Current opinion in psychiatry · 2012
Genetic correlates of medical comorbidity associated with schizophrenia and treatment with antipsychotics.
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Ferentinos Panagiotis, Dikeos Dimitris
Аннотация
PURPOSE OF REVIEW: High comorbidity rates for various medical conditions have been documented in schizophrenia, being explained by factors either inherent to the disease or associated with antipsychotic treatment. The aim of this study is to review the genetic factors contributing to medical comorbidity in schizophrenia.
RECENT FINDINGS: Based on clinical genetic studies in schizophrenia, comorbid impaired glucose tolerance/type 2 diabetes mellitus, most autoimmune disorders and cardiac autonomic dysregulation have the strongest evidence for familial predisposition. Similarly, of antipsychotic-induced adverse drug reactions, tardive dyskinesia, neuroleptic malignant syndrome, and antipsychotic-induced weight gain have some evidence for familial clustering. On the molecular genetic level, schizophrenia seems to share specific genes with type 2 diabetes mellitus and with autoimmune disorders. Various genes have been proposed to account for the reduced incidence of rheumatoid arthritis and cancer in schizophrenic patients and their relatives. Many pharmacogenetic association studies have pinpointed numerous, though often contradictory or poorly replicated, genes of modest effect size for tardive dyskinesia, neuroleptic malignant syndrome, clozapine-induced agranulocytosis, hyperprolactinaemia, antipsychotic-induced weight gain, and antipsychotic-induced QT prolongation.
SUMMARY: Unravelling the genetic underpinnings of medical comorbidity associated with schizophrenia and its treatment is expected to highlight new pathogenetic pathways in both schizophrenia and comorbid medical conditions, and introduce personalized treatment strategies for schizophrenia patients.
RECENT FINDINGS: Based on clinical genetic studies in schizophrenia, comorbid impaired glucose tolerance/type 2 diabetes mellitus, most autoimmune disorders and cardiac autonomic dysregulation have the strongest evidence for familial predisposition. Similarly, of antipsychotic-induced adverse drug reactions, tardive dyskinesia, neuroleptic malignant syndrome, and antipsychotic-induced weight gain have some evidence for familial clustering. On the molecular genetic level, schizophrenia seems to share specific genes with type 2 diabetes mellitus and with autoimmune disorders. Various genes have been proposed to account for the reduced incidence of rheumatoid arthritis and cancer in schizophrenic patients and their relatives. Many pharmacogenetic association studies have pinpointed numerous, though often contradictory or poorly replicated, genes of modest effect size for tardive dyskinesia, neuroleptic malignant syndrome, clozapine-induced agranulocytosis, hyperprolactinaemia, antipsychotic-induced weight gain, and antipsychotic-induced QT prolongation.
SUMMARY: Unravelling the genetic underpinnings of medical comorbidity associated with schizophrenia and its treatment is expected to highlight new pathogenetic pathways in both schizophrenia and comorbid medical conditions, and introduce personalized treatment strategies for schizophrenia patients.