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Parasitic conjoined twins: external, internal (fetuses in fetu and teratomas), and detached (acardiacs)†
Article first published online: 25 OCT 2001
Copyright © 2001 Wiley-Liss, Inc.
Volume 14, Issue 6, pages 428–444, November 2001
How to Cite
Spencer, R. (2001), Parasitic conjoined twins: external, internal (fetuses in fetu and teratomas), and detached (acardiacs). Clin. Anat., 14: 428–444. doi: 10.1002/ca.1079
This article was adapted from the forthcoming book, Conjoined Twins: Embryology, Pathogenesis, and Review of the Literature, by Rowena Spencer, to be published by The Johns Hopkins University Press.
- Issue published online: 25 OCT 2001
- Article first published online: 25 OCT 2001
- Manuscript Revised: 14 MAR 2001
- Manuscript Received: 12 OCT 2000
- parasitic conjoined twins;
During the course of researching the embryologic etiology of conjoined twins, more than 1260 individual cases were collected from the literature and the reported abnormal anatomy tabulated and evaluated in the light of known embryology. It soon became apparent that the association of conjoined twins and their parasites with fetuses in fetu, acardiacs, and teratomas was more frequent than could be attributed to chance. These anomalous fetuses form a continuum, strongly suggesting that they are all variations of abnormal conjoined twinning, with the site of union and the extent of damage (or defect) of one embryo resulting in (1) an externally attached parasitic twin, (2) an enclosed fetus in fetu, (3) an internal teratoma, or (4) an acardiac connected via the placenta. Common patterns among them are a family history of twinning, the predominance of females, and the frequent presence of a twin or triplet accompanying the malformation. The several reports of chromosomal abnormality suggest that perhaps, at least on occasion, it is a genetically imperfect embryo that develops into a defective fetus. Of singular importance is the fact that rarely, if ever, is either a functional heart or a competent brain found in any of these abnormal fetuses, suggesting that the etiology of all of them is a primary cardiac malformation with secondary disruption in the development of the brain. Clin. Anat. 6:428–444, 2001. © 2001 Wiley-Liss, Inc.