RESUMEN
OBJECTIVE: Clozapine is a second-generation antipsychotic used for treatment-resistant schizophrenia. Despite its effectiveness, clozapine is largely underused due to serious side effects such as leukopenia or neutropenia. We aimed to review whether to continue, discontinue or rechallenge clozapine treatment after such haematological side effects. METHODS: We reviewed and summarized the literature on the use of clozapine, how to deal with its side effects, and suitable options in case of any haematological problems. Then, we described several cases successfully treated with clozapine and lithium after development of neutropenia or leukopenia. RESULTS: We present three patients with treatment-resistant schizophrenia. While they had demonstrated poor response to multiple antipsychotic trials, clozapine was started. Clozapine induced neutropenia; or leukopenia developed in some cases that was successfully reversed after lithium onset. Increased serious side effects related with coprescription of lithium and clozapine were not observed. CONCLUSION: Lithium increases neutrophil and total white blood cell count as a side effect that may be useful in patients who develop neutropenia or leukopenia while being treated with clozapine.
Asunto(s)
Miembro 1 de la Subfamilia B de Casetes de Unión a ATP/genética , Agranulocitosis/genética , Alelos , Clozapina/efectos adversos , Variación Genética/genética , Gemelos Monocigóticos/genética , Subfamilia B de Transportador de Casetes de Unión a ATP , Adulto , Agranulocitosis/inducido químicamente , Agranulocitosis/diagnóstico , Humanos , Masculino , Esquizofrenia Paranoide/tratamiento farmacológico , Esquizofrenia Paranoide/genéticaRESUMEN
The aim of this study was to elucidate the chronic effects of tobacco smoking on the P300, a neurophysiological index of cognitive function. Prospective study participants were recruited from a family medicine polyclinic. We selected 32 right-handed smokers who had smoked more than 15 cigarettes per day, by inhalation, for more than 2 years. The control population consisted of 32 right-handed, age-matched healthy individuals who had never smoked. Event-related potentials (ERPs) were recorded with the auditory "oddball" two-tone discrimination task. The data from the central (Cz) and frontal (Fz) electrodes were analyzed. The P300 and N1 amplitudes at Fz were lower in the study population compared to the control group. The early component of ERP, the measure of mental speed (N1) latency at Fz was prolonged in the study group compared to the controls, possibly because early cognitive processes such as sensory input or initial encoding of sensory information were delayed in this group. For those who smoke, a decreased N1 amplitude might indicate delayed information processing and possibly short-term memory disturbance. Thus, chronic tobacco smoking may produce prefrontal cognitive dysfunction.
