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BackgroundIron (Fe) status of neonates born to women carrying multiple fetuses might be compromised as a consequence of the high prevalence of maternal Fe deficiency and anemia coupled with an increased risk of preterm birth. This study aimed to characterize and identify determinants of anemia in this neonatal population.MethodsUmbilical cord blood obtained from 183 neonates was utilized to assess hemoglobin (Hb), ferritin (SF), soluble transferrin receptor (sTfR), hepcidin, serum Fe, erythropoietin, folate, vitamin B-12, C-reactive protein, and interleukin-6. Associations with maternal Fe status were explored.ResultsCord Hb or SF did not change significantly as a function of gestational age at birth (25–38 wks). Neonates born to women who were obese prior to pregnancy or smoked cigarettes during pregnancy had a 4–5-fold greater odds of anemia at birth. Cord sTfR was the strongest indicator of cord Hb (P < 0.0001), and it was significantly associated with maternal sTfR at mid-gestation (P = 0.01) and delivery (P = 0.002). Cord Fe indicators were significantly associated with cord hepcidin, but not maternal hepcidin.ConclusionScreening for Fe status in neonates born to women carrying multiple fetuses is warranted, especially for those born to smokers or to women who are obese at entry into pregnancy.

The terminology and diagnostic criteria presently used by pathologists to report invasive placentation is inconsistent and does not reflect current knowledge of the pathogenesis of the disease or the needs of the clinical care team. A consensus panel was convened to recommend terminology and reporting elements unified across the spectrum of PAS specimens (i.e., delivered placenta, total or partial hysterectomy with or without extrauterine tissues, curetting for retained products of conception). The proposed nomenclature under the umbrella diagnosis of placenta accreta spectrum (PAS) replaces the traditional categorical terminology (placenta accreta, increta, percreta) with a descriptive grading system that parallels the guidelines endorsed by the International Federation of Gynaecology and Obstetrics (FIGO). In addition, the nomenclature for hysterectomy specimens is separated from that for delivered placentas. The goal for each element in the system of nomenclature was to provide diagnostic criteria and guidelines for expected use in clinical practice.

Eosinophilic/T-cell chorionic vasculitis (ETCV) is an inflammatory lesion of placental fetal vessels. In contrast to acute chorionic vasculitis, inflammation in ETCV is seen in chorionic vessel walls opposite the amnionic surface. It is not known whether inflammation in ETCV consists of maternal cells from the intervillous space or fetal cells migrating from the vessel. We used fluorescent in situ hybridization (FISH) to differentiate fetal versus maternal cells in ETCV. Placentas with ETCV, previously identified for a published study, were used. Infant sex in each case was identified using the electronic medical record. For male infants, 3-μm sections were cut from archived tissue blocks from placentas involving ETCV and stained with fluorescent X- and Y-chromosome centromeric probes. A consecutive hematoxylin/eosin-stained section was used for correlation. FISH analysis was performed on 400 interphase nuclei at the site of ETCV to determine the proportion of XX, XY, X, and Y cells. Of 31 ETCV cases, 20 were female and 10 were male (1 sex not recorded). Six of 10 cases with male infants had recuts with visible ETCV. In these 6 cases the average percentages (ranges) of XY cells, X-only cells, and Y-only cells in the region of inflammation were 81 (70–90), 11 (6–17), and 8 (2–14), respectively. There was a 2:1 female:male infant ratio in ETCV. Similar to acute chorionic vasculitis, the inflammation in ETCV is of fetal origin. It is still unknown, however, whether the stimulus for ETCV is of fetal or maternal origin.

Abstract Objectives Indications for cholecystectomy have changed dramatically over the past three decades. Cystoisospora belli has been reported in cholecystectomy specimens of immunocompetent patients. The present study was designed to determine the prevalence and clinical association of C belli in the gallbladder. Methods The study included retrospective review of cholecystectomy specimens (n = 401) removed for various indications, and a prospective cohort of cholecystectomy specimens (n = 22) entirely submitted for histologic evaluation. Correlations of presence of C belli with age, sex, clinical indication, and abnormalities of preoperative laboratory values were assessed by Fisher exact test. Results C belli was identified in 39/401 (9.7%) of the retrospective cohort, and 6/22 (27.3%) of the entirely submitted specimens. The presence of C belli showed no correlation with age, sex, clinical indication, or laboratory abnormalities. Conclusions C belli resides in a latent state in the gallbladder and may be best considered a commensal organism.

Collagenous mucosal inflammatory disease is a rare gastrointestinal disorder that involves the columnar lining of gastric and intestinal mucosa and is characterized by a distinct subepithelial collagen deposition. Recent clinical and pathological evidence have indicated that collagenous mucosal inflammatory disease can be extensive disease that may concomitantly involve several gastrointestinal sites at the same time. This entity, however, occurs infrequently in children. It is even less common to find concomitant depositions of collagen in the mucosa of gastrointestinal sites other than the colon. Only two cases in pediatric literature reported concomitant involvement, one with gastric and colonic involvement and the other one with gastroduodenocolitis. We are reporting a 15-month-old boy who presented with severe diarrhea and diffuse edema secondary to hypoalbuminemia. Further testing documented protein losing enteropathy (PLE) associated with collagenous colitis.

