3 resultados para Sexually Transmitted Diseases.

em CORA - Cork Open Research Archive - University College Cork - Ireland


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Background: Human papillomavirus (HPV) causes cervical cancer and external genital warts. The purpose of this study is to document the genotype distribution of HPV in females aged between 18 and 34 who self-referred to an STI clinic with visible external genital warts (EGW). Scrapings were taken from visible external genital warts (EGW). These scrapings were analysed by PCR for the presence of HPV DNA. Positive samples were then genotyped by means of a commercially available assay (LiPA). A comparison of genotyping results determined by the LiPA assay and direct amplicon DNA sequencing was also performed. Results: Ninety-two patients out of 105 samples (88%) had detectable levels of HPV DNA. The majority of individuals with EGW (66%) showed the presence of two or more genotypes. The most common HPV genotypes present in the study population were HPV-6, HPV-11, HPV-16, HPV-18, HPV-33 and HPV-53. Potential effects of vaccination on HPV molecular epidemiology indicate that 40% of the patients could have been protected from the high risk genotypes HPV-16 and HPV-18.Conclusion: This is the first report of the molecular epidemiology of external genital warts in women aged between 18 and 34 from Ireland based on results from a LiPA assay. The study shows that most individuals are infected with multiple genotypes including those with high oncogenic potential and that the newly available HPV vaccines could have a significant impact on prevalence of the most common HPV genotypes in this study population.

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Objective: The burden of sexually transmitted infections (STIs) rests with young people, yet in Ireland there has been very little research into this population. The purpose of this study was to determine the incidence rate and establish risk factors that predict STI occurrence among adolescents in Ireland. Design: Routine diagnostic, demographic and behavioural data from first-time visits to three screening centres in the southwest of Ireland were obtained. Univariate and multivariable logistic regression models were used to assess risk factors that predict STI occurrence among adolescents. Results: A total of 2784 first-time patients, aged 13–19 years, received 3475 diagnoses between January 1999 and September 2009; 1168 (42%) of adolescents had notifiable STIs. The incidence rate of STIs is 225/100 000 person-years. Univariate analysis identified eligible risk factors (p<0.2) for inclusion in the multivariable model. Multivariable logistic regression showed the dominant risk factors for STI diagnosis to be: males who sometimes [odds ratio (OR) 2.02] or never (OR 1.83) use condoms; and females 18–19 years (OR 2.26) and 16–18 years (OR 1.8), with 2 (OR 1.33) or 3+ (OR 1.56) partners in the last 12 months, who are non-intravenous drug users (OR 0.72), are most likely to receive a positive STI diagnosis. Conclusions: STI diagnosis has become increasingly common in Ireland. The proportion of notifications among those aged under 20 years is increasing. These data illustrate the significance of age, condom use and number of sexual partners as risk factors for STI diagnosis. Furthermore, providing data for the first time, we report on the high incidence rate of STIs among adolescents in Ireland. The high levels of risk-taking behaviour and STI acquisition are highlighted and suggest that there is a need for an integrated public health approach to combat this phenomenon in the adolescent population.

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Sex differences occur in most non-communicable diseases, including metabolic diseases, hypertension, cardiovascular disease, psychiatric and neurological disorders and cancer. In many cases, the susceptibility to these diseases begins early in development. The observed differences between the sexes may result from genetic and hormonal differences and from differences in responses to and interactions with environmental factors, including infection, diet, drugs and stress. The placenta plays a key role in fetal growth and development and, as such, affects the fetal programming underlying subsequent adult health and accounts, in part for the developmental origin of health and disease (DOHaD). There is accumulating evidence to demonstrate the sex-specific relationships between diverse environmental influences on placental functions and the risk of disease later in life. As one of the few tissues easily collectable in humans, this organ may therefore be seen as an ideal system for studying how male and female placenta sense nutritional and other stresses, such as endocrine disruptors. Sex-specific regulatory pathways controlling sexually dimorphic characteristics in the various organs and the consequences of lifelong differences in sex hormone expression largely account for such responses. However, sex-specific changes in epigenetic marks are generated early after fertilization, thus before adrenal and gonad differentiation in the absence of sex hormones and in response to environmental conditions. Given the abundance of X-linked genes involved in placentogenesis, and the early unequal gene expression by the sex chromosomes between males and females, the role of X- and Y-chromosome-linked genes, and especially those involved in the peculiar placenta-specific epigenetics processes, giving rise to the unusual placenta epigenetic landscapes deserve particular attention. However, even with recent developments in this field, we still know little about the mechanisms underlying the early sex-specific epigenetic marks resulting in sex-biased gene expression of pathways and networks. As a critical messenger between the maternal environment and the fetus, the placenta may play a key role not only in buffering environmental effects transmitted by the mother but also in expressing and modulating effects due to preconceptional exposure of both the mother and the father to stressful conditions.