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Successful pregnancy following conservative surgical therapy of an invasive molar gestation.

Introduction

Gestational trophoblastic disease is an abnormal pregnancy occurring from an aberrant fertilization event. This maternal tumor is unique because it arises from fetal tissue. (1) An invasive molar gestation is a variation of a hydatiform mole where the hydropic villi invade the uterine wall or blood vessels and develops only after uterine evacuation of a molar pregnancy. (2,3) Excessive trophoblastic overgrowth and penetration of trophoblastic elements into the myometrium are distinguishing features of an invasive molar gestation which tends to be locally invasive and usually does not result in widespread metastatic disease. (4)

Persistent gestational trophoblastic disease is normally treated with single agent chemotherapy with methotrexate. Medical treatment failures are usually treated by hysterectomy. Treatment of invasive molar gestation by conservative surgical excision has been described in the literature. However, 7 of 22 patients in one trial required additional chemotherapy following the surgical excision for persistent [beta]-hCG elevations. (5)

Case

A 24-year-old woman presented to our facility with the presumed diagnosis of an intramural ectopic pregnancy. Six months prior to admission, she underwent a suction curettage for a presumed incomplete abortion with pathology showing some hydropic changes of the villi. She was placed on oral contraceptives and had regular monthly menses until 2 months prior to admission. A pregnancy test was obtained and was positive but serial levels of beta-hCG plateaued.

[FIGURE 1 OMITTED]

The patient was hemodynamically stable with no discomfort. Her quantitative [beta]-hCG on admission was 6283 IU. Transvaginal ultrasound (See Figure 1) revealed a cystic structure within the uterine wall with a marked increase in vascularity, suspicious for intramural ectopic pregnancy. Because of the lack of symptoms, a normal CBC, renal, and liver function tests and the fact that her HCG levels were already plateauing, it was decided to attempt to treat her with single dose methotrexate. She was given one dose of 50 mg/ [m.sup.2] of intramuscular Methotrexate, and her beta-hCG levels decreased to 5777 IU on the second day after methotrexate injection.

Follow-up quantitative [beta]-hCG values initially fell to 5081 IU but then plateaued at 5011 IU. Repeat ultrasound showed increased size and vascularity of the cystic mass along with a small amount of cul-de-sac fluid. At this point, the diagnosis of invasive molar gestation as opposed to intramural ectopic pregnancy was suspected. She underwent a chest x-ray, which was normal. Her follow-up platelet count had fallen to 71,000 but there was no other evidence of bone marrow suppression. She underwent leucovorin rescue as the thrombocytopenia was felt to be due to the methotrexate. Her platelet count improved to 121,000 after one dose of leucovorin. Further methotrexate therapy, even in the context of a multi-dose regimen, was felt to be contraindicated. Interventional radiology was consulted and performed a uterine artery embolization in an attempt to decrease blood flow to the area in case surgical intervention was necessary.

Her quantitative [beta]-hCG initially dropped following the uterine artery embolization but then began to rise once again to a level of 3342 IU. Laparoscopic findings included a markedly edematous left tube, left broad ligament, and left proximal round ligament, marked dilation of the vessels in the left broad ligament and infundibulopelvic ligament and a 2 cm x 2 cm x 3 cm mass protruding from the left posterior wall of the uterus (See Figure 2). Laparotomy was performed and the round ligaments were ligated and divided in order to reduce the time needed for hysterectomy in case of excessive bleeding. A bladder flap was developed, the anterior sheath of the broad ligaments opened, and the ligaments were penetrated lateral to the ascending branches of the uterine artery. A Penrose drain was passed through these defects to provide a tourniquet effect to the ascending branches of the uterine arteries. A rubber-shod clamp was placed over the proximal left tube and dilated vessels in an attempt to interrupt collateral blood flow. The serosa overlying the mass was injected with dilute vasopressin and the serosa was opened using a monopolar electrosurgical device. The mass had a capsule that was immediately beneath the serosa and extended into the myometrium and contained villous-like material and dense tissue. The capsule and its contents were removed using the monopolar electrosurgical device. Flowseal and Gelfoam were placed in the base of the myometrial incision, and the defect was then closed using 2-0 chromic. The serosa was closed using 3-0 vicryl in a baseball suture fashion, and the Penrose drain was removed. The total estimated blood loss for the procedure was 300 mL. The pathologic evaluation of the tissue revealed an invasive molar gestation.

Her quantitative [beta]-hCG levels remained negative for over 1 year. She then became pregnant and underwent a Cesarean delivery at 36 weeks gestation due to concern for uterine rupture if labor were to occur. Small bowel was noted to be adherent to the uterine fundus. The uterine wall was intact.

Conclusion

The initial treatment for persistent trophoblastic disease in the form of invasive molar gestation is single agent chemotherapy with methotrexate. (7) If chemotherapy fails or is contraindicated and future fertility is desired, conservative surgical excision may be appropriate for treatment and definitive diagnosis. In our case, this approach led to negative [beta]-hCG levels for greater than 1-year post therapy and the subsequent delivery of a viable infant.

References

(1.) Berkowitz RS. Goldstein DP. Chorionic tumors. N Engl J Med. 1996;23:1740-8.

(2.) Stenchever MA, Droegemueller W, Herbst AL, Mishell D. Gestational Trophoblastic Disease. In Comprehensive Gynecology. St Louis: Mosby; 2001. p. 1047-51.

(3.) Kennedy AW. Persistent nonmetastatic gestational trophoblastic disease. Semin Oncol. 1995;22:161-5.

(4.) Cunningham FG, Gant NF, Leveno KJ, Gilstrap III LC, Hauth JC, Wenstrom KD: Diseases and Abnormalities of the Placenta. In Williams Obstetrics 21st Edition. Seils A, Noujaim SR, Davis K. New York: McGraw-Hill; 2001. p. 827-52.

(5.) Kanazawa K, Sasagawa M, Suzuki T, Takeuchi S. Clinical evaluation of focal excision of myometrial lesion for treatment of invasive hydatidiform mole. Acta Obstet Gynecol Scand. 1988;67:487-92.

Shon P. Rowan, MD

Michael L. Stitely, MD

Roger C. Toffle, MD

WVU School of Medicine

Department of Obstetrics and

Gynecology
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Article Details
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Title Annotation:Scientific Article
Author:Rowan, Shon P.; Stitely, Michael L.; Toffle, Roger C.
Publication:West Virginia Medical Journal
Article Type:Case study
Geographic Code:1U5WV
Date:May 1, 2010
Words:1024
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