Congenital GATA1-mutated myeloproliferative disorder in trisomy 21 complicated by placental fetal thrombotic vasculopathy

Loh, Tracy Jiezhen; Duan, Lian; Iyer, Prasad; Lam, Joyce Ching Mei; Kuick, Chik Hong; Aung, Aye C.L.; Chang, Kenneth Tou En

doi:10.1016/j.humpath.2014.07.019

Cited by 14 publications

(7 citation statements)

References 16 publications

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“…As described above, high grade FVM (fetal thrombotic vasculopathy) has the highest rate of associated adverse outcomes, particularly CNS abnormalities (cerebral palsy, neonatal encephalopathy, perinatal stroke, intracranial hemorrhage) . Less well established associations with placental FVM include maternal diabetes and a variety of fetal/neonatal abnormalities including necrotizing enterocolitis, congenital leukemia, neonatal alloimmune thrombocytopenia, gastroschisis, and non‐cardiac congenital malformations .…”

Section: Clinical Correlationsmentioning

confidence: 99%

Fetal vascular malperfusion, an update

Redline

Ravishankar

2018

APMIS

147

104

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Fetal vascular malperfusion is the most recent term applied to a group of placental lesions indicating reduced or absent perfusion of the villous parenchyma by the fetus. The most common etiology of malperfusion is umbilical cord obstruction leading to stasis, ischemia, and in some cases thrombosis. Other contributing factors may include maternal diabetes, fetal cardiac insufficiency or hyperviscosity, and inherited or acquired thrombophilias. Severe or high grade fetal vascular malperfusion is an important risk factor for adverse pregnancy outcomes including fetal growth restriction, fetal CNS injury, and stillbirth. Overall recurrence risk for subsequent pregnancies is low.

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Section: Clinical Correlationsmentioning

confidence: 99%

Fetal vascular malperfusion, an update

Redline

Ravishankar

2018

APMIS

147

104

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“…5 Last, hypercoagulable states due to fetal or maternal thrombophilia have also been associated with FTV. 4,11 Loh et al 4 report a case of fetal myeloproliferative disease, which resulted in hypercoagulable state and consequent FTV.…”

Section: Discussionmentioning

confidence: 99%

Fetal thrombotic vasculopathy: A case report and literature review

Peleja

Martinelli²,

Ribeiro³

et al. 2016

Rev. Assoc. Med. Bras.

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“…Shorter length of umbilical cord in DS compared with controls has been well documented. 14,18 Several authors 17,19 have described macroscopic occlusive thrombi in chorionic vessels and wedge-shaped pale zones within the villous parenchyma.…”

Section: Gross Pathology and Histopathologymentioning

confidence: 99%

“…A complete histopathologic evaluation of the placenta is emphasized, as most notable findings are observed microscopically. Leukocytosis with left-shifted hematopoietic elements and myeloid blasts can be seen within vessels of the umbilical cord, chorionic plate, and chorionic villi 12,16,17,[19][20][21][22] (Figure 2, A through D). These mononuclear blasts are characterized by large, lobulated nuclei with open chromatin, high nuclear to cytoplasmic ratio, prominent nucleoli, and associated apoptosis (Figure 2, E).…”

Section: Gross Pathology and Histopathologymentioning

confidence: 99%

“…Fetal vascular malformation with organizing thrombi containing blasts and associated downstream avascular villi are the histopathologic correlates to the grossly identified chorionic villous tree thrombi and pale zones within the parenchyma, respectively. 12,16,17,[19][20][21]23 It is believed that these fetal vascular malformation changes result from the hypercoagulable state triggered by the myeloproliferative disease in the fetus. Presence of fetal vascular malformation in TAM placentas may also help explain sudden perinatal clinical deterioration caused by thromboembolic spread to the fetal circulation via the umbilical vein.…”

Section: Gross Pathology and Histopathologymentioning

confidence: 99%

See 1 more Smart Citation

Placental Pathology in Down Syndrome–Associated Transient Abnormal Myelopoiesis

Kuo

Kumarapeli²

2019

Archives of Pathology &Amp; Laboratory Medicine

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Transient abnormal myelopoiesis is a hematopoietic disorder that occurs in up to 10% of neonates with Down syndrome. It is characterized by leukocytosis and the presence of circulating blast cells harboring truncating GATA1 mutations with variable multiorgan system involvement. Placental involvement of transient abnormal myelopoiesis is infrequently described. Placental examination and identifying features related to transient abnormal myelopoiesis could be one of the early, if not the only, means of diagnosis of this condition in affected stillbirths, premature infants, and a subset of asymptomatic neonates. This article provides an overview of the placental pathology in transient abnormal myelopoiesis with review of the literature, and also discusses the important differential diagnoses.

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Congenital GATA1-mutated myeloproliferative disorder in trisomy 21 complicated by placental fetal thrombotic vasculopathy

Cited by 14 publications

References 16 publications

Fetal vascular malperfusion, an update

Fetal vascular malperfusion, an update

Fetal thrombotic vasculopathy: A case report and literature review

Placental Pathology in Down Syndrome–Associated Transient Abnormal Myelopoiesis

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