Pathoanatomical Lesions in Placentas With Excessively Hypercoiled Umbilical Cords: Frequent Detection of Massive Perivillous Fibrin Deposition.

This study focused to investigate a possible association of extensive umbilical hypercoiling (displaying an umbilical coiling index [UCI] of at least 1.0 coils/cm), clinical outcome, and associated pathoanatomical placental lesions. Of the 771 singleton placentas from the second and third trimesters submitted for pathoanatomical evaluation, 15 cases (2%) displayed extensive hypercoiling. There was an association of excessive hypercoiling with hypotrophy of fetuses and children (11 cases) and fetal demise (12 cases). Thin cord syndrome and umbilical stricture were observed in 9 cases and 4 cases, respectively. Seven of the 15 cases with excessive umbilical hypercoiling showed increased placental fibrin deposition (47% of the cases with hypercoiling), in 4 cases sufficient for rendering the diagnosis of massive perivillous fibrin deposition. Signs of maternal vascular malperfusion (n = 6) and chorangiosis (n = 2) were also detected in cases with hypercoiling. Recurrence of excessive umbilical hypercoiling was observed in 2 families, suggesting a genetic predisposition for the development of this lesion. Extensive hypercoiling could be a hitherto underrecognized pathogenetic factor for the development of massive perivillous fibrin deposition. A high UCI measured in the second trimester by ultrasound may be predictive of fetal hypotrophy, and intensified fetal monitoring is warranted, particularly if there is a history of hypercoiling and adverse fetal outcome.

Massive Perivillous Fibrin Deposition of an Enterovirus A-Infected Placenta Associated With Stillbirth: A Case Report.

Massive perivillous fibrin deposition (MFD) is a morphologically defined severe placental lesion associated with perinatal morbidity and mortality. The etiology is unknown, and recurrence risk in subsequent pregnancies is assumed to be high. In most cases, a pathologic immune reaction is supposed to be responsible for the lesion. We report a case of a pregnant woman's suffering from hand, foot, and mouth disease in the 20th gestational week. Subsequently, MFD developed in the placenta and was followed by intrauterine growth restriction and stillbirth in the 29th gestational week. Enterovirus A with high homology to Coxsackievirus A16 was detected in the placenta by means of immunohistochemisty and reverse transcription polymerase chain reaction. This infection could be a rare cause of MFD and should be taken into consideration in the differential diagnosis of the individual etiology. Recurrence risk of virus-related MFD is expected to be lower than in MFD without infectious association.

Discordancy for a Villous Maturation Defect in a Dizygotic Twin Placenta.

Background: Dizygotic twin pregnancies with discordant manifestation of abnormalities with unclear etiology are of interest because they arise in the same environment. Case report: We present a dizygotic third trimester twin placenta with discordant villous maturation, one placenta lacking developed syncytiocapillary membranes. The twins were eutrophic with no perinatal or postnatal complications. Conclusions: Discordant manifestation of villous maturation in dizygotic twin placentas could be a hint for a genetic rather than an environmental etiology. Villous maturation defect may be underrecognized and has been associated with perinatal morbidity and stillbirth in the late third trimester. Proper recognition is important because of the increased recurrence risk of villous dysmaturity.

Measurement site for waist circumference affects its accuracy as an index of visceral and abdominal subcutaneous fat in a Caucasian population.

Following experts' consensus, waist circumference (WC) is the best anthropometric obesity index. However, different anatomic sites are used, and currently there is no universally accepted protocol for measurement of WC. In this study, we compare the associations between WC measured at different sites with total visceral adipose tissue (VAT) volume and cardiometabolic risk. Cross-sectional data were obtained from 294 adults and 234 children and adolescents. In addition, longitudinal data were provided in 75 overweight adults before and after dietary-induced weight loss. WC was measured below the lowest rib (WC(rib)), above the iliac crest (WC(iliac crest)), and midway between both sites (WC(middle)). Volumes of VAT and abdominal subcutaneous adipose tissue (SAT) were obtained using MRI. Cardiometabolic risk included blood pressure, plasma lipids, glucose, and homeostasis model (HOMA index). WC differed according to measurement site as WC(rib) < WC(middle) < WC(iliac crest) (P < 0.001) in children and women, and WC(rib) < WC(middle), WC(iliac crest) (P < 0.001) in men. Elevated WC differed by 10-20% in females and 6-10% in males, dependent on measurement site. In men and children, all WC had similar relations with VAT, SAT, and cardiometabolic risk factors. In women, WC(rib) correlated with weight loss-induced decreases in VAT (r = 0.35; P < 0.05). By contrast, WC(iliac crest) had the lowest associations with VAT and cardiometabolic risk factors in women. Each WC had a stronger correlation with SAT than with VAT, suggesting that WC is predominantly an index of abdominal subcutaneous fat. There is need for a unified measurement protocol.

