Biological Markers that Predict the Treatment Response of Paroxetine in Panic Disorder.
- Author:
Joo Eon PARK
1
;
Bum Hee YU
Author Information
1. Department of Psychiatry, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. bhyu@smc.samsung.co.kr
- Publication Type:Original Article
- Keywords:
Panic disorder;
Beta-adrenergic receptors;
Treatment response;
Paroxetine
- MeSH:
Anxiety;
Anxiety Disorders;
Appointments and Schedules;
Biomarkers*;
Body Mass Index;
Depression;
Diagnostic and Statistical Manual of Mental Disorders;
Drug Therapy;
Humans;
Panic Disorder*;
Panic*;
Paroxetine*;
Receptors, Adrenergic, beta
- From:Journal of Korean Neuropsychiatric Association
2005;44(2):238-246
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: Previons studies reported altered beta-adrenergic receptor (betaAR) responsiveness in panic disorder, but few studies reported to see the effect of pharmacotherapy on betaAR function in panic patients. This investigation examined betaAR responsiveness in patients with panic disorder before and after pharmacotherapy with paroxetine. METHODS: After assessment using the Anxiety Disorder Interview Schedule for DSM-IV, 27 acute panic patients whose illness duration did not exceed 1 year were assigned to 12 weeks of paroxetine treatment. Twenty seven normal control subjects with no previous history of major medical and psychiatric illnesses were matched by age, sex, exercise, and body mass index. The Hamilton rating scale for anxiety (HAM-A), Hamilton rating scale for depression (HAM-D), Spielberger state-trait anxiety inventory-State (STAI-S) and Trait (STAI-T), acute panic inventory (API), anxiety sensitivity index (ASI), and Beck depression index (BDI) were performed to assess clinical states in the panic patients before and after treatment. The HAM-A, HAM-D, STAI-S and STAI-T, and BDI were also performed in the normal control subjects. We measured the betaAR density (Bmax), affinity (1/Kd), and sensitivity (cyclic AMP ratio of isoproterenol-stimulated cAMP to basal cAMP) in all subjects. RESULTS: Panic patients showed much lower scores of the HAM-A, STAI-S, STAI-T, API, ASI, HAM-D, and BDI after 12 weeks of paroxetine treatment than those before the treatment. There was no significant difference in the means of Bmax and cAMP ratio between control subjects and panic patients before and after the treatment. However, pretreatment Kd (R2=0.314, beta=-0.876, p=0.001) and Bmax (R2=0.230, beta=-0.575, p=0.019) significantly accounted for API scores after the treatment and change of Bmax according to the treatment accounted for the improvement of anxiety sensitivity (R2=0.353, beta=0.594, p=0.015). The pretreatment Kd value was significantly higher in the panic patients compared with that of control subjects (78.35+/-26.20 vs. 59.15+/-29.33, p=0.014), which was significantly reduced after the treatment (79.43+/-26.83 vs. 56.38+/-28.79, p=0.002). The pretreatment Kd value significantly accounted for the improvement of API scores (R2=0.316, beta=0.562, p=0.029) and the decrease in trait anxiety (R2=0.246, beta=-0.513, p=0.025). CONCLUSION: In acute panic patients, only betaAR affinity was reduced before the treatment, which was contrary to our expectation. Decreased betaAR affinity was normalized after paroxetine treatment. Decreased betaAR affinity and increased betaAR density before the treatment predicted good treatment response in acute panic patients. Thus, betaAR affinity and density could be useful biological markers that predict the treatment response of paroxetine in panic disorder.
