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Partial hydatidiform mole with subsequent trophoblastic tumor; a case report
European Journal of Obstetrics & Gynecology and Reproductrve 0 1991 Elsevier Science Publishers B.V. 0028-2243/91/$03.50
EUROBS
Biology,
40 (1991)
73-11
13
01091
Partial hydatidiform mole with subsequent trophoblastic tumor; a case report Lars 0. Vejerslev ’ Department
of Medical
2 Obstetrics
‘, Gorm
Larsen 2 and Marianne
Genetics, The John F. Kennedy and Gynecology and 3 Pathology, Accepted
Institute, Aalborg
for publication
Jacobsen 3
Glosirup/Copenhagen, Hospital N., Aalborg,
and Departments Denmark
of
2 July 1990
Summary A case of partial hydatidiform mole revealed by genetic marker analysis one maternal and two paternal chromosome complements. Levels of serum human chorionic gonadotropin were persistently elevated during follow-up. Avillous curettage specimens prior to chemotherapy were morphologically suspicious for gestational choriocarcinoma. It is still uncertain whether the risk for gestational choriocarcinoma preceded by partial mole exceeds the risk related to non-molar abortions. Careful follow-up with serial serum human chorionic gonadotropin levels is required to detect persistent disease. Partial
mole;
Triploidy;
Trophoblastic
tumor
Introduction Complete hydatidiform moles (CMM) are generally diploid, of paternal origin, and without an embryo [l-3]. Partial hydatidiform moles (PHM) are essentially always triploid, diandric with an embryo, parts of embryonic origin, or villous vessels with fetal red blood cells indicating previous presence of an embryo [4-61. Distinction between CHM with a coexisting normal conceptus and PHM may be difficult without genetic marker analysis [7]. Persistent trophoblastic disease requiring cytostatic treatment has been reported in 5.7 to 36% of CHM, including 2 to 3% associated with gestational choriocarcinoma [8]. In contrast, clinical residual disease referable to PHM is rarely reported [9-211. Correspondence: Dr. Lars 0. Vejerslev, Department Genetics, The John F. Kennedy Institute, Gl. DK-2600 Glostrup, Denmark.
of Medical Landevej 7,
This report describes a patient who after primary evacuation of a triploid, diandric PHM presented with persistent trophoblastic disease suspicious for choriocarcinoma on repeated curettage.
Case report A 26-year-old Caucasian primigravida was referred to hospital for ultrasound scanning at 23 weeks’ gestation because the uterus was small for date by clinical examination. The sonogram revealed a mass with a mixed echo pattern and a translucent area of which the largest diameter was 6 cm, consistent with a molar pregnancy with an empty gestational sac. Uterine evacuation revealed placental tissue with vesicles from 1 to 20 mm in diameter.
14
Fig. Partial hydatidiform mole. (a) Villi with characteristic an d eosin (X 25). (b) Villi with edema, focal syncytiotrophoblastic
stall oped outlines pro11 iferation
Histological examination confirrred the diagno, sis of hydatidiform mole presenting villous cystic enlargement and mild focal, troph.oblastic hyperplasia (Figs. la and b). The presence of villi with characteristic scalloped outlines, morphologically normal villi, and fetal membranes (amnion and
TABLE
I
Genetic
markers Sex
Pat. Mat. Mole
XY XX XXX
in partial
mole
Chromosome Chromosome
showing
triploidy
with
heteromorphism No.
an extra
and slight tropboblastic byperplasia. Hematoxylin and vacuolization. Hematoxylin and eosin ( x 90).
ck ken) was in accordance with the criteria for Pl IM. Chromosome analysis and HEA determination were performed on cultured stromal cells and enzyme analysis on cystic villi stored at - 20°C after separation from decidual tissue and blood clots
chromosome
*
set of paternal Enzyme
3
13
14
15
21
22
ab ab abb
ab cc/d abc
ab cd sac
ab cc sac
ab cd aad
ab cd abd
origin
locus
HLA
locus
PGM
ACP
CL0
A
B
2+1+ l+l2+1+
A B AB
l-l 2-l l-l
2.25 2,23 2
13.44 44’ 12,13
* a, b, c and d are symbols and do not represent specific heteromorphisms. * * The splits of the HLA-antigen B12 (Bw44 and Bw45) were not distinguished.
