ABSTRACT
Preeclampsia is a pregnancy-specific disorder, of which one of its major subtypes, the placental subtype is considered a response to an ischemic placental environment, impacting fetal growth and pregnancy outcome. Inflammatory immune responses have been linked to metabolic and inflammatory disorders as well as reproductive failures. In healthy pregnancy, immune regulatory mechanisms prevent excessive systemic inflammation. However, in preeclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differentiation of T-helper cell subsets creating a cytotoxic environment in utero. Recognition events that facilitate immune interaction between maternal decidual T cells, NK cells, and cytotrophoblasts are considered an indirect cause of the incomplete remodeling of spiral arteries in preeclampsia. The mechanisms involved include the activation of immune cells and the subsequent secretion of cytokines and placental growth factors affecting trophoblast invasion, angiogenesis, and eventually placentation. In this review, we focus on the role of excessive systemic inflammation as the result of a dysregulated immune system in the development of preeclampsia. These include insufficient control of inflammation, failure of tolerance toward paternal antigens at the fetal-maternal interface, and subsequent over- or insufficient activation of immune mediators. It is also possible that external stimuli, such as bacterial endotoxin, may contribute to the excessive systemic inflammation in preeclampsia by stimulating the release of pro-inflammatory cytokines. In conclusion, a disrupted immune system might be a predisposing factor or result of placental oxidative stress or excessive inflammation in preeclampsia. Preeclampsia can thus be considered a hyperinflammatory state associated with defective regulation of the immune system proposed as a key element in the pathological events of the placental subtype of this disorder.
ABSTRACT
INTRODUCTION: Occupational injuries in medical students are concerning, especially in countries with a high prevalence of bloodborne infections. With more HIV-infected patients on antiretroviral treatment, appropriate post-exposure prophylaxis (PEP) depends on knowledge of source patients' infection status and treatment response. This study determined the number and type of exposure incidents, reporting practices, and PEP use among medical students at the University of Pretoria, South Africa. METHODOLOGY: Data were collected from an anonymous voluntary questionnaire completed by medical students from years 1 to 6 of study as well as from incident records archived at the Department of Family Medicine. Data were described and tests of association performed in Stata 11. RESULTS: Thirteen percent of students overall and 21% of senior students reported an incident in the preceding year. The majority of incidents occurred during phlebotomy, with fatigue and work pressure found to be major contributing factors. Underreporting was common and many students displayed a lack of risk awareness and a preference for managing the incident privately. Although 59% knew the HIV-status of the source patient, less than a third knew the viral load and only 16.9% the regimen. Side-effects on antiretroviral treatment used for PEP were common and only about three-quarters of the students completed the course. CONCLUSIONS: We recommend targeted training, especially in the senior years, together with improving the work environment through attention to working hours, sharps disposal and ready availability of safety devices, improved reporting systems, individualised PEP, and possibly the implementation of an occupational injury support line.
