Impact of Chlamydia trachomatis in the reproductive setting: British Fertility Society Guidelines for practice

Chlamydia trachomatis infection of the genital tract is the most common sexually transmitted infection and has a world-wide distribution. The consequences of infection have an adverse effect on the reproductive health of women and are a common cause of infertility. Recent evidence also suggests an adverse effect on male reproduction. There is a need to standardise the approach in managing the impact of C. trachomatis infection on reproductive health. We have surveyed current UK practice towards screening and management of Chlamydia infections in the fertility setting. We found that at least 90% of clinicians surveyed offered screening. The literature on this topic was examined and revealed a paucity of solid evidence for estimating the risks of long-term reproductive sequelae following lower genital tract infection with C. trachomatis. The mechanism for the damage that occurs after Chlamydial infections is uncertain. However, instrumentation of the uterus in women with C. trachomatis infection is associated with a high risk of pelvic inflammatory disease, which can be prevented by appropriate antibiotic treatment and may prevent infected women from being at increased risk of the adverse sequelae, such as ectopic pregnancy and tubal factor infertility. Recommendations for practice have been proposed and the need for further studies is identified

Risk of death after first admission for cardiovascular diseases by country of birth in The Netherlands: a nationwide record-linked retrospective cohort study

OBJECTIVE: To examine differences in short- (28 days) and long-term (5 years) risk of death in patients hospitalised for the first time for various cardiovascular diseases (CVD) by country of birth and/or parental country of birth. DESIGN: A nationwide prospective cohort of CVD patients. Settings: Entire Netherlands. PATIENTS: 118 691 patients hospitalised for the first time for various CVDs were identified through the national hospital discharge, the Dutch population and the cause-of-death registers. MAIN OUTCOME MEASURES: Differences in short-term and long-term risk of death. Cox proportional hazard models were used to estimate the mortality hazard ratios. RESULTS: After adjusting for age, compared with Dutch patients, Turkish, other non-Western and Western migrants had both a short- and long-term higher risk, while Suriname patients had only a long-term higher risk of total-mortality and combined-CVD mortality. These higher rates were driven mainly by an increased risk of short-term (hazard ratio 3.21; 95% CI 1.03 to 10.03) and long-term (2.29; 1.14 to 4.60) mortality following congestive heart failure (CHF) among Turkish; short-term (1.56; 1.10 to 2.20) and long-term (1.50; 1.11 to 2.01) mortality following cerebrovascular accident (CVA) among the other non-Western migrants; short-term mortality following CVA (1.10; 1.01 to 1.19) and long-tem mortality following CVA (1.10; 1.03 to 1.17), and, to a lesser extent, CHF and myocardial infarction among Western migrants; and a long-term mortality following CVA (1.29; 1.05 to 1.57) among Surinamese patients. CONCLUSION: Higher mortality after a first episode of CVD was found in ethnic minority patients than in Dutch patients. These differences hardly changed after adjusting for possible confounders, suggesting that treatment and secondary prevention strategies may be less effective in these groups. More research is needed to explain the possible causes of these inequalitie

Immunological analysis of treatment interruption after early highly active antiretroviral therapy

We longitudinally evaluated HIV-specific T-cell immunity after discontinuation of highly active antiretroviral therapy (HAART). After treatment interruption (TI), some individuals could maintain a low plasma viral load (50,000 copies/mL). Before HAART was initiated, plasma viral load was similar. After TI, the numbers of CD8+ T cells increased more in individuals without viral control, whereas individuals maintaining a low viral load showed a more pronounced increase in HIV-specific CD8+ T-cell numbers. No differences were seen in the number or percentage of cytokine-producing HIV-1-specific CD4+ T cells, or in proliferative capacity of T cells. Four weeks after TI, the magnitude of the total HIV-1-specific CD8+ T-cell response (IFN-γ+ and/or IL-2+ and/or CD107a+) was significantly higher in individuals maintaining viral control. Degranulation contributed more to the overall CD8+ T-cell response than cytokine production. Whether increased T-cell functionality is a cause or consequence of low viral load remains to be elucidated