**
75
under a stereomicroscope [6]. HLA- and enzyme types were studied at the University Institute of Forensic Genetics, Copenhagen. The karyotype was 69,XxX and polymorphisms were consistent with fertilization of an ovum by two sperm as described for PHM (Table I). Quantitative serum human chorionic gonadotropin (se-hCG) levels at day 1 after evacuation were 16000 IU/l and increased at day 27 to 30000 IU/l (performed by radioimmunoassay at the Hormone Department, Statens Seruminstitut). An ultrasoundscan indicated retained intra-uterine tissue, and uterine curretage was performed on day 40. Histological examination revealed sheets of proliferating cyto- and syncytiotrophoblast with atypia and superficial invasion of the myometrium (Figs. 2a and b). No villous structures were identified, and the morphology was suspicious for choriocarcinoma. The patient was referred to the Department of Obstetrics and Gynecology, Arhus for cytostatic treatment.
Fig. 2. Trophoblastic tumor villous structure. Hematoxylin
Discussion To our knowledge, the present case is the first observation of trophoblastic tumor following PHM diagnosed both by morphology and genetic markers. Consistent with our findings, Gaber et al. [20] observed persistent hCG elevation and invasion of myometrium in a PHM with a triploid karyotype. The findings of avillous trophoblast in postmolar curettage specimens may indicate the presence of gestational choriocarcinoma, which has not been described so far. Definite proof of the diagnosis is not possible by curettage alone, as villous structures could be buried deep in the uterine wall. However, sheets of proliferating cytoand syncytiotrophoblast with atypia and superficial myometrial invasion are indeed suspicious of choriocarcinoma. Previous reports on PHM or hydatidiform mole with a fetus ‘followed by invasive growth, metas-
after reevacuation at day 40. (a) Shea& of proliferating atypical syncytioand eosin (X 25). (b) Trophoblast superficially invading the myometrium, Hematoxylin and eosin (X 150).
and cytotrophoblast which shows focal
without necrosis.
TABLE Persistent Author
II trophoblastic
disease
and reference
Jones and Lauersen [9] Stone and Bagshawe [lo] Szulman and Surti [ll] S&man et al. [12] Berkowitz et al. [13] Szulman et al. [14] Looi and Sivanesaratnam [15] Czemobilsky et al. [16] Franke et al. [17] Smith et al. [18] Wong and Ma [19] Gaber et al. [20] Mostoufi-Zadeh et al. [21]
in partiai
hydatidiform
mole and hydatidiform
mole
with
a fetus
Year
No.
Ascertainment
Karyotype
Treatment
1975 1976 1978 197x 1979 1981 1981 1982 1983 1984 1984 1986 1987
1 5 1 1 1 1 1 1 1 2 4 1 8
Mole + fetus Partial mole Partial mole + fetus Partial mole + fetus Mole + fetus Partial mole Mole + fetus Partial mole Partial mole Partial mole Partial mole Partial mole Partial mole
Triploid Triploid -
Methotrexate Chemotherapy Chemotherapy Actinomycin-D Methotrexate Bleomycin + hysterectomy Methotrexate + hysterectomy Methotrexate Methotrexate + hysterectomy Chemotherapy Single agent Methotrexate + hysterectomy Methotrexate
tases or cytostatic treatment are shown in Table II. Administration of cytostatics may or may not indicate persistent trophoblastic disease. Szulman and Surti [ll] stated that one patient treated with chemotherapy after evacuation of a triploid partial mole probably would have been treated expectantly at the time of publication. In one series without development of trophoblastic tumor, irregular heavy vaginal bleeding following evacuation prompted administration of methotrexate in one patient [16]. Without genetic marker analysis the observation of fetal parts in a molar specimen could be consistent with either PHM or twin gestation comprising a CHM and a normal conception [7]. In the latter an increased malignant potential as for CHM could be expected in spite of the observation of fetal parts. Unequivocal distinction between PHM with a fetus and twin gestation implies analysis of genetic markers on fetal tissue, apparently normal and cystic villi. Triploidy with three paternal chromosome complements in morphologically complete moles emphasizes that without characterization of chromosomal origin triploidy may comprise genetically partial as well as complete moles [22]. Secondly, a period without follow-up between molar evacuation and malignancy raises the possibility for an intervening non-molar pregnancy [15]. Differences in morphological criteria and indications for cytostatic treatment may account for
