Amitriptyline is an old drug but is still prevalently used as the first-line treatment for a variety of common diseases. Surprisingly, knowledge of sexual risks with amitriptyline comes from only one clinical trial and several case reports from three decades ago. In the current study, a systematic review of the literature following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) related to amitriptyline and sexual dysfunction (SD) was performed. The frequency, gender-difference, types, disease-specificity and time course of SD, and the relationship between SD and nonsexual adversity were studied. A total of 14 publications, including 8 qualified randomized clinical trials, were eligible. The frequency of SD in overall, male and female patients was 5.7, 11.9 and 1.7%, respectively. SD was six-fold higher in men than women. The frequency of SD was 6.9% in depressive patients compared with 0.8% in non-depressive patients ( p = .008), and gradually decreased at 8 weeks after treatment ( p = .02). Amitriptyline impacted arousal and libido more than orgasm and ejaculation in male patients but mainly libido in female patients. SD was significantly correlated with insomnia linearly whereas somnolence and nausea dually. Therefore, amitriptyline-associated SD mainly occurs in depressive and male patients, disturbs each phase of the sexual response cycle in men but mainly libido in women, gradually decreases under long-term treatment, and can be predicted by the co-existence of insomnia, somnolence or nausea during treatment. Clinicians should caution and tailor the gender and disease vulnerability of amitriptyline in their practice.
Zolpidem, a non-benzodiazepine hypnotic drug, shows a high affinity for the BZ1 (ω1) subtypes of the modulatory sites within the GABAA receptor complex, but classical benzodiazepines (diazepam, lorazepam) have a non-specific affinity profile at ω1 and ω2 subtypes of the GABAA receptor. Therefore, zolpidem is thought to be safer than benzodiazepines. We present five cases with withdrawal delirium, seizure, acute psychosis and orofacial dyskinesia that developed following cessation of zolpidem. Adverse effects such as withdrawal seizure and withdrawal delirium have been rarely reported in relation to zolpidem. Chemically unrelated to benzodiazepines, zolpidem is thought to have fewer adverse effects, but shares a pharmacokinetic profile with the benzodiazepines. It is advised that the normal criteria for the prescription of benzodiazepines also be used when prescribing non-benzodiazepine sedatives and hypnotics, as they act upon the same receptor, namely, the benzodiazepine-GABA-chloride complex. However, at higher than recommended doses for extended periods of time, the addictive potential of zolpidem may be similar to that of the benzodiazepines. It is possible that zolpidem abandons its selectivity for the BZ1 receptors and demonstrates all the actions of classic benzodiazepines.
Objective: There is a significant relationship between obesity and common mental symptoms (depression and anxiety symptoms). But the association between depression (or anxiety symptoms) and serum leptin is still unclear and controversial, despite the growing body of evidence supporting the existence of “leptin resistance” in obese persons. So we investigated whether common mental symptoms, obesity, and the interactive effect of these two factors have a relationship with leptin in obese patients who were candidates for bariatric surgery. Methods: In all, 139 participants (mean age: 31.4 years, standard deviation: 9.3 years, 73.4% female) were enrolled at an obesity treatment center in southern Taiwan. Serum leptin levels and body mass index (BMI) were measured. The Chinese Health Questionnaire and Taiwanese Depression Questionnaire were administered. Results: The mean BMI of our participants was 39.4 kg/m 2 (±6.8), and the mean leptin level was 24.5 ng/mL (±9.4). In the multivariate regression models, Chinese Health Questionnaire-by-BMI and Taiwanese Depression Questionnaire-by-BMI interaction terms remained significant predictors of leptin level ( β =0.16, P <0.0001; β =0.04, P <0.0001, respectively), after adjustment for age, sex, and history of hypertension, diabetes, and hyperlipidemia, despite the inverse correlation between Chinese Health Questionnaire (or Taiwanese Depression Questionnaire) and leptin. In addition, female patients had significantly higher leptin levels than male patients. Conclusion: The present findings confirmed that the relationship between common mental symptoms and leptin is modulated by obesity in severely obese patients. Future studies should focus on further measures of leptin receptors or signaling on the basis of these interactive effects in psychiatry. Keywords: leptin, depression, anxiety, common mental disorder, obesity
Objective. To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the monoamine oxidase A (MAOA) promoter and exon 3 of the dopamine D4 receptor (DRD4) gene in heroin addiction modulate the vulnerability of individuals to heroin addiction. Methods. Eight hundred and ninety-four male heroin addicts without other psychiatric disorders, were recruited as subjects. Another community 180 males were selected randomly as controls. Results. The geno-distribution of the DRD4 exon 3 VNTR polymorphism in controls was in Hardy–Weinberg equilibrium (HWEχ2=0.925), but the distribution in heroin addicts was not (HWEχ2=28.35). The long-repeat alleles of the DRD4 exon 3 VNTR polymorphism were found more frequently in the heroin addicts (P=0.019). However, the long-repeat alleles of the MAOA promoter VNTR polymorphism were not (P=0.828). No interaction between these two VNTR polymorphisms was found by using multiple logistic regression analysis (P=0.261). Conclusion. The long-repeat allelic variants (>4-repeats) and 2-repeat allele of the DRD4 exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to heroin addiction in Chinese men, but the MAOA promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of heroin dependence.
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