Multiple thromboembolic events in fetofetal transfusion syndrome in triplets contributing to the understanding of pathogenesis of hydranencephaly in combination with polymicrogyria

Mittelbronn, Michel; Beschorner, Rudi; Schittenhelm, Jens; Capper, David; Goeppert, Benjamin; Meyermann, Richard; Meyer‐Wittkopf, M.; Mackensen-Haen, S

doi:10.1016/j.humpath.2006.07.005

Cited by 14 publications

(7 citation statements)

References 11 publications

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“…Polymicrogyria is thought to occur during or after the neuronal migration period. 25 It has been described before in case reports of infants with TTTS, [26][27][28] and in the infant in our study it may have been due to a vascular insult that occurred after the fetal MRI, performed at about 20 weeks in this patient. Multiple types of brain injury have been described in infants with TTTS.…”

Section: Discussionsupporting

confidence: 58%

Fetal and postnatal brain MRI in premature infants with twin–twin transfusion syndrome

et al. 2012

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Section: Discussionsupporting

confidence: 58%

Fetal and postnatal brain MRI in premature infants with twin–twin transfusion syndrome

et al. 2012

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“…Therefore, the majority of defects caused by tissue damage through vascular disruption occur in structures supplied by the most peripheral vasculature, such as the distal limbs and the embryonic intestine (Jones, 1991;Los et al, 1999). Birth defects that were attributed to vascular disruption include terminal limb reductions (Kino, 1975;Hoyme et al, 1982), hydranencephaly/porencephaly (Hoyme et al, 1981a;Mittelbronn et al, 2006), gastroschisis (Hoyme et al, 1981b;Komuro et al, 2003), small intestinal atresia (Louw and Barnard, 1955;Cragan et al, 1994) and Poland anomaly (Shalev and Hall, 2003;Puvabanditsin et al, 2005). However, there are no known experimental models for the complete range of birth defects caused by vascular disruption.…”

Section: Vascular Disruptionmentioning

confidence: 99%

Teratogenic mechanisms of medical drugs

Gelder

Rooij

Miller

et al. 2010

Human Reproduction Update

168

125

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BACKGROUND Although prescription drug use is common during pregnancy, the human teratogenic risks are undetermined for more than 90% of drug treatments approved in the USA during the past decades. A particular birth defect may have its origins through multiple mechanisms and possible exposures, including medications. A specific pathogenic process may result in different outcomes depending upon factors such as embryonic age at which a drug is administered, duration and dose of exposure and genetic susceptibility. This review focuses on the teratogenic mechanisms associated with a number of medications. METHODS We used three methods to identify the teratogenic mechanisms of medications: the MEDLINE and EMBASE databases, two recent books on teratogenic agents and a list of drugs classified as U.S. Food and Drug Administration class D or X. Mechanisms were included only if they are associated with major structural birth defects and medications that are used relatively frequently by women of reproductive age. RESULTS We identified six teratogenic mechanisms associated with medication use: folate antagonism, neural crest cell disruption, endocrine disruption, oxidative stress, vascular disruption and specific receptor- or enzyme-mediated teratogenesis. Many medications classified as class X are associated with at least one of these mechanisms. CONCLUSIONS Identifying teratogenic mechanisms may not only be relevant for etiologic and post-marketing research, but may also have implications for drug development and prescribing behavior for women of reproductive age, especially since combinations of seemingly unrelated prescription and over the counter medications may utilize similar teratogenic mechanisms with a resultant increased risk of birth defects.

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“…In the past, much attention has been paid to the consideration that thrombotic material and the like could be recirculated into the surviving twin, thus causing CNS damage. This hypothesis has recently been reawakened by the publication of Mittelbronn et al ( 2006 ) . They described triplets with TTTS and a macerated fetus; the triplets had hydranencephaly and cortical polymicrogyria, and one had further visceral "thrombotic" events found at autopsy.…”

Section: Fetus Papyraceusmentioning

confidence: 99%