69,XXY -
the assumption of residual trophoblastic disease in some of the cases listed in Table II. However, on present grounds PHM appears to imply a significant risk for persistent trophoblastic disease; in one series comparable to the approximately 10% in CHM [20]. Whether choriocarcinoma following PHM is more frequent than following a non-molar pregnancy remains to be elucidated. As illustrated by the present case, patients with PHM require careful follow-up by serial se-hCG titers. Acknowledgements This work was supported by the Dagmar Marshall Foundation and the Danish Medical Research Council, grants No. 12-4122, 12-4514 and 12-5580. References 1 Jacobs PA, Wilson CM, Sprenkle YA, Rosenhein NB, Migeon BR. Mechanism of origin of complete hydatidiform moles. Nature 1980;286:714-716. 2 Lawler SD, Povey S, Fisher RA, Pickthall VJ. Genetic studies on hydatidiform moles. II. The origin’of complete moles. Ann Hum Genet 1982;46:209-222. 3 Vejerslev LO, Dissing J, Hansen HE, Poulsen H. Hydatidiform mole: genetic markers in diploid abortuses with macroscopic villous enlargement. Cancer Genet Cytogenet 1987;26:143-155. 4 Jacobs PA, Szulman AE, Funkhouser J, Matsuura JS, Wilson CC. Human triploidy: relationship between parental origin of the additional haploid complement and develop-
77
5
6
7
8
9 10 11
12 13
ment of partial hydatidiform mole. Ann Hum Genet 1982;46:223-231. Lawler SD, Fisher RA, Pickthall VJ, Povey S, Evans MW. Genetic studies on hydatidiform moles. I. The origin of partial moles. Cancer Genet Cytogenet 1982;5:309-320. Vejerslev LO, Dissing J, Hansen HE, Poulsen H. Hydatidiform mole: genetic origin in polyploid conceptuses. Hum Genet 1987;76:11-19. Vejerslev LO, Dueholm M, Nielsen FH. Hydatidiform mole: cytogenetic marker analysis in twin gestation. Am J Obstet Gynecol 1986;155:614-617. Lurain JR. Natural history. In: Szulman AE, Buchsbaum HJ (eds). Gestational Trophoblastic Disease, 1st edn, New York: Springer-Verlag, 1987:69-76. Jones WB, Lauersen NH. Hydatidiform mole with coexistent fetus. Am J Obstet Gynecol 1975;122:267-272. Stone M, Bagshawe KD. Hydatidiform mole: two entities. Lancet 1916;i:535. Szulman AE, Surti U. The syndromes of hydatidiform mole. I. Cytogenetic and morphological correlations. Am J Obstet Gynecol 1978;131:665-671. Szulman AE, Surti U, Berman M. Patient with partial mole requiring chemotherapy. Lancet 1978;ii:1099. Berkowitz RS, Goldstein DP, Marean AR, Bernstein MR. Proliferative sequelae after evacuation of partial hydatidiform mole. Lancet 1979;ii:804-805.
14 Szulman AE, Wong LC, Hsu C. Residual trophoblastic disease in association with partial hydatidiform mole. Obstet Gynecol 1981;57:392-394. 15 Looi LM, Sivanesaratnam V. Malignant evolution with fatal outcome in a patient with partial hydatidiform mole. Aust N Z J Obstet Gynaecol 1981;21:51-52. 16 Czernobilsky B, Barash A, Lancet M. Partial moles: a clinicopathologic study of 25 cases. Obstet Gynecol 1982; 59:75-77. 17 Franke HR, Risse EKJ, Kenemans P, Vooijs GP, Stolk JG. Epidemiologic features of hydatidiform mole in The Netherlands. Obstet Gynecol 1983;62:613-616. 18 Smith EB, Szulman AE, Hinshaw W, Tyrey L, Surti S, Hammond CB. Human chorionic gonadotropin levels in complete and partial hydatidiform moles a.nd nonmolar abortuses. Am J Obstet Gynecol 1984;149:129-132. 19 Wong LC, Ma H-K The syndrome of partial mole. Arch Gynecol 1984;234:161-166. 20 Gaber LW, Redline RW, Mostoufi-Zadeh M, Driscoll SG. Invasive partial mole. Am J Clin Path01 1986;85:722-724. 21 Mostoufi-Zadeh M, Berkowitz RS, Driscoll SG. Persistence of partial mole. Am J Clin Path01 1987;87:377-380. 22 Vejerslev LO, Fisher RA, Surti U, Wake N. Hydatidiform mole: Cytogenetically unusual cases and their implications for the present classification. Am J Obstet Gynecol 1987;157:180-184.