Villitis of unknown etiology and chronic deciduitis are not associated with human papilloma virus and enterovirus infection.

Villitis of unknown etiology (VUE) and chronic deciduitis with plasma cells (CD) are supposed to be non infectious placental lesions caused by a pathologic immune reaction similar to a host versus graft mechanism. In some investigations, infection of human trophoblastic cells with human papilloma virus (HPV) has been described, and a relationship with miscarriage, preeclampsia, and chronic inflammatory placental lesions has been suspected. Infection with enterovirus, especially Coxsackievirus, has been observed in cases with spontaneous abortion and adverse perinatal outcome, respectively. We investigated 20 cases with VUE and 30 cases with chronic deciduitis with plasma cells. The placenta specimens were analyzed for expression of HPV capsid protein by immunohistochemistry, for presence of HPV DNA via polymerase chain reaction (PCR), and for presence of enterovirus mRNA using RT-PCR, respectively. VUE was associated with maternal diseases: atopic lesions in 21%, other autoimmune diseases in 15.5%, and obesity in 31.5%, respectively. Birth weight below the 10th percentile was detected in 63% of the cases with VUE. Chronic deciduitis was associated with preterm labor and preterm premature rupture of membranes (26%). Intrauterine fetal demise occurred in 5 cases with CD (18.5%). HPV DNA, HPV capsid protein, and enterovirus mRNA were not detected in all investigated VUE or CD cases. Our investigations show that a causal role for enterovirus and human papilloma virus in the development of VUE and CD is unlikely. Therefore, HPV vaccination is unlikely to reduce the incidence of VUE and CD in the future.

Discordancy for Placental Massive Perivillous Fibrin Deposition and Fetal Growth in Dichorionic Twins after In Vitro Fertilization.

Massive perivillous fibrin deposition (MFD) is a placental lesion of unknown etiology associated with perinatal morbidity and mortality and recurrence risk in subsequent pregnancies. We report a 34 weeks' gestation dizygotic twin pregnancy with discordancy for MFD and for intrauterine growth restriction after in vitro fertilization (IVF). Only the smaller twin corresponding to the placenta affected by MFD showed intrauterine growth restriction, with a weight below the 3rd percentile according to gestational age. The affected placenta showed a moderate increase in decidual lymphocytes. No difference in expression of complement factor C4d in umbilical veins could be observed. Development of MFD in one of the dizygotic placentas may be due to a pathologic immune response to one of the different fetal genotypes as semiallografts. The pathogenetic role of IVF as an environmental factor for development of MFD is unclear.

Association of pericardial fat with liver fat and insulin sensitivity after diet-induced weight loss in overweight women.

Pericardial adipose tissue (PAT) is positively associated with fatty liver and obesity-related insulin resistance. Because PAT is a well-known marker of visceral adiposity, we investigated the impact of weight loss on PAT and its relationship with liver fat and insulin sensitivity independently of body fat distribution. Thirty overweight nondiabetic women (BMI 28.2-46.8 kg/m(2), 22-41 years) followed a 14.2 ± 4-weeks low-calorie diet. PAT, abdominal subcutaneous (SAT), and visceral fat volumes (VAT) were measured by magnetic resonance imaging (MRI), total fat mass, trunk, and leg fat by dual-energy X-ray absorptiometry and intrahepatocellular lipids (IHCL) by ((1))H-magnetic resonance spectroscopy. Euglycemic hyperinsulinemic clamp (M) and homeostasis model assessment of insulin resistance (HOMA(IR)) were used to assess insulin sensitivity or insulin resistance. At baseline, PAT correlated with VAT (r = 0.82; P < 0.001), IHCL (r = 0.46), HOMA(IR) (r = 0.46), and M value (r = -0.40; all P < 0.05). During intervention, body weight decreased by -8.5%, accompanied by decreases of -12% PAT, -13% VAT, -44% IHCL, -10% HOMA2-%B, and +24% as well as +15% increases in HOMA2-%S and M, respectively. Decreases in PAT were only correlated with baseline PAT and the loss in VAT (r = -0.56; P < 0.01; r = 0.42; P < 0.05) but no associations with liver fat or indexes of insulin sensitivity were observed. Improvements in HOMA(IR) and HOMA2-%B were only related to the decrease in IHCL (r = 0.62, P < 0.01; r = 0.65, P = 0.002) and decreases in IHCL only correlated with the decrease in VAT (r = 0.61, P = 0.004). In conclusion, cross-sectionally PAT is correlated with VAT, liver fat, and insulin resistance. Longitudinally, the association between PAT and insulin resistance was lost suggesting no causal relationship between the two.