Both overweight and obesity have been identified as risk factors for sexual dysfunction in men, but the relationship between sexual function and amount of body fat in females is still obscure. There are few reported studies in women assessing the relationship between female sexual function index (FSFI) and body weight. The aim of this study was to identify the frequency of female sexual dysfunction (FSD) among obese and overweight women. A total of 45 obese and overweight and 30 age-matched voluntary healthy women serving as a control group were evaluated by a detailed medical and sexual history, including the FSFI questionnaire. Serum prolactin, cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), dehydroepiandrosterone-SO 4 (DHEA-S), testosterone, estradiol and sex hormone-binding globulin (SHBG) levels were measured. No significant difference was observed between controls and patients in terms of the FSH, LH, estradiol, free thyroxine and thyrotropin (TSH), testosterone and DHEA-S levels. The comparison of total FSFI scores between patients and controls showed no significant difference (P ¼ 0.74). As the FSFI score of p26.55 indicated FSD, 86% of obese patients and 83% of controls were considered to have sexual dysfunction. The mean total FSFI score was 22.1±4.3 for obese patients and 23.1±3.7 for healthy women. FSFI scores were not correlated with any of the anthropometric measurements (body mass index (BMI), waist-to-hip ratio (WHR) and fat percent). The levels of total testosterone and DHEA-S were not correlated with total FSFI scores. We found a significant negative correlation between BMI and orgasm (P ¼ 0.007, r ¼ À0.413). Satisfaction was also negatively correlated with BMI (P ¼ 0.05, r ¼ À0.305) and weight (P ¼ 0.03, r ¼ À0.326). Testosterone levels were negatively correlated with only satisfaction domain scores of FSFI (P ¼ 0.01, r ¼ À0.385). We found that 86% of obese women and 83% of controls had sexual dysfunction. Although obesity does not seem to be a major contributor to sexual dysfunction, it affects several aspects of sexuality.

These results support the idea that adalimumab might be beneficial for severity of AP.

Long-term clinical use of methotrexate is connected with a raised risk of liver injury and fibrosis. Leflunomide is a disease-modifying drug. Leflunomide has a powerful inhibitory effect on nuclear factor kappa B activation. Leflunomide also presents antioxidant activity. In this experimental study, we aimed to investigate the effects of leflunomide treatment on methotrexate-induced hepatotoxicity. Materials and methods: Thirty-nine rats were divided into 4 groups. A single dose of 20mg/kg methotrexate was injected intraperitoneally for methotrexate-induced hepatotoxicity. After induction, leflunomide (10 mg/kg) was administered into the stomach for consecutive 5 days. Then, serum samples and homogenated liver tissues were collected for analyzed serum alanine aminotransferase, alkaline phosphatase, superoxide dismutase activity, myeloperoxidase activity, glutathione levels and assessment of histopathology. Results: Leflunomide treatment significantly ameliorated total histopathologic score according to semiquantitative scale compared to the untreated group, (Pathological score 1.1+0.7 versus 5.1+2 respectively, p<0,01). Leflunomide treatment significantly ameliorated Kuppfer cell activation. (Elevation of the activated Kupffer cells score were 0.2+0.6 and 2.5+1.01 respectively, p = 0.001). The serum alanine aminotransferase, alkaline phosphatase levels were lower and glutathione levels, myeloperoxidase activity, and superoxide dismutase activity were similar between leflunomide treated and untreated methotrexate toxicity groups. Conclusion: Leflunomide treatment ameliorated methotrexate induced liver toxicity in this experimental model.