Benign Tumors and Chorangiosis

  • Kurt Benirschke
  • Graham J. Burton
  • Rebecca N. Baergen


With rare exceptions, vascular tumors are the only benign tumors of the placenta. Tumors designated as chorioangiomas, chorangiomas, fibroangiomyxomas, fibromas, and the many other names that have been applied in the past are essentially similar, relatively common neoplasms of the placenta. Three large reviews have been published that bring together most of the literature. DeCosta et al. (1956) found about 250 case reports and listed all the synonyms applied previously. They also made reference to the frequency of hydramnios and associated fetal angiomas. Fox (1967), who also reviewed the often confusing nomenclature, indicated that Clarke described the first such tumor in 1798. Since then, the review by Siddall (1924) encompassed 130 cases, that by Marchetti (1939) comprised 209 cases, and Fox traced another 127 cases. Fox accounted for 344 published cases and gave incidence figures of one in 9,000 to one in 50,000 placentas. When careful study of placentas is undertaken, the real prevalence may be as high as one in 100 pregnancies, according to some authors (e.g., Wentworth 1965, who found one in 77); although in our experience, this number is somewhat excessive. Wallenburg (1971) provided 13 new cases and summarized publications between 1939 and 1970. His reported incidence in consecutively collected placentas was one in 117. These authors provided an extensive literature documentation that would be redundant to repeat. Bashiri et al. (2002) found a significant risk of preterm delivery in patients with chorangiomas. Soma et al. (1991) found that the tumor existed in 0.2% of placentas in Japanese women but was more common (2.5–7.6%) in the high altitude population of Nepal (Soma 2001). This is similar to the higher frequency of chorioangioma observed in placentas of women living at altitude by Reshetnikova et al. (1996). We have seen chorioangiomas associated with chronic vascular thrombi and elevated NRBCs in the fetal circulation. Thus, a hypoxic stimulus is inferred to lead to excessive villous capillary proliferative stimulation. While still speculative, such angiogenesis may well be regulated by such vascular growth factors as demonstrated to occur in the placenta by Jackson et al. (1994). A more detailed consideration of the placental villous adaptation to hypoxia can be found in the contribution by Kaufmann et al. (1993), and the paper by Kadyrov et al. (1998) provided information on how anemic women produce increased placental angiogenesis in early development. The control of angiogenesis is complex, but it is an essential aspect of placentation and regulation during anemia, preeclampsia, and other pathologic states in pregnancy. There are numerous factors now being explored, and many have significant impact on the villous vascularization. A detailed review was provided by Sherer and Abulafia (2001) that is too complex, however, for the brief consideration possible in this chapter. Guschmann (2002, 2003) and his colleagues in Berlin (Guschmann et al. 2003) have described various angiogenesis factors in chorangiomas. It was their experience that high expression of angiopoietin-1 and 2 and their receptors was demonstrated in chorangiomas, while VEGF was uniform with the normal villi, but variability existed. Further remarkable in their series was that 72% of accompanying babies were of female gender, and tumors occurred much more commonly in the first pregnancy. North et al. (2001) studied immunoreactivity for a variety of antigens in chorangiomas and juvenile angiomas. Thus, FcgammaRII, Lewis Y antigen, merosin, and GLUT1 were found to be highly expressed in the small placental vessels and angiomas, but not in control blood vessels or those of granulomas etc.


Placenta Previa Fetal Circulation Smooth Muscle Tumor Fetal Demise Turner Syndrome Patient 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  • Kurt Benirschke
    • 1
  • Graham J. Burton
    • 2
  • Rebecca N. Baergen
    • 3
  1. 1.La JollaUSA
  2. 2.Physiological LaboratoryUniversity of Cambridge Centre for Trophoblast ResearchCambridgeUK
  3. 3.Department of Pathology and Laboratory Medicine New York-Presbyterian HospitalWeill Medical College of Cornell UniversityNew YorkUSA

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