Psicosis como presentación del síndrome antifosfolípido primario / Psychosis as debut of antiphospholipid syndrome

Introducción. El síndrome antifosfolípido (SAF) es un trastorno autoinmune que determina un estado de hipercoagulabilidad caracterizado por eventos trombóticos, abortos de repetición y la presencia de anticuerpos antifosfolípido. Puede presentarse de manera aislada (SAF primario) o asociado a lupus eritematoso sistémico u otras enfermedades autoinmunes (SAF secundario). Las manifestaciones neuropsiquiátricas del SAF incluyen jaqueca, epilepsia, corea, demencia y psicosis. Se realiza una revisión bibliográfica de la sintomatología neuropsiquiátrica en general y psicótica en particular de los pacientes afectos de SAF. Caso clínico. Mujer de 23 años afecta de un SAF primario que comenzó con manifestaciones clínicas únicamente neuropsiquiátricas consistentes en sintomatología psicótica (dos episodios de clínica delirante) y movimientos anormales coreiformes y hemibalísticos que inicialmente se interpretaron como clínica conversiva. Conclusiones. Se discute la patogénesis de la sintomatología motora y psicótica. La etiología de los síntomas neuropsiquiátricos todavía no se conoce con claridad, pero la trombosis de pequeños vasos en el cerebro podría explicar parte de los síntomas. Asimismo, se revisa el papel que la medicación antipsicótica y antitrombótica tiene para estos pacientes.En la actualidad, nuestra paciente se mantiene asintomática sin necesidad de terapia antipsicótica y recibe tratamiento únicamente con un agente antiagregante y otro antipalúdico (AU)

Introduction. Antiphospholipid syndrome (APS) is an autoimmune disorder which causes an hypercoagulation state characterized by thrombotic events, repetitive miscarriages and the presence of antiphospholipid antibodies. APS may be an isolated disease (primary APS) or associated to systemic lupus erythematous or another autoimmune conditions (secondary APS). Neuropsychiatric manifestations accompanying APS include migraine, epilepsy, chorea, dementia or psychosis. Detailed descriptions of clinical cases are lacking, and correlations between clinical and analytical findings are far from being well known. We review literature concerning neuropsychiatric manifestations in general and psychosis in particular, in patients suffering from AFS.Case report. A 23 years-old female who presented a primary AFS with a clinical debut consisting of neuropsychiatric manifestations characterized by psychosis (with two delusion episodes) and abnormal movements such as choreiform and hemiballistic movements, initially understood as conversive symptoms. Conclusions. We discuss the pathogenesis of the psychotic and motor manifestations. The etiology is nowadays not completely understood, but cerebral small vessel thrombosis might explain part of the manifestations. We also review the role of antipsychotic and antithrombotic medication for these patients. Currently, our patient remains asymptomatic without any antipsychotic agent, only being treated with antiagregant and antipalludic therapy (AU)

[Psychosis as debut of antiphospholipid syndrome]. / Psicosis como presentacion del sindrome antifosfolipido primario.

INTRODUCTION: Antiphospholipid syndrome (APS) is an autoimmune disorder which causes an hypercoagulation state characterized by thrombotic events, repetitive miscarriages and the presence of antiphospholipid antibodies. APS may be an isolated disease (primary APS) or associated to systemic lupus erythematous or another autoimmune conditions (secondary APS). Neuropsychiatric manifestations accompanying APS include migraine, epilepsy, chorea, dementia or psychosis. Detailed descriptions of clinical cases are lacking, and correlations between clinical and analytical findings are far from being well known. We review literature concerning neuropsychiatric manifestations in general and psychosis in particular, in patients suffering from AFS. CASE REPORT: A 23 years-old female who presented a primary AFS with a clinical debut consisting of neuropsychiatric manifestations characterized by psychosis (with two delusion episodes) and abnormal movements such as choreiform and hemiballistic movements, initially understood as conversive symptoms. CONCLUSIONS: We discuss the pathogenesis of the psychotic and motor manifestations. The etiology is nowadays not completely understood, but cerebral small vessel thrombosis might explain part of the manifestations. We also review the role of antipsychotic and antithrombotic medication for these patients. Currently, our patient remains asymptomatic without any antipsychotic agent, only being treated with antiagregant and antipalludic therapy.

