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Classic illustration
Europ. J. Obstet. Gynec. reprod. Biol., 18 (1984) 239-240
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Elsevier EJO 00137
Classic illustration
Fig. 1. This figure is taken from the thesis of B.J.C. den Hartog (1933) called ‘Het chorionepithehoma malignum van den man en zijn biologische beteekenis: Fig. 116. Geval VII (S. 11644). Paraffinecoupe No. 3 uit retroperitoneaal knobbeltje K2. Vergrooting 167 x . Mola-achtig vormsel in lymphvat. Het stroma is oedemateus, vrij celrijk. Het syncytium bevat vacuolen. Er zijn geen cellen van Langhans.
In 1933 B.J.C. den Hartog had already discussed in his thesis the development of chorionepithelium as a product of male germ cells. The more mature zygote of man would not have the ability to form this epithelium. Even hydatidiform mole-like structures appeared to be found in males. Until 1977 it was considered that the pathogenesis of hydatidiform mole was due to retention of a blighted ovum with cessation of the villous stromal circulation and continued secretory activity of the trophoblast, nourished by maternal blood. This resulted in hydropic degeneration of the villus stroma and trophoblastic proliferation. Another theory was that the abnormality was primarily sited in the trophoblast, which caused stromal hydropic degeneration. Cytogenetic studies in 1968 by Baggish et al. showed that in 88% of hydatidiform mole cases a sex chromatin body was found. It was therefore concluded that the hydatidiform mole was predominantly female. Recent cytogenetic studies, however, indicate that there are two forms of hydatidiform moles, namely complete hydatidiform moles and partial moles. Complete hydatidiform moles have in most instances a 46XX chromosome constitution and are of androgenetic origin (Kajii and Ohama, 1977). Approx. 3-13% of hydatidiform moles are reported to have 46XY karyotype. 0028-2243/84/%03.00 0 1984 Elsevier Science Publishers B.V.
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The possible causes of diploid androgenesis are the preservation of only the male chromosomes, in 46XX hydatidiform moles one ovum is fertilized by two sperms, a diploid sperm or by a haploid sperm followed by duplication of its chromosomes. In 1980, Jacobs et al. reported that fertilization by a haploid sperm, followed by duplication without cytokinesis, may probably result in the androgenesis of the 46XX hydatidiform mole. In 46XY hydatidiform moles fertilization of one ovum by two sperms may have taken place. Partial moles have been reported to comprise various chromosomal abnormalities, such as triploidy (69 chromosomes) and trisomy 16. We therefore may conclude that in 1933 Den Hartog had already assumed that a hydatidiform mole is a paternal tumor. H.R. FRANKE Amsterdam References Den Hartog, B.J. (1933): Het chorionepithelioma malignum van den man en zijn biologische beteekenis. Thesis, Amsterdam. Fox, H. (1978): Pathology of the placenta. Major problems in pathology, Vol. 7. Editor: J.L. Bennington. W.B. Saunders, London. Baggish, M.S., Woodruff, J.D., Tow, S.H., et al. (1968): Sex chromatin pattern in hydatidiform mole. Amer. J. Obstet. Gynec., 102, 362-370. Kajii, T. and Ohama, K. (1977): Androgenetic origin of hydatidiform mole. Nature, 268, 633-634. Surti, U., Szulman, A.E. and O’Brien, S. (1979): Complete (classic) hydatidiform mole with 46XY karyotype of paternal origin. Hum. Genet., 51, 153-155. Jacobs, P.A., Wilson, C.M., Sprenkle, J.A., et al. (1980): Mechanism of origin of complete hydatidiform mole. Nature, 286, 714-716. Vassilakos, P., Riotton, G. and Kajii, T. (1977): Hydatidiform mole: two entities. A morphological and cytogenetic study with some clinical considerations. Amer. J. Obstet. Gynec., 127, 167-170. Franke, H.R. (1983): Gestational trophoblastic disease in the Netherlands. Thesis, Amsterdam.
