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Indian Journal of Cancer
Medknow Publications on behalf of Indian Cancer Society
ISSN: 0019-509X EISSN: 1998-4774
Vol. 39, Num. 3, 2002, pp. 116-118

Indian Journal of Cancer, Vol. 39, No. 3, (July - September 2002), pp. 116-118

Metastatic Invasive Mole in the Urinary Bladder

Bhawna Malhotra, M.D., Senior Research Associate, Renu Misra, M.D., Associate Professor

Department of Obstetrics & Gynecology, All India Institute of Medical Sciences, New Delhi, India.

Code Number: cn02006


We report an unusual case of invasive mole metastasized to the urinary bladder. The patient presented with hematuria one month after evacuation of a molar pregnancy. The serum chorionic gonadotropin levels regressed spontaneously following transurethral cystoscopic resection of the tumour. Metastasis of an invasive mole to the urinary bladder has not been previously reported.


Invasive mole follows approximately 10 to 15 per cent of complete hydatidiform moles.1 They are characterized by the persistence of edematous chorionic villi with trophoblastic proliferation invading into the myometrium. Invasive moles rarely metastasize and the most common sites of metastatic lesions are lung, vagina, parametrium and pelvis. Brain, liver, spleen, kidneys and retroperitoneum are the other reported rare sites of metastatic mole.2-4 To the best of our knowledge, metastasis of an invasive mole to the urinary bladder has not been reported in the literature, though choriocarcinoma of the urinary bladder has been described in a case report.5 The presence of villi in the metastatic trobhoblastic tissue differentiates an invasive mole from choriocarcinoma. We present a case of metastatic mole in the urinary bladder diagnosed one month after the evacuation of hydatidiform mole.


A 31-year-old primipara presented in the outpatient department of Gynaecology at All India Institute of Medical Sciences, New Delhi, with the complaints of hematuria for three days and irregular vaginal bleeding for ten days. One month back, she had undergone uterine evacuation for a molar pregnancy at a period of three and a half months gestation at a peripheral hospital. She had not attended any follow-up nor serum chorionic gonadotropin levels (hCG) had been assayed before or after the evacuation. Her previous menstrual history was unremarkable. Her past obstetric history included a cesarean section at term two years back.

The general and systemic examination revealed no abnormality. On local examination, the external genitalia and urethral meatus were healthy. The speculum examination revealed a healthy vagina and cervix with minimal bleeding from the cervical os. On bimanual pelvic examination, the uterus was anteverted and multiparous size. There was no tenderness or adnexal mass palpable in any of the fornices. The urine examination confirmed hematuria with no evidence of infection on microscopy or culture. Routine serum biochemistry and chest X-ray were normal. Her serum beta-hCG was 406 MIU\ml. The pelvic ultrasound showed a space-occupying lesion in the urinary bladder with mucosal thickening and irregularity in the posterior bladder wall. The uterus and bilateral ovaries were unremarkable.

The cystoscopy confirmed a solitary lobulated growth, 2.5 x 1.0 cm in size, arising near the right ureteric orifice and extending to the trigone; bleeding on touch. The growth was resected using the resectoscope at the same sitting, followed by a uterine curettage. The histopathology of both the specimens was similar and consistent with hydatidiform mole, with areas of hemorrhage and necrosis in the bladder specimen.

The metastatic work-up revealed no evidence of metastasis at any other site. In view of low levels of serum beta-hCG, she was kept under surveillance with serial quantitative beta-hCG determinations to consider chemotherapy if beta-hCG levels plateau or rise. Post-operatively, beta-hCG fell rapidly to 37mIU\n1 at one week and <5mlU\ml at two weeks following the resection of the tumour. The subsequent beta-hCG levels were negative till 18months of follow-up.


