Cause of fetal demise in first‐trimester parvovirus infection: anemia, placentitis or myocarditis?

Chalouhi, G. E.; Benedetti, Sara; Alby, Caroline; Benzina, N.; Ville, Y.

doi:10.1002/uog.13416

Cited by 5 publications

(2 citation statements)

References 5 publications

(4 reference statements)

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“…Hydrops fetalis, massive edema in the fetus associated with death in utero or at birth, is best characterized, and B19V is important in the consideration of the differential diagnosis of nonimmune hydrops. Hydrops follows most commonly midtrimester infection of the mother but may occasionally occur with earlier-and latertrimester transmission (485)(486)(487). B19V exposure in early pregnancy may increase the rate of spontaneous abortion.…”

Section: Clinical Manifestations Diseases Caused By B19v Infectionmentioning

confidence: 99%

Human Parvoviruses

2017

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Parvovirus B19 (B19V) and human bocavirus 1 (HBoV1), members of the large Parvoviridae family, are human pathogens responsible for a variety of diseases. For B19V in particular, host features determine disease manifestations. These viruses are prevalent worldwide and are culturable in vitro, and serological and molecular assays are available but require careful interpretation of results. Additional human parvoviruses, including HBoV2 to -4, human parvovirus 4 (PARV4), and human bufavirus (BuV) are also reviewed. The full spectrum of parvovirus disease in humans has yet to be established. Candidate recombinant B19V vaccines have been developed but may not be commercially feasible. We review relevant features of the molecular and cellular biology of these viruses, and the human immune response that they elicit, which have allowed a deep understanding of pathophysiology.

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Section: Clinical Manifestations Diseases Caused By B19v Infectionmentioning

confidence: 99%

Human Parvoviruses

2017

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“…Additionally, in immunocompromised patients, PVB19 can lead to prolonged anemia, myocarditis, hepatitis, and pneumonia [ 9 , 10 ]. Infection with PVB19 in pregnancy, even though it has no teratogenic effects, may lead to severe outcomes like spontaneous abortion, fetal hydrops, or intrauterine fetal death [ 11 , 12 , 13 , 14 ] in approximately 10% of infected fetuses, especially when it happens in the first two trimesters of pregnancy [ 15 ]. The estimated risk of transplacental infection is up to 33% [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Seroepidemiology of Human Parvovirus B19 Infection among the Population of Vojvodina, Serbia, over a 16-Year Period (2008–2023)

Vuković,

Patić,

Ristić

et al. 2024

Viruses

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This study aimed to estimate the serological status and dynamic changes in the prevalence of Parvovirus B19 (PVB19) antibodies within the general population residing in the northern part of the Republic of Serbia (Province of Vojvodina) during a 16-year period. Serum samples were analyzed for Human PVB19-specific IgM and IgG antibodies using enzyme-linked immunosorbent assay (ELISA). Throughout the study period, the overall seroprevalence was 49.51%. Approximately 10% of patients exhibited a serologic profile positive for PVB19 IgM antibodies. Notably, seroprevalence varied significantly, ranging from 9.12% in the pediatric cohort (ages 1–4 years) to 65.50% in the adult demographic (40–59 years old). Seroprevalence was higher (51.88%) among women compared to men (42.50%). Immunologically naive pregnant women in the age groups 26–36 and 36–45 years had 45% (OR = 0.55, 95% CI: 0.31–1.00) and 52% (OR = 0.48; 95% CI: 0.24–0.94) lower odds of having negative IgM and IgG compared to those in age group 16–25 years old. Improved knowledge of the epidemiology of PVB19 may assist clinicians in the differential diagnosis of PVB19 clinical manifestations. The PVB19 detection is particularly important for monitoring individuals in risk groups such as women of reproductive age, medical staff, patients with hematological disorders, and those with immunodeficiency.

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The prediction of fetal death with a simple maternal blood test at 24-28 weeks: a role for angiogenic index-1 (PlGF/sVEGFR-1 ratio)

Chaiworapongsa

Romero

Erez

et al. 2017

American Journal of Obstetrics and Gynecology

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Objective To determine if maternal plasma concentrations of angiogenic and anti-angiogenic factors measured at 24–28 weeks of gestation can predict subsequent fetal death. Methods A case-cohort study was designed to include 1000 randomly selected subjects and all remaining fetal deaths (cases) from a cohort of 4006 women with a singleton pregnancy, enrolled at 6–22 weeks of gestation, in a pregnancy biomarker cohort study. The placentas of all fetal deaths were histologically examined by pathologists who used a standardized protocol and were blinded to patient outcomes. Placental growth factor (PlGF), soluble endoglin (sEng), and soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) concentrations were measured by ELISA assays. Quantiles of the analyte concentrations (or concentration ratios) were estimated as a function of gestational age among women who delivered live neonates but did not develop preeclampsia or deliver small-for-gestational–age (SGA) newborns. A positive test was defined as analyte concentrations (or ratios) <2.5th and 10th centiles [PlGF, PlGF/sVEGFR-1 (angiogenic index-1), and PlGF/sEng)] or >90th and 97.5th centiles (sVEGFR-1 and sEng). Inverse probability weighting was used to reflect the parent cohort when estimating the relative risk. Results There were 11 fetal deaths and 829 controls with samples available for analysis between 24–28 weeks of gestation. Three fetal deaths occurred prior to 28 weeks and eight at or after 28 weeks of gestation. The rate of placental lesions consistent with maternal vascular underperfusion was 33.3% (1/3) among those who had a fetal death before 28 weeks and 87.5% (7/8) of those who had this complication at or after 28 weeks of gestation. The maternal plasma angiogenic index-1 value was below the 10th centile in 63.6% (7/11) of the fetal death group and in 11.1% (92/829) of the controls. The angiogenic index-1 value was <2.5th centile in 54.5% (6/11) of the fetal death group and in 3.7% (31/829) of the controls. An angiogenic index-1 value <2.5th centile had the largest positive likelihood ratio for predicting fetal death >24 weeks (14.6; 95% CI, 7.7–27.7) and a relative risk of 29.1 (95% CI, 8.8–97.1), followed by sEng >97.5thcentile and PlGF/sEng <2.5th, both with a positive likelihood ratio of 13.7 (95% CI, 7.3–25.8) and a relative risk of 27.4 (95% CI, 8.2–91.2). Among women without a fetal death whose plasma angiogenic index-1 concentration ratio was below the 2.5th centile, 61% (19/31) developed preeclampsia or delivered an SGA neonate; when the 10th centile was used as the cut-off, 37% (34/92) of women had these adverse outcomes. Conclusions 1) A maternal plasma angiogenic index-1 value below the 2.5th centile (0.126) at 24–28 weeks of gestation carries a 29-fold increase in the risk of subsequent fetal death and identifies 55% of subsequent fetal deaths with a false-positive rate of 3.5%; and 2) 61% of women who have a false-positive test result will subsequently experience adverse pregnancy outcomes.

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Cause of fetal demise in first‐trimester parvovirus infection: anemia, placentitis or myocarditis?

Cited by 5 publications

References 5 publications

Human Parvoviruses

Human Parvoviruses

Seroepidemiology of Human Parvovirus B19 Infection among the Population of Vojvodina, Serbia, over a 16-Year Period (2008–2023)

The prediction of fetal death with a simple maternal blood test at 24-28 weeks: a role for angiogenic index-1 (PlGF/sVEGFR-1 ratio)

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