239
Elsevier EJO 00137
Classic illustration
Fig. 1. This figure is taken from the thesis of B.J.C. den Hartog (1933) called ‘Het chorionepithehoma malignum van den man en zijn biologische beteekenis: Fig. 116. Geval VII (S. 11644). Paraffinecoupe No. 3 uit retroperitoneaal knobbeltje K2. Vergrooting 167 x . Mola-achtig vormsel in lymphvat. Het stroma is oedemateus, vrij celrijk. Het syncytium bevat vacuolen. Er zijn geen cellen van Langhans.
In 1933 B.J.C. den Hartog had already discussed in his thesis the development of chorionepithelium as a product of male germ cells. The more mature zygote of man would not have the ability to form this epithelium. Even hydatidiform mole-like structures appeared to be found in males. Until 1977 it was considered that the pathogenesis of hydatidiform mole was due to retention of a blighted ovum with cessation of the villous stromal circulation and continued secretory activity of the trophoblast, nourished by maternal blood. This resulted in hydropic degeneration of the villus stroma and trophoblastic proliferation. Another theory was that the abnormality was primarily sited in the trophoblast, which caused stromal hydropic degeneration. Cytogenetic studies in 1968 by Baggish et al. showed that in 88% of hydatidiform mole cases a sex chromatin body was found. It was therefore concluded that the hydatidiform mole was predominantly female. Recent cytogenetic studies, however, indicate that there are two forms of hydatidiform moles, namely complete hydatidiform moles and partial moles. Complete hydatidiform moles have in most instances a 46XX chromosome constitution and are of androgenetic origin (Kajii and Ohama, 1977). Approx. 3-13% of hydatidiform moles are reported to have 46XY karyotype. 0028-2243/84/%03.00 0 1984 Elsevier Science Publishers B.V.
240
The possible causes of diploid androgenesis are the preservation of only the male chromosomes, in 46XX hydatidiform moles one ovum is fertilized by two sperms, a diploid sperm or by a haploid sperm followed by duplication of its chromosomes. In 1980, Jacobs et al. reported that fertilization by a haploid sperm, followed by duplication without cytokinesis, may probably result in the androgenesis of the 46XX hydatidiform mole. In 46XY hydatidiform moles fertilization of one ovum by two sperms may have taken place. Partial moles have been reported to comprise various chromosomal abnormalities, such as triploidy (69 chromosomes) and trisomy 16. We therefore may conclude that in 1933 Den Hartog had already assumed that a hydatidiform mole is a paternal tumor. H.R. FRANKE Amsterdam References Den Hartog, B.J. (1933): Het chorionepithelioma malignum van den man en zijn biologische beteekenis. Thesis, Amsterdam. Fox, H. (1978): Pathology of the placenta. Major problems in pathology, Vol. 7. Editor: J.L. Bennington. W.B. Saunders, London. Baggish, M.S., Woodruff, J.D., Tow, S.H., et al. (1968): Sex chromatin pattern in hydatidiform mole. Amer. J. Obstet. Gynec., 102, 362-370. Kajii, T. and Ohama, K. (1977): Androgenetic origin of hydatidiform mole. Nature, 268, 633-634. Surti, U., Szulman, A.E. and O’Brien, S. (1979): Complete (classic) hydatidiform mole with 46XY karyotype of paternal origin. Hum. Genet., 51, 153-155. Jacobs, P.A., Wilson, C.M., Sprenkle, J.A., et al. (1980): Mechanism of origin of complete hydatidiform mole. Nature, 286, 714-716. Vassilakos, P., Riotton, G. and Kajii, T. (1977): Hydatidiform mole: two entities. A morphological and cytogenetic study with some clinical considerations. Amer. J. Obstet. Gynec., 127, 167-170. Franke, H.R. (1983): Gestational trophoblastic disease in the Netherlands. Thesis, Amsterdam.