RESUMO
Recent evidence suggests a possible relationship between the immune system and schizophrenia spectrum disorders (SSDs), as neuroinflammation appears to play a role in major psychiatric conditions. Neuroinflammation is as a broad concept representing a physiological protective response to infection or injury, but in some cases, especially if chronic, it may represent an expression of maladaptive processes, potentially driving to clinical dysfunction and neurodegeneration. Several studies are concurrently highlighting the importance of microglia, the resident immune cells of the central nervous system, in a huge number of neurodegenerative diseases, including multiple sclerosis, Alzheimer's and Parkinson's diseases, as well as SSDs. A more fundamental phenomenon of maladaptive coupling of microglia may contribute to the genesis of dysfunctional brain inflammation involved in SSDs, from the onset of their neurophenomenological evolution. Clozapine and other antipsychotic drugs seem to express a provable immunomodulant effect and a more specific action on microglia, while neuroactive steroids and nonsteroidal anti-inflammatory drugs may reduce some SSDs symptoms in add-on therapy. Given these theoretical premises, this article aims to summarize and interpret the available scientific evidence about psychotropic and anti-inflammatory drugs that could express an immunomodulant activity on microglia.
RESUMO
BACKGROUND: Clozapine may be considered the first-line option for treatment-resistant schizophrenia (TRS), a condition that occurs in more than 30% of patients with schizophrenia. Despite its efficacy for treating TRS, clozapine use is limited by the occurrence of several adverse effects in more than 70% of cases. Clozapine does not typically affect lung function, although a few cases have been reported in the literature. CASE PRESENTATION: To gain a better understanding of this rare event, here we report the case study of a young female with TRS, who was treated with clozapine and developed medium and bilateral pleural effusion relief with contiguous atelectasis and polyserositis. Two weeks after stopping clozapine, the follow-up chest scan showed complete remission of the pulmonary condition. We postulate that clozapine might have caused, in this case, a specific immunoinflammatory response leading to serosal complications. CONCLUSION: Although the underlying mechanisms of this adverse effect are not completely understood, early manifestations, such as benign eosinophilia, fever, and flu-like symptoms need to be considered a potential warning to facilitate an early diagnosis and carefully manage pulmonary complications related to clozapine treatment.