ABSTRACT
Objective: Analog triptorelin is one of the effective agonists for the treatment of reproductive disorders, particularly prostate cancer. Due to results of previous studies, we hypothesized that obsessive-compulsive disorder (OCD can be effectively treated with the long-term administration of a gonadotropin-releasing hormone (GnRH) analog, namely triptorelin. The aim of this study was to evaluate the effectiveness of triptorelin injection in clients with OCD. Method : This randomized single-blind clinical trial was performed on 30 clients with OCD who had a Yale-Brown score of > 17 after 8 weeks of treatment. The participants were randomly assigned into two groups of triptorelin and placebo. The clients in the intervention group were treated with Selective serotonin reuptake inhibitors (SSRIs), including fluoxetine, in addition to triptorelin three times a month for at least 8 weeks. Clients in the control group received injection of distilled water as placebo three times in addition to the routine treatment. The outcome was evaluated by Yale-Brown OCD scale (Y-BOCS) at the baseline, as well as 4, 8, and, 20 weeks after the end of the treatment. Results: The mean scores of Y-BOCS in the intervention and control groups was 30.5 ±67.6 and 30.5 ±67.6, respectively, before intervention, indicating no significant difference between the two groups (P = 0.0.8). The comparison of Y-BOCS scores after the intervention showed a significant difference between the two groups in the scores 4 (P = 0.01), 8 (P < 0.005), and 20 (P < 0.005) weeks after the treatment. With regards to the side effects of the medicine, 6.7% (n = 1) of the clients in the control group developed headache and 66.7% (n = 10) had late period in intervention group. The results revealed a significant difference between the two groups in terms of side effects (P < 0.005). Conclusion: The results of this study showed triptorelin decreased the symptoms of OCD. The effectiveness of triptorelin in the treatment of symptoms in clients with OCD was confirmed in our study. However, due to the limited research addressing this domain, future studies are suggested to clarify this conclusion.
ABSTRACT
BACKGROUND: The relationship between depression and increased oxidative stress is well known. DNA damage by oxidation factors is an important cause of the aging process in psychiatric disorders. AIMS: Owing to the scarcity of human studies and high inconsistencies in studies of the effects of antidepressants on DNA damage, the current study was undertaken to investigate the effects of depression and its treatment on DNA damage. METHODS: In a 15-week open-label study of citalopram (n = 25) and sertraline (n = 20), levels of DNA damage were measured by comet assay, proinflammatory (Interlukin-6 (IL-6)) and oxidative DNA damage (8-hydroxy-2'-deoxyguanosine (8-OHdG)) markers by ELISA, and gene expression of base excision repair enzymes (8-oxoguanine glycosylase (OGG1) and poly (ADP)-ribose polymerase-1 (PARP1)) by quantitative real-time polymerase chain reaction in healthy control patients (n = 14), with depression at the baseline and the same patients after week 15. RESULTS: DNA damage, 8-OHdG, IL-6 and expression of PARP1 were elevated in patients with depression compared with the healthy controls (p < 0.001). Selective serotonin reuptake inhibitor (SSRI) therapy could significantly reduce the depression score (p < 0.01), DNA damage (p < 0.001), as well as 8-OHdG and IL-6 (p < 0.0001). Nevertheless, the expression of PARP1 and OGG1 showed no significant changes after treatment. CONCLUSIONS: This is the first study on the effect of SSRIs on the DNA damage and some of the repair enzymes in depression. Based on the results, depression can cause increased DNA damage. This damage is followed by activation of compensatory mechanisms whereby the expression of DNA damage repair enzymes is elevated. Finally, the treatment of psychiatric disorder by antidepressants can lower the level of oxidative DNA damage.
Subject(s)
Citalopram/administration & dosage , DNA Damage/drug effects , Depressive Disorder/drug therapy , Selective Serotonin Reuptake Inhibitors/administration & dosage , Sertraline/administration & dosage , Adult , Case-Control Studies , Citalopram/pharmacology , Comet Assay , DNA Glycosylases/genetics , Depressive Disorder/genetics , Female , Humans , Male , Middle Aged , Oxidative Stress/drug effects , Poly (ADP-Ribose) Polymerase-1/genetics , Selective Serotonin Reuptake Inhibitors/pharmacology , Sertraline/pharmacologyABSTRACT
Progressive dementia in conjunction with multiple bone fractures in a previously healthy young man led to the investigation of the underlying cause. The differential diagnoses (most importantly hypoparathyroidism) were limited given basal ganglia calcifications on the brain computed tomographic scan. Electronic search of the key words basal ganglia calcification, osteoporosis, and dementia revealed a rare condition termed Nasu-Hakola disease or polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy. This very rare and potentially fatal genetic disease is characterized by pathological fractures, multiple lytic bone lesions, and presenile dementia. We report an Iranian patient with this disease and a review of the literature.