG1, IgG2, IgG3, IgG4) and their relationship with latent Toxoplasma gondii infection, an established risk factor for BD and SZ.ResultsAlthough lower levels of IgG, IgG1, IgG2, IgG4 and IgA were found among BD as compared to HC and/or SZ, after adjustment for confounding variables, only low levels of IgG and IgG1 in BD remai- ned significant. Strikingly highest levels of antibodies to T. gondii (but not CMV) infection in BD and SZ were associated with lowest levels of IgG3 and IgG4 levels as compared to controls.ConclusionsSchizophrenia and bipolar disorder patients with latent T. gondii specific infection may be more vulnerable to changes in immuno-inflammatory processes than controls with similar latent infectious state. Simultaneous sequential immunological monitoring both in steady state and active disease phases in the same BD and SZ patients are warranted to understand the role of Toxoplasma gondii latency in these disorders.

BackgroundEvidence suggests that neurotropic infectious agents might be involved in bipolar disorder. So far, few have been written for the association between parasitic infection and bipolar disorder. Filariasis is a parasitic disease acting ruthlessly via mosquitos and affecting more than 120 million people worldwide. We present here, to our knowledge, the first description of a filariasis infected manic bipolar disorder patient fully improved in terms of psychiatric symptoms by anti-heminthic treatment.Case presentationThe patient is a 31 years-old man native of Congo. At inclusion, he presented a severe manic episode with dangerous behaviour unresolved by classic treatments. A diagnosis of filariasis bancrofti infection was made after the discovery of a systemic hypereosinophilia. Therefore, a bi-therapy of anthelmintics was conducted allowing a successful improvement with clear reduction of agitation and aggressive behaviours that could not be attributed to a modification of psychotropic treatments or filarial encephalopathy or acute disseminated encephalomyelitis.ConclusionThe ineffectiveness of psychotropic treatment of a manic episode requires the evaluation of co-morbid medical conditions such as infections which can interfere with adequate mood stabilizing medication. Filariasis by inducing chronic inflammation and immunopathologic reactions seems to play a major role in infected affective disorders patients by changing levels of cytokines of the Th1 system or indirectly damaging the brain tissue. The beneficial combination of antihelmintics and mood stabilizers, in this case, could be explained by the potential of such association to downregulate neuroinflammation and excitotoxicity processes.Altogether, these data pinpoint the requirement to explore the parasitic infectious status in case of bipolar disorder patients resistant to classic treatments and originating or living in endemic geographical areas.

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Background A high prevalence of cannabis use disorder has been reported in subjects suffering from schizophrenia, fuelling intense debate about whether schizophrenia with pre-onset cannabis use disorder may be a distinct entity with specific features or whether cannabis use disorder can precipitate schizophrenia in genetically vulnerable subjects.Methods We retrospectively assessed schizophrenia subjects with and without pre-onset cannabis use disorder on the basis of their clinical features, assessed categorically and dimensionally with the operational criteria checklist for psychotic illnesses (OCCPI). We also investigated whether the two groups could be differentiated on the basis of a history of psychiatric disorders in first-degree relatives. A principal component factor analysis of the OCCPI items was used to identify specific symptom dimensions. The relationships between symptom dimensions and cannabis status were analysed by point-biserial correlation analysis to control for sex and age at time of the assessment and illness duration.ResultsOne hundred and seventy-one subjects with a diagnosis of schizophrenia were included. Among them, forty-one patients (18.2 % of the sample) had a cannabis use disorder before or at the time of the onset of schizophrenia. We found similar results in symptoms patterns or family history between patients with and without pre-onset cannabis use disorder.ConclusionsOur results clearly argue against cannabis-associated schizophrenia being a relevant distinct clinical entity of schizophrenia with specific features.