TITLE: Psicosis como presentacion del sindrome antifosfolipido primario.Introduccion. El sindrome antifosfolipido (SAF) es un trastorno autoinmune que determina un estado de hipercoagulabilidad caracterizado por eventos tromboticos, abortos de repeticion y la presencia de anticuerpos antifosfolipido. Puede presentarse de manera aislada (SAF primario) o asociado a lupus eritematoso sistemico u otras enfermedades autoinmunes (SAF secundario). Las manifestaciones neuropsiquiatricas del SAF incluyen jaqueca, epilepsia, corea, demencia y psicosis. Se realiza una revision bibliografica de la sintomatologia neuropsiquiatrica en general y psicotica en particular de los pacientes afectos de SAF. Caso clinico. Mujer de 23 años afecta de un SAF primario que comenzo con manifestaciones clinicas unicamente neuropsiquiatricas consistentes en sintomatologia psicotica (dos episodios de clinica delirante) y movimientos anormales coreiformes y hemibalisticos que inicialmente se interpretaron como clinica conversiva. Conclusiones. Se discute la patogenesis de la sintomatologia motora y psicotica. La etiologia de los sintomas neuropsiquiatricos todavia no se conoce con claridad, pero la trombosis de pequeños vasos en el cerebro podria explicar parte de los sintomas. Asimismo, se revisa el papel que la medicacion antipsicotica y antitrombotica tiene para estos pacientes. En la actualidad, nuestra paciente se mantiene asintomatica sin necesidad de terapia antipsicotica y recibe tratamiento unicamente con un agente antiagregante y otro antipaludico.

QTc interval in a sample of long-term schizophrenia inpatients.

This naturalistic study attempted to determine the prevalence of prolonged QTc interval in a relatively large population of inpatients hospitalized with chronic schizophrenia, and to explore QTc relationship with demographic variables, metabolic parameters and prescribed treatments. All inpatients from a Spanish long-term psychiatric hospital were cross-sectionally investigated to determine the prevalence of QTc prolongation and metabolic syndrome. The sample with a DSM-IV diagnosis of schizophrenia included 171 Caucasian inpatients, all of Spanish origin. A prolonged QTc interval was defined as >450 ms in men and >470 ms in women. The relationships between QTc and other continuous variables were assessed using a linear regression model with QTc as the dependent variable. Only 10 patients (6%) had a prolonged QTc interval; one case was possibly explained by hypokalemia. Three patients (2%) had a QTc > 500 ms. Gender, old age (> or = 50 years old), current smoking, systolic blood pressure, HDL cholesterol and history of arrhythmia were found to have significant effects on QTc interval in a linear regression analysis. After controlling for significant variables, the mean QTc interval was not significantly influenced by antipsychotic dose, type of antipsychotic treatment, the use of depot antipsychotics, or the number of different antipsychotics prescribed. Our study focused on long-term schizophrenia inpatients with frequent antipsychotic polypharmacy and high antipsychotic doses, and suggested that after excluding the case with hypokalemia length of QTc was associated with history of arrhythmias and with metabolic factors, while the effects of antipsychotic compound or class were not so evident.

Hiponatremia por oxcarbazepina / Oxcarbezepine-induced hyponatremia

Con los años, desde su instauración como tratamiento anticomicial, se han publicado numerosos casos clínicos que relacionan la utilización de oxcarbazepina y la aparición de hiponatremia (sodio sérico < 135 mmol/l), tanto en monoterapia como en combinación con otros fármacos. Se describen posibles mecanismos de acción por los que la oxcarbazepina puede producir hiponatremia, como la liberación inadecuada de vasopresina (SIADH) o el incremento de agua y la pérdida secundaria de sodio ¿mayor sensibilidad tubular a la vasopresina. A partir del caso de un varón de 40 años diagnosticado de esquizofrenia resistente que, tras varias semanas de tratamiento con oxcarbazepina, presenta astenia y fatigabilidad en relación con sodio sérico en 124 mmol/l, revisamos todos los casos clínicos publicados desde 1987 hasta la actualidad centrándonos en las dosis de fármaco administradas, el tratamiento concomitante, la edad y el sexo del paciente, el sodio sérico en sangre periférica, los síntomas presentados y el tratamiento recibido. Se proponen incrementos lentos y graduales de la dosis al introducir la oxcarbazepina, así como determinaciones plasmáticas para evitar un posible descenso del sodio sérico por debajo de 135 mmol/l (AU)

Since oxcarbazepine was establishment as an antiepileptic treatment, numerous case reports have been published associating the use of this drug with the development of hyponatremia (serum sodium < 135 mmol/l), both in monotherapy and associated with other drugs. Possible mechanisms of action through which oxcarbazepine can produce hyponatremia are described, such as an increase in antidiuretic hormone release ¿ syndrome of inappropriate antidiuretic hormone secretion (SIADH) ¿or by means of increase water and secondary sodium loss¿ increased renal tubule sensitivity to antidiuretic hormone. Based on the case of a 40-year-old man with a diagnosis of paranoid schizophrenia, who developed weakness and fatigue closely related to serum sodium of 124 mmol/l after several weeks of oxcarbazepine treatment, we review all the cases published from 1987 to date. The doses of the drug administered, concomitant treatment, patient age and sex, serum sodium in peripheral blood, symptoms, and the treatment received are discussed. We recommend slow and gradual dose increases when oxcarbazepine is introduced, as well as plasma monitoring, to avoid possible decreases in serum sodium below 135 mmol/l (AU)