Complete hydatidiform moles are recognized to have a potential for developing uterine invasion or distant metastases (which represent the normal capacity of the trophoblast for implantation). Approximately 20 per cent of patients with primary hydatidiform mole develop malignant sequelae, the majority of which are invasive moles.6 Invasive mole may perforate through the myometrium resulting in uterine perforation and intraperitoneal bleedmg.7 Direct vascular invasion and metastasis rarely occur in invasive moles; the most common site reported is the lung.2,8

The metastatic mole is frequently diagnosed incorrectly as choriocarcinomar.2 The diagnosis of invasive mole rests on the demonstration of complete hydatidiform mole invading the myometrium or the presence of villi in the metastatic lesion (as was present in our case). Myometrial invasion is difficult to document on pelvic ultrasound and also in uterine curettings unless there is sufficient myometrium to demonstrate invasion. The metastatic lesion may not be available for the pathological diagnosis in all the cases.

The use of prophylactic chemotherapy following molar evacuation remains controversial. Although it has been shown to reduce the incidence of persistent or metastatic gestational trophoblastic neoplasia, it is not routinely recommended. The low morbidity and mortality achieved by monitoring patients with serial beta-hCG levels and instituting only indicated chemotherapy outweighs, the potential risk and small benefit of routine prophylactic chemotherapy.1,6 The role of chemotherapy in the management of invasive mole is debatable, with the evidence of spontaneous regression of metastatic mole in the literature.2,8 Ring reported two patients with histologically proven metastases from hydatidiform mole to the lungs, which regressed spontaneously following hysterectomy without additional chemotherapy.8 In a review of twenty cases of invasive mole, Wilson et al reported that no additional therapy was administered for metastatic lesion in three cases all of whom recovered with disappearance of metastatic lesion.2

In our patient, the metastatic mole in the urinary bladder was detected one month after the evacuation of molar pregnancy due to the occurrence of hematuria. Since beta-hCG was low at that time, it is possible that serum hCG levels were already regressing following molar evacuation when hematuria resulted from necrosis and degeneration of the metastatic mole. It remains uncertain whether cystoscopic resection of the metastatic mole provided any additional benefit in the management of our case.

We did not consider chemotherapy in our case as the beta-hCG was already low and thereafter declined rapidly to become negative. Low beta-hCG levels before treatment and negative hCG as early as one week following treatment has been reported in association with histologically proven metastatic mole.2 Pronounced degenerative changes in the trophoblasts along with hyalinization were found to correlate with low or declining levels of beta-hCG.

Though experience in the management of metastatic mole is limited, we believe that surgical removal of the metastatic lesion should be done whenever possible. It would provide tissue diagnosis as well as hasten the resolution of the disease. In our opinion, chemotherapy should not be withheld in the presence of metastasis in association with high hCG titer since invasive mole can perforate to result in a potentially fatal hemorrhage.


  1. Hammond CB. Gestational trophoblastic neoplasms. In: Scott JR, DiSaia PJ, Spellacy WN, eds. Danforth's Obstetrics and Gynecology, 8th edn. Philadelphia: Lippincott Williams & Wilkins; 1999. pp. 927-37.
  2. Wilson RB, Hunter IS, Dockerty MB. Chorioadenoma destruens. Am J Obstet Gynecol 1961;81:546-59.
  3. Song HZ, Yang XY, Xiang Y. Forty-five years' experience of the treatment of choriocarcinoma and invasive mole. Int J Gynecol Obstet 1998;160:S77-83.
  4. Makangee A, Nadvi SS, Dellen JRV. Invasive mole presenting as a spinal extradural tumour: Case report. Neurosurgery 1996;38:191-3.
  5. Yishai D, Atad J, Bornstein J, et al. Choriocarcinoma of the bladder: Report of a case of primary tumour or late metastasis of a molar pregnancy. J Reprod Med 1995;40:482-4.
  6. ACOG Technical Bulletin. Management of gestational trophoblastic disease. Int J Gynecol Obstet 1993;142:308-15.
  7. Mackenzie F, Mathers A, Kennedy J, Invasive hydatidiform mole presenting as an acute primary haemoperitoneum. Br J Obstet Gynecol 1993;100:953-4.
  8. Ring AM. The concept of benign metastasizing hydatidiform moles. Am J Clin Path 1972;58:111-7.

Copyright 2002 - Indian Journal of Cancer.

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