EUROBS
Biology,
40 (1991)
73-11
13
01091
Partial hydatidiform mole with subsequent trophoblastic tumor; a case report Lars 0. Vejerslev ’ Department
of Medical
2 Obstetrics
‘, Gorm
Larsen 2 and Marianne
Genetics, The John F. Kennedy and Gynecology and 3 Pathology, Accepted
Institute, Aalborg
for publication
Jacobsen 3
Glosirup/Copenhagen, Hospital N., Aalborg,
and Departments Denmark
of
2 July 1990
Summary A case of partial hydatidiform mole revealed by genetic marker analysis one maternal and two paternal chromosome complements. Levels of serum human chorionic gonadotropin were persistently elevated during follow-up. Avillous curettage specimens prior to chemotherapy were morphologically suspicious for gestational choriocarcinoma. It is still uncertain whether the risk for gestational choriocarcinoma preceded by partial mole exceeds the risk related to non-molar abortions. Careful follow-up with serial serum human chorionic gonadotropin levels is required to detect persistent disease. Partial
mole;
Triploidy;
Trophoblastic
tumor
Introduction Complete hydatidiform moles (CMM) are generally diploid, of paternal origin, and without an embryo [l-3]. Partial hydatidiform moles (PHM) are essentially always triploid, diandric with an embryo, parts of embryonic origin, or villous vessels with fetal red blood cells indicating previous presence of an embryo [4-61. Distinction between CHM with a coexisting normal conceptus and PHM may be difficult without genetic marker analysis [7]. Persistent trophoblastic disease requiring cytostatic treatment has been reported in 5.7 to 36% of CHM, including 2 to 3% associated with gestational choriocarcinoma [8]. In contrast, clinical residual disease referable to PHM is rarely reported [9-211. Correspondence: Dr. Lars 0. Vejerslev, Department Genetics, The John F. Kennedy Institute, Gl. DK-2600 Glostrup, Denmark.
of Medical Landevej 7,
This report describes a patient who after primary evacuation of a triploid, diandric PHM presented with persistent trophoblastic disease suspicious for choriocarcinoma on repeated curettage.
Case report A 26-year-old Caucasian primigravida was referred to hospital for ultrasound scanning at 23 weeks’ gestation because the uterus was small for date by clinical examination. The sonogram revealed a mass with a mixed echo pattern and a translucent area of which the largest diameter was 6 cm, consistent with a molar pregnancy with an empty gestational sac. Uterine evacuation revealed placental tissue with vesicles from 1 to 20 mm in diameter.
14
Fig. Partial hydatidiform mole. (a) Villi with characteristic an d eosin (X 25). (b) Villi with edema, focal syncytiotrophoblastic
stall oped outlines pro11 iferation
Histological examination confirrred the diagno, sis of hydatidiform mole presenting villous cystic enlargement and mild focal, troph.oblastic hyperplasia (Figs. la and b). The presence of villi with characteristic scalloped outlines, morphologically normal villi, and fetal membranes (amnion and
TABLE
I
Genetic
markers Sex
Pat. Mat. Mole
XY XX XXX
in partial
mole
Chromosome Chromosome
showing
triploidy
with
heteromorphism No.
an extra
and slight tropboblastic byperplasia. Hematoxylin and vacuolization. Hematoxylin and eosin ( x 90).
ck ken) was in accordance with the criteria for Pl IM. Chromosome analysis and HEA determination were performed on cultured stromal cells and enzyme analysis on cystic villi stored at - 20°C after separation from decidual tissue and blood clots
chromosome
*
set of paternal Enzyme
3
13
14
15
21
22
ab ab abb
ab cc/d abc
ab cd sac
ab cc sac
ab cd aad
ab cd abd
origin
locus
HLA
locus
PGM
ACP
CL0
A
B
2+1+ l+l2+1+
A B AB
l-l 2-l l-l
2.25 2,23 2
13.44 44’ 12,13
* a, b, c and d are symbols and do not represent specific heteromorphisms. * * The splits of the HLA-antigen B12 (Bw44 and Bw45) were not distinguished.
