ABSTRACT
Nitric oxide (NO) is thought to be involved in the pathogenesis of schizophrenia as well as many neuropsychiatric disease. Asymmetric dimethylarginine (ADMA) reduces the level of NO by inhibiting nitric oxide synthase (NOS) enzyme. In this study it is aimed to be investigated ADMA in patients with first-episode schizophrenia. In this study, according to DSM-IV diagnostic criteria for schizophrenia-like psychotic disorder, 49 male first-episode schizophrenia patients-whose mean age was 23.4±3.5 year-and age and education matched 30 healthy male subjects were included for comparison. ADMA levels of the patients were measured before and after 2 months of therapy. In order to rule out the conditions that may affect the levels of ADMA, people whose physical examination and laboratory findings were within normal range were included in the study. In this study plasma ADMA levels of first-episode schizophrenia patients and control group were 3.6±1.5 µmol/L and 1.02±1.02 respectively. After 2 months of antipsychotic treatment plasma ADMA levels of the schizophrenia patients decreased compared to baseline. There was no relationship between the ADMA levels and the clinical severity of the disease. It is considered to be the role of ADMA in the etiopathogenesis of schizophrenia.
Subject(s)
Antipsychotic Agents/therapeutic use , Arginine/analogs & derivatives , Nitric Oxide/metabolism , Schizophrenia/drug therapy , Schizophrenia/metabolism , Adult , Arginine/blood , Arginine/drug effects , Humans , Male , Middle Aged , Treatment Outcome , Young AdultABSTRACT
PATIENT: Male, 25 FINAL DIAGNOSIS: Post Traumatic Stress Disorder Symptoms: Insomnia ⢠nightmares ⢠spontaneous ejaculation MEDICATION: Paroxentine Clinical Procedure: - Specialty: Psychiatry. OBJECTIVE: Unusual clinical course. BACKGROUND: Sexual dysfunction is reported to occur more frequently in posttraumatic stress disorder (PTSD) patients than in the general population. Herein, we present the case of a patient with spontaneous ejaculation that developed when severity of PTSD symptoms increased. CASE REPORT: Our patient was a 25-year-old single man admitted to a psychiatric polyclinic because of PTSD symptoms and concurrent spontaneous ejaculations. He was diagnosed with PTSD after clinical interviews. Organic pathology to explain spontaneous ejaculations was not detected. Paroxetine treatment was initiated and PTSD symptoms and frequency of spontaneous ejaculations were decreased at the clinical follow-up. CONCLUSIONS: Assessment of the presented case in the light of the literature indicates that his re-experiencing (flashbacks, nightmare) and hyperarousal (symptoms of anxiety specific to PTSD) led to an increase in adrenergic system activation and, consequently, spontaneous ejaculation without sexual stimulus. The effect of Paroxetine in decreasing the frequency of spontaneous erection and ejaculation in the presented case is thought to have occurred via control of PTSD symptoms and their adverse effects on ejaculation. Treatment based on a consideration of PTSD symptoms and autonomic instability might increase the positive outcome rate in such patients.