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COVID-19 and hydatidiform mole.
Abbas, AM, Ahmed, L, Salem, AS, Elsamman, SH, Refai, A, Fathy, SK, Ahmed, OA, Shalotut, AS, AbdelWahab, RA
American journal of reproductive immunology (New York, N.Y. : 1989). 2020;(5):e13310
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Abstract
The emergence of coronavirus disease 2019 (COVID-19) as a pandemic threatens the entire world resulting in severe consequences for people's health. Pregnant patients with COVID-19 had immune dysregulation that could result in abnormal pregnancy outcomes such as hydatidiform mole (HM), recurrent pregnancy loss, and early-onset preeclampsia. In this article, we tried to summarize the possible association between COVID-19 and the HM's development by reviewing the role of NOD-Like Receptor (NLR) Family Pyrin Domain Containing 7 (NLRP7), cytokines, zinc, and leukocytes in the pathogenesis of HM.
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Intracellular Pathogen Infections and Immune Response in Autism.
Abib, RT, Gaman, A, Dargél, AA, Tamouza, R, Kapczinski, F, Gottfried, C, Leboyer, M
Neuroimmunomodulation. 2018;(5-6):271-279
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Abstract
BACKGROUND/AIMS: Perinatal exposure to infections during critical developmental periods is a promising area of study in autism spectrum disorder (ASD). Epidemiological data has highlighted this relationship, pointing out significant correlations between perinatal exposure to pathogens and the occurrence of ASD. The aim of this review is to critically examine the present state of the art on intracellular pathogenic infection during pregnancy and postnatally, pointing out possible correlations with the development of ASD. METHODS We reviewed and collected studies concerning potential associations between intracellular pathogens like viral, bacterial, and parasite infection and the risk of ASD. RESULTS We included 14 publications, considering bacterial and/or viral infection that demonstrated the potential to trigger ASD. Nine case-control studies were included and 5 of them reported an association between infections and ASD. One of the 2 cohorts investigated demonstrated that maternal infection increased the risk of ASD in the offspring. Three cross-sectional studies demonstrated that ASD patients presented with chronic infections and active neuroinflammatory processes. Most of the reports suggest inflammatory response as a common factor, and interleukin 6 appears to be a key-player in this process. CONCLUSION The immune responses generated by organisms that cause perinatal maternal infection, i.e., bacteria, viruses, or parasites, have been associated with the development of autism in offspring. Physiological changes transmitted from the mother during chronic or acute inflammation should be further investigated so that modulatory preventive measures can be developed.
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Impact of Timing of Influenza Vaccination in Pregnancy on Transplacental Antibody Transfer, Influenza Incidence, and Birth Outcomes: A Randomized Trial in Rural Nepal.
Katz, J, Englund, JA, Steinhoff, MC, Khatry, SK, Shrestha, L, Kuypers, J, Mullany, LC, Chu, HY, LeClerq, SC, Kozuki, N, et al
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2018;(3):334-340
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Abstract
BACKGROUND Maternal influenza vaccination protects mothers and their infants in low resource settings, but little is known about whether the protection varies by gestational age at vaccination. METHODS Women of childbearing age in rural southern Nepal were surveilled for pregnancy, consented and randomized to receive maternal influenza vaccination or placebo, with randomization stratified on gestational age (17-25 or 26-34 weeks). Enrollment occurred in 2 annual cohorts, and vaccinations occurred from April 2011 through September 2013. RESULTS In sum, 3693 women consented and enrolled, resulting in 3646 live births. Although cord blood antibody titers and the rise in maternal titers were generally greater when women were vaccinated later in pregnancy, this was not statistically significant. The incidence risk ratio (IRR) for maternal influenza in pregnancy through 6 months postpartum was 0.62 (95% confidence interval [CI]: 0.35, 1.10) for those vaccinated 17-25 weeks gestation and 0.89 (95% CI: 0.39, 2.00) for those 26-34 weeks. Infant influenza IRRs were 0.73 (95% CI: 0.51, 1.05) for those whose mothers were vaccinated earlier in gestation, and 0.63 (95% CI: 0.37, 1.08) for those later. Relative risks (RR) for low birthweight were 0.83 (95% CI: 0.71, 0.98) and 0.90 (95% CI: 0.72, 1.12) for 17-25 and 26-34 weeks gestation at vaccination, respectively. IRRs did not differ for small-for-gestational age or preterm. No RRs were statistically different by timing of vaccine receipt. CONCLUSIONS Vaccine efficacy did not vary by gestational age at vaccination, making maternal influenza immunization programs easier to implement where women present for care late in pregnancy. CLINICAL TRIALS REGISTRATION NCT01034254.