**
75
under a stereomicroscope [6]. HLA- and enzyme types were studied at the University Institute of Forensic Genetics, Copenhagen. The karyotype was 69,XxX and polymorphisms were consistent with fertilization of an ovum by two sperm as described for PHM (Table I). Quantitative serum human chorionic gonadotropin (se-hCG) levels at day 1 after evacuation were 16000 IU/l and increased at day 27 to 30000 IU/l (performed by radioimmunoassay at the Hormone Department, Statens Seruminstitut). An ultrasoundscan indicated retained intra-uterine tissue, and uterine curretage was performed on day 40. Histological examination revealed sheets of proliferating cyto- and syncytiotrophoblast with atypia and superficial invasion of the myometrium (Figs. 2a and b). No villous structures were identified, and the morphology was suspicious for choriocarcinoma. The patient was referred to the Department of Obstetrics and Gynecology, Arhus for cytostatic treatment.
Fig. 2. Trophoblastic tumor villous structure. Hematoxylin
Discussion To our knowledge, the present case is the first observation of trophoblastic tumor following PHM diagnosed both by morphology and genetic markers. Consistent with our findings, Gaber et al. [20] observed persistent hCG elevation and invasion of myometrium in a PHM with a triploid karyotype. The findings of avillous trophoblast in postmolar curettage specimens may indicate the presence of gestational choriocarcinoma, which has not been described so far. Definite proof of the diagnosis is not possible by curettage alone, as villous structures could be buried deep in the uterine wall. However, sheets of proliferating cytoand syncytiotrophoblast with atypia and superficial myometrial invasion are indeed suspicious of choriocarcinoma. Previous reports on PHM or hydatidiform mole with a fetus ‘followed by invasive growth, metas-
after reevacuation at day 40. (a) Shea& of proliferating atypical syncytioand eosin (X 25). (b) Trophoblast superficially invading the myometrium, Hematoxylin and eosin (X 150).
and cytotrophoblast which shows focal
without necrosis.
TABLE Persistent Author
II trophoblastic
disease
and reference
Jones and Lauersen [9] Stone and Bagshawe [lo] Szulman and Surti [ll] S&man et al. [12] Berkowitz et al. [13] Szulman et al. [14] Looi and Sivanesaratnam [15] Czemobilsky et al. [16] Franke et al. [17] Smith et al. [18] Wong and Ma [19] Gaber et al. [20] Mostoufi-Zadeh et al. [21]
in partiai
hydatidiform
mole and hydatidiform
mole
with
a fetus
Year
No.
Ascertainment
Karyotype
Treatment
1975 1976 1978 197x 1979 1981 1981 1982 1983 1984 1984 1986 1987
1 5 1 1 1 1 1 1 1 2 4 1 8
Mole + fetus Partial mole Partial mole + fetus Partial mole + fetus Mole + fetus Partial mole Mole + fetus Partial mole Partial mole Partial mole Partial mole Partial mole Partial mole
Triploid Triploid -
Methotrexate Chemotherapy Chemotherapy Actinomycin-D Methotrexate Bleomycin + hysterectomy Methotrexate + hysterectomy Methotrexate Methotrexate + hysterectomy Chemotherapy Single agent Methotrexate + hysterectomy Methotrexate
tases or cytostatic treatment are shown in Table II. Administration of cytostatics may or may not indicate persistent trophoblastic disease. Szulman and Surti [ll] stated that one patient treated with chemotherapy after evacuation of a triploid partial mole probably would have been treated expectantly at the time of publication. In one series without development of trophoblastic tumor, irregular heavy vaginal bleeding following evacuation prompted administration of methotrexate in one patient [16]. Without genetic marker analysis the observation of fetal parts in a molar specimen could be consistent with either PHM or twin gestation comprising a CHM and a normal conception [7]. In the latter an increased malignant potential as for CHM could be expected in spite of the observation of fetal parts. Unequivocal distinction between PHM with a fetus and twin gestation implies analysis of genetic markers on fetal tissue, apparently normal and cystic villi. Triploidy with three paternal chromosome complements in morphologically complete moles emphasizes that without characterization of chromosomal origin triploidy may comprise genetically partial as well as complete moles [22]. Secondly, a period without follow-up between molar evacuation and malignancy raises the possibility for an intervening non-molar pregnancy [15]. Differences in morphological criteria and indications for cytostatic treatment may account for
