Journal of affective disorders · 2014
Increased platelet intracellular calcium ion concentration is specific to bipolar disorder.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Dubovsky Steven L, Daurignac Elsa, Leonard Kenneth E
Аннотация
BACKGROUND: Increased baseline ([Ca(2+)]B) and agonist-stimulated ([Ca(2+)]s) free intracellular calcium ion concentrations ([Ca(2+)]i) are well-replicated findings in bipolar disorder, but whether this finding is specific to that condition and if so, whether it is a marker of the mood disorder or a feature seen in other disorders such as psychosis has remained unclear.
METHODS: Platelet [Ca(2+)]i was assessed in 15 inpatients with psychotic and nonpsychotic mania, 17 schizophrenia inpatients, and 17 matched controls.
RESULTS: Platelet [Ca(2+)]B and [Ca(2+)]s were significantly higher than controls in bipolar disorder but not schizophrenia. Variability of [Ca(2+)]B was significantly increased in bipolar disorder regardless of the presence of psychosis, but not in schizophrenia.
LIMITATIONS: Use of antipsychotic drugs by the majority of both patient groups may have obscured elevated [Ca(2+)]i in schizophrenia, or may have masked a difference between psychotic and nonpsychotic bipolar disorder. Measurement of [Ca(2+)]i is too labor intensive to become a routine test for diagnosis or prediction of treatment response.
CONCLUSIONS: Elevated intracellular Ca(2+) signaling may be a marker of primary cellular hyperactivity that could contribute to comorbid conditions such as hypertension and neuronal apoptosis. Since lithium and carbamazepine attenuate increased [Ca(2+)]i, further research may demonstrate a correlation between normalization of [Ca(2+)]i and response to one of these medications, and further research may clarify whether a subgroup of patients may respond well to calcium channel antagonists.
METHODS: Platelet [Ca(2+)]i was assessed in 15 inpatients with psychotic and nonpsychotic mania, 17 schizophrenia inpatients, and 17 matched controls.
RESULTS: Platelet [Ca(2+)]B and [Ca(2+)]s were significantly higher than controls in bipolar disorder but not schizophrenia. Variability of [Ca(2+)]B was significantly increased in bipolar disorder regardless of the presence of psychosis, but not in schizophrenia.
LIMITATIONS: Use of antipsychotic drugs by the majority of both patient groups may have obscured elevated [Ca(2+)]i in schizophrenia, or may have masked a difference between psychotic and nonpsychotic bipolar disorder. Measurement of [Ca(2+)]i is too labor intensive to become a routine test for diagnosis or prediction of treatment response.
CONCLUSIONS: Elevated intracellular Ca(2+) signaling may be a marker of primary cellular hyperactivity that could contribute to comorbid conditions such as hypertension and neuronal apoptosis. Since lithium and carbamazepine attenuate increased [Ca(2+)]i, further research may demonstrate a correlation between normalization of [Ca(2+)]i and response to one of these medications, and further research may clarify whether a subgroup of patients may respond well to calcium channel antagonists.