Eosinophilic/T-cell chorionic vasculitis (ETCV) is characterized by mixed T-cell, eosinophilic, and histiocytic infiltrates within the chorionic vessel wall. We sought to better characterize this lesion with respect to other pathologic correlates and the T-cell populations involved. Epidemiologic data and other pathologic diagnoses, including concurrent chronic villitis (CV), were tabulated for each case of ETCV diagnosed at our institution over a 6-year period. CD3, CD25, FOXP3, and dual FOXP3-CD3 immunostains were used to identify regulatory T-cell populations in ETCV and CV. Cells positive for CD3, FOXP3, and CD25 were quantitated by manual counts of ×40 fields at the sites of ETCV and CV, and FOXP3:CD3 and CD25:CD3 ratios were calculated. Digital analysis of ETCV and CV using the dual FOXP3-CD3 immunostain was also performed on select cases. Of 31 ETCV cases, 10 (32%) were accompanied by CV and 13 (42%) by a thrombus in the vessel affected by ETCV. The mean Treg cell marker: CD3 ratios in ETCV ranged from 0.18 to 0.26 by manual count and digital analysis, but the counts did not statistically differ by method. The mean Treg cell marker:CD3 ratios in CV ranged from 0.37 to 0.39 by manual count and 0.19 by digital analysis, but these counts also did not statistically differ by method. Chronic villitis was seen in one-third of ETCV cases. FOXP3+ and CD25+ regulatory T cells represent a significant subpopulation of T cells in ETCV and CV, suggesting that they may play a role in these entities.

Maternal T cells and fetal macrophages constitute the primary infiltrate of chronic villitis of unknown etiology (CVUE), but the role of CD25+/FOXP3+ regulatory T (Treg) cells in CVUE has not been examined. Moreover, little is known about the expression of immune markers, such as the major histocompatibility complex (MHC) class II antigen, human leukocyte antigen–DR (HLA-DR), in trophoblasts in this disease. We, therefore, examined CVUE placentas for the presence of Treg cells and aberrant activation of HLA-DR in trophoblasts. Sequential formalin-fixed, paraffin-embedded tissue sections from 8 CVUE placentas and 10 control placentas were stained by immunohistochemistry with antibodies for CD3, CD4, CD8, CD20, CD25, FOXP3, CD56, CD68, HLA-DR, STAT-1, and phosphorylated STAT-1 [P-(Y701)-STAT-1]. T cells and histiocytes were confirmed as the inflammatory infiltrate in CVUE. In areas of CVUE, histiocytes strongly expressed HLA-DR and nuclear P-(Y701)-STAT-1, and the relative numbers of CD25+/FOXP3+ Treg cells were increased, compared with control placentas. In 5 of 8 CVUE cases, there was patchy nuclear expression of P-(Y701)-STAT-1 in syncytiotrophoblast most extensively involved by villitis, but no other marker examined was detected in the trophoblast cell layer. We confirmed the influx of T cells and histiocytes in CVUE. Our results are the 1st, to our knowledge, to identify increased numbers of Treg cells in CVUE vs noninflamed placentas. However, we were unable to verify HLA-DR expression in trophoblasts of placentas with CVUE, suggesting that this does not contribute to the influx of T cells. Our observation that P-(Y701)-STAT-1 expression in a syncytiotrophoblast is restricted to regions of inflammation suggests that the JAK–STAT-1 pathway is aberrantly activated in these cells.

Anterior diaphragmatic defects with pericardial involvement are extremely rare and diagnostically challenging entities encountered perinatally. While a majority of diaphragmatic defects occur in isolation, others are associated with multiple defects forming a complex of syndromes such as Pentalogy of Cantrell. Liver herniation into the pericardial sac poses a particular challenge and can mimic a pericardial tumor on prenatal ultrasound, yielding a different management course. The following case is an unusual presentation of a 30 week gestation female with an anterior diaphragmatic defect with liver herniation mimicking as a pericardial tumor, diagnosed at time of autopsy. Postmortem studies also found multiple congenital anomalies including an atrioventricular defect and midline gumline defect suggesting at least a partial Pentalogy of Cantrell or variant. Early recognition and screening for associated anomalies are essential for management in this subset of patients.

This study investigates the hypotheses that (1) the fetal inflammatory response to intra-amniotic infection can occur in early stages of maternal inflammatory response and (2) a difference in early cord inflammation exists at different sites in the cord. Placentas accessioned in our department over a 4-year period with a differential in umbilical vessel inflammation between proximal and distal sections were evaluated for cord inflammation using a 0 to 4 graded scale. Cases were also evaluated for acute chorionic vasculitis and extent of maternal inflammatory response. Of 5566 placentas, 1004 (18%) had some degree of cord inflammation; 120 (12%) had a differential in inflammation between the 2 cord sites. Greater cord inflammation was divided almost equally between proximal (59) and distal (61) sections. Twenty-two cases had 1 or both arteries involved in 1 cord section only. The proximal section had the greater degree of inflammation in 21 (95%) of these cases. Early or no maternal inflammatory response was seen in 63 of 120 cases (52%). Acute chorionic vasculitis was identified in 57 of 106 cases (54%) with at least 2 chorionic vessels present. Fetal inflammatory response can be seen in early amniotic infection, occasionally without finding maternal inflammatory response. The absence of differences in cord vein inflammation depending on cord site and the finding that arteritis occurs close to the placental cord insertion site suggest that cord vessel blood flow dynamics play a role in neutrophil margination. At least 2 cord sections representing proximal and distal sites are recommended to exclude fetal inflammatory response.