RESUMEN
Panic disorder has been associated with both an increased risk of coronary events as well as an increased risk of stroke. Hemoconcentration, with both a decrease in plasma volume and an increase in plasma viscosity, is a possible contributor to the risk of acute ischemic events. Our objectives were to demonstrate the process of hemoconcentration in response to induced panic symptoms and to assess the effect of pretreatment with ethinyl estradiol on panic-induced hemoconcentration. Fifteen male patients with panic disorder and 10 male healthy volunteers were included in a double-blind cross-over placebo-controlled design consisting of two injections of pentagastrin following randomized pretreatment with placebo and ethinyl estradiol. Plasma levels of hematocrit and hemoglobin were assessed at baseline and post-injections, and used to calculate an indirect estimation of the change in plasma volume. Pentagastrin-induced panic symptoms were associated with a mean decrease in plasma volume of 4.8% in the placebo pretreatment condition. Pretreatment with ethinyl estradiol attenuated this effect. The acute hemoconcentration observed in relation to pentagastrin-induced panic symptoms may be relevant to the increased risk of stroke and acute coronary events found in patients with panic disorder.
Asunto(s)
Viscosidad Sanguínea/efectos de los fármacos , Estrógenos/farmacología , Etinilestradiol/farmacología , Trastorno de Pánico/sangre , Pánico/efectos de los fármacos , Pentagastrina/efectos adversos , Volumen Plasmático/efectos de los fármacos , Estudios Cruzados , Método Doble Ciego , Estrógenos/administración & dosificación , Etinilestradiol/administración & dosificación , Hematócrito , Hemoglobinas/análisis , Humanos , Masculino , Pentagastrina/farmacología , Escalas de Valoración PsiquiátricaRESUMEN
OBJECTIVE: The primary objective of this study was to assess whether pentagastrin-induced panic symptoms are associated with release of free fatty acids (FFAs) in a manner that could explain the mechanism of correlations observed between serum cholesterol levels and frequency and severity of panic attacks in patients with panic disorder (PD). A secondary objective was to assess whether pretreatment with ethinyl estradiol (EE) attenuates pentagastrin-induced release of FFAs. METHODS: A double-blind, crossover, placebo-controlled study was conducted in which patients with PD and healthy volunteers received 2 injections of pentagastrin, 7-10 days apart, with randomization of the order of pretreatment with placebo and EE. RESULTS: We found a statistically significant, time-dependent release of FFAs in response to pentagastrin challenge. However, this release of FFAs was not attenuated by pretreatment with EE. CONCLUSIONS: These results support the hypothesis that release of FFAs in association with panic attacks occurs in a manner similar to the stress-induced lipolysis model. This suggests a possible mechanism for the elevated serum cholesterol levels observed in patients with PD. However, the occurrence of a delayed increase in low-density lipoprotein (LDL) cholesterol following induction of a panic attack remains to be tested in studiesincorporating a placebo injection visit and timed measurements of LDL cholesterol.