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The role of the complement system in first-time pathologic first-trimester miscarriage was investigated. In this case-control study, tissue samples of 126 women with pathologic miscarriage and termination of normal pregnancies were assessed. The pathologic pregnancy group consisted of 40 women with missed miscarriage, 13 women with incomplete miscarriage and 10 women with a blighted ovum. The control group consisted of 63 normal-appearing pregnancies. Immunoreactivity for C4d, Bb and MBL was evaluated in the deciduas and villous trophoblasts separately using a semi-quantitative histological scoring system (H-score). C4d and Bb H-scores were higher and MBL H-score was reduced in the deciduas and villous tissues from pathologic miscarriage compared to termination of pregnancies (p = .003 and p = .001; p = .011 and p < .001; p < .001 and p < .001, respectively). C4d and Bb activities were increased and MBL activity was decreased in human first-time pathologic first-trimester miscarriage. We suggest that three complement pathways may play a role in human first-time pathologic first-trimester miscarriage. Impact statement Previous studies focussed on complement proteins related to a single complement pathway in cases often associated with antiphospholipid syndrome (APS) or recurrent miscarriage. In APS-related cases, the classical pathway is activated. In antibody-dependent and in antibody-independent mouse models of foetal loss, classical and alternative pathways are activated, respectively. Lectin pathway deficiency has been reported in some recurrent miscarriage. The complement pathway or pathways, which have a role in human pathologic miscarriage was the starting point of this study. There has been no study done till now reporting the role of the three complement pathways in human pathologic miscarriage. In this study, we found increased classical and alternative complement pathway activities and decreased lectin pathway activity in tissues from first-time pathologic human miscarriage.

Peters plus syndrome is a rare congenital disorder that includes ocular anterior segment defects of the classic Peter’s anomaly, and is mostly associated with craniofacial and skeletal defects. A 21-week fetus was referred for further evaluation due to a suspicion of fetal hydrocephalus. An ultrasound examination revealed hyperechogenic lenses, microphthalmia, hypotelorism, retrognathia, mild ventriculomegaly, absence of the cavum septum pellucidum, and short stature. Amniocentesis and further microarray analysis revealed normal chromosomal copy numbers including the gene B3GALTL. In utero mort fetalis occurred at the 23rd gestational week. Ultrasound and fetal autopsy findings were suggestive of Peters plus syndrome, but the absence of the B3GALTL gene mutation made the diagnosis Peters plus-like syndrome. Obstetricians should consider Peters plus-like syndrome with prenatal detection of ocular anomalies along with craniofacial and skeletal anomalies with the absence of B3GALTL gene mutation.

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Gastrointestinal bleeding is a rare but potentially life-threatening manifestation of eosinophilic gastrointestinal disorders (EGIDs). Here, we describe a case series comprising 5 pediatric patients between 7 and 12 years of age, who presented to the emergency department with hematemesis and were subsequently diagnosed with EGID. Accompanying allergic history, peripheral eosinophilia, and total IgE elevation were common. Despite a more severe presentation, response to medical and dietary therapy was favorable. A comprehensive review of the literature revealed 26 other cases with similar findings that reinforced the importance of prompt recognition and early dietary and immunomodulating therapy in the control of this disease.