69,XXY -
the assumption of residual trophoblastic disease in some of the cases listed in Table II. However, on present grounds PHM appears to imply a significant risk for persistent trophoblastic disease; in one series comparable to the approximately 10% in CHM [20]. Whether choriocarcinoma following PHM is more frequent than following a non-molar pregnancy remains to be elucidated. As illustrated by the present case, patients with PHM require careful follow-up by serial se-hCG titers. Acknowledgements This work was supported by the Dagmar Marshall Foundation and the Danish Medical Research Council, grants No. 12-4122, 12-4514 and 12-5580. References 1 Jacobs PA, Wilson CM, Sprenkle YA, Rosenhein NB, Migeon BR. Mechanism of origin of complete hydatidiform moles. Nature 1980;286:714-716. 2 Lawler SD, Povey S, Fisher RA, Pickthall VJ. Genetic studies on hydatidiform moles. II. The origin’of complete moles. Ann Hum Genet 1982;46:209-222. 3 Vejerslev LO, Dissing J, Hansen HE, Poulsen H. Hydatidiform mole: genetic markers in diploid abortuses with macroscopic villous enlargement. Cancer Genet Cytogenet 1987;26:143-155. 4 Jacobs PA, Szulman AE, Funkhouser J, Matsuura JS, Wilson CC. Human triploidy: relationship between parental origin of the additional haploid complement and develop-
77
5
6
7
8
9 10 11
12 13
ment of partial hydatidiform mole. Ann Hum Genet 1982;46:223-231. Lawler SD, Fisher RA, Pickthall VJ, Povey S, Evans MW. Genetic studies on hydatidiform moles. I. The origin of partial moles. Cancer Genet Cytogenet 1982;5:309-320. Vejerslev LO, Dissing J, Hansen HE, Poulsen H. Hydatidiform mole: genetic origin in polyploid conceptuses. Hum Genet 1987;76:11-19. Vejerslev LO, Dueholm M, Nielsen FH. Hydatidiform mole: cytogenetic marker analysis in twin gestation. Am J Obstet Gynecol 1986;155:614-617. Lurain JR. Natural history. In: Szulman AE, Buchsbaum HJ (eds). Gestational Trophoblastic Disease, 1st edn, New York: Springer-Verlag, 1987:69-76. Jones WB, Lauersen NH. Hydatidiform mole with coexistent fetus. Am J Obstet Gynecol 1975;122:267-272. Stone M, Bagshawe KD. Hydatidiform mole: two entities. Lancet 1916;i:535. Szulman AE, Surti U. The syndromes of hydatidiform mole. I. Cytogenetic and morphological correlations. Am J Obstet Gynecol 1978;131:665-671. Szulman AE, Surti U, Berman M. Patient with partial mole requiring chemotherapy. Lancet 1978;ii:1099. Berkowitz RS, Goldstein DP, Marean AR, Bernstein MR. Proliferative sequelae after evacuation of partial hydatidiform mole. Lancet 1979;ii:804-805.
14 Szulman AE, Wong LC, Hsu C. Residual trophoblastic disease in association with partial hydatidiform mole. Obstet Gynecol 1981;57:392-394. 15 Looi LM, Sivanesaratnam V. Malignant evolution with fatal outcome in a patient with partial hydatidiform mole. Aust N Z J Obstet Gynaecol 1981;21:51-52. 16 Czernobilsky B, Barash A, Lancet M. Partial moles: a clinicopathologic study of 25 cases. Obstet Gynecol 1982; 59:75-77. 17 Franke HR, Risse EKJ, Kenemans P, Vooijs GP, Stolk JG. Epidemiologic features of hydatidiform mole in The Netherlands. Obstet Gynecol 1983;62:613-616. 18 Smith EB, Szulman AE, Hinshaw W, Tyrey L, Surti S, Hammond CB. Human chorionic gonadotropin levels in complete and partial hydatidiform moles a.nd nonmolar abortuses. Am J Obstet Gynecol 1984;149:129-132. 19 Wong LC, Ma H-K The syndrome of partial mole. Arch Gynecol 1984;234:161-166. 20 Gaber LW, Redline RW, Mostoufi-Zadeh M, Driscoll SG. Invasive partial mole. Am J Clin Path01 1986;85:722-724. 21 Mostoufi-Zadeh M, Berkowitz RS, Driscoll SG. Persistence of partial mole. Am J Clin Path01 1987;87:377-380. 22 Vejerslev LO, Fisher RA, Surti U, Wake N. Hydatidiform mole: Cytogenetically unusual cases and their implications for the present classification. Am J Obstet Gynecol 1987;157:180-184.