Persistent Fetal Circulation Syndrome
"Persistent Fetal Circulation Syndrome" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A syndrome of persistent PULMONARY HYPERTENSION in the newborn infant (INFANT, NEWBORN) without demonstrable HEART DISEASES. This neonatal condition can be caused by severe pulmonary vasoconstriction (reactive type), hypertrophy of pulmonary arterial muscle (hypertrophic type), or abnormally developed pulmonary arterioles (hypoplastic type). The newborn patient exhibits CYANOSIS and ACIDOSIS due to the persistence of fetal circulatory pattern of right-to-left shunting of blood through a patent ductus arteriosus (DUCTUS ARTERIOSUS, PATENT) and at times a patent foramen ovale (FORAMEN OVALE, PATENT).
| Descriptor ID |
D010547
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| MeSH Number(s) |
C08.381.423.694 C16.614.694
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| Concept/Terms |
Persistent Fetal Circulation Syndrome- Persistent Fetal Circulation Syndrome
- Pulmonary Hypertension, Familial Persistent, of the Newborn
- ACD-MPV
- ACD MPV
- ACDMPV
- Alveolar Capillary Dysplasia With Misalignment Of Pulmonary Veins
- Persistent Fetal Circulation
- Circulation, Persistent Fetal
- Familial Persistent Pulmonary Hypertension of the Newborn
- Fetal Circulation, Persistent
- Hypertension, Pulmonary, of Newborn, Persistent
- Misalignment of the Pulmonary Vessels
- Persistent Pulmonary Hypertension of Newborn
- Alveolar Capillary Dysplasia With Misalignment Of Pulmonary Veins And Other Congenital Anomalies
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Below are MeSH descriptors whose meaning is more general than "Persistent Fetal Circulation Syndrome".
Below are MeSH descriptors whose meaning is more specific than "Persistent Fetal Circulation Syndrome".
This graph shows the total number of publications written about "Persistent Fetal Circulation Syndrome" by people in this website by year, and whether "Persistent Fetal Circulation Syndrome" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 2000 | 0 | 1 | 1 |
| 2002 | 1 | 0 | 1 |
| 2007 | 1 | 0 | 1 |
| 2010 | 0 | 1 | 1 |
| 2011 | 2 | 0 | 2 |
| 2012 | 3 | 0 | 3 |
| 2013 | 2 | 0 | 2 |
| 2014 | 2 | 0 | 2 |
| 2015 | 1 | 0 | 1 |
| 2016 | 4 | 0 | 4 |
| 2017 | 1 | 1 | 2 |
| 2018 | 1 | 0 | 1 |
| 2019 | 6 | 0 | 6 |
| 2020 | 1 | 1 | 2 |
| 2021 | 3 | 0 | 3 |
| 2022 | 3 | 0 | 3 |
| 2023 | 4 | 0 | 4 |
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Below are the most recent publications written about "Persistent Fetal Circulation Syndrome" by people in Profiles.
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Further refinement of the differentially methylated distant lung-specific FOXF1 enhancer in a neonate with alveolar capillary dysplasia. Clin Epigenetics. 2023 10 21; 15(1):169.
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Single Cell Multiomics Identifies Cells and Genetic Networks Underlying Alveolar Capillary Dysplasia. Am J Respir Crit Care Med. 2023 09 15; 208(6):709-725.
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Histologic features and decreased lung FOXF1 gene expression in severe bronchopulmonary dysplasia without a genetic diagnosis of alveolar capillary dysplasia. Pediatr Pulmonol. 2023 10; 58(10):2746-2749.
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Prenatal Detection of a FOXF1 Deletion in a Fetus with ACDMPV and Hydronephrosis. Genes (Basel). 2023 02 23; 14(3).
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High-level gonosomal mosaicism for a pathogenic non-coding CNV deletion of the lung-specific FOXF1 enhancer in an unaffected mother of an infant with ACDMPV. Mol Genet Genomic Med. 2022 11; 10(11):e2062.
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Variable expressivity in a four-generation ACDMPV family with a non-coding hypermorphic SNV in trans to the frameshifting FOXF1 variant. Eur J Hum Genet. 2022 10; 30(10):1182-1186.
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Do paternal deletions involving the FOXF1 locus on chromosome 16q24.1 manifest with more severe non-lung anomalies? Eur J Med Genet. 2022 Jun; 65(6):104519.
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Patent Ductus Arteriosus. Pediatr Rev. 2021 Nov; 42(11):632-634.
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Perturbation of semaphorin and VEGF signaling in ACDMPV lungs due to FOXF1 deficiency. Respir Res. 2021 Jul 27; 22(1):212.
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Lung-specific distant enhancer cis regulates expression of FOXF1 and lncRNA FENDRR. Hum Mutat. 2021 06; 42(6):694-698.