Volume 5, Issue 4 pp. 241-249

Placental site trophoblastic tumor. Report of three cases and review of the literature

J. How

J. How

Department of Obstetrics and Gynecology, University of Melbourne, Mercy Hospital for Women and Austin Hospital, and Departments of Pathology of

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J. Scurry

J. Scurry

Mercy Hospital for Women,

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P. Grant

P. Grant

Department of Obstetrics and Gynecology, University of Melbourne, Mercy Hospital for Women and Austin Hospital, and Departments of Pathology of

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K. Sapountzis

K. Sapountzis

Mercy Hospital for Women,

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A. Ostor

A. Ostor

Royal Women’s Hospital, and

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D. Fortune

D. Fortune

Austin Hospital, and

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J. Armes

J. Armes

Cytopath Histology and Cytology Laboratory, Melbourne, Australia

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First published: July/August 1995
Citations: 4
Address for correspondence: Dr J. Scurry, Pathology, Mercy Hospital for Women, Clarendon Street, East Melbourne, Victoria 3002, Australia.

Abstract

Three cases of placental site trophoblast tumor (PSTT) are added to 74 cases in the English language literature. One case presented with an anorexic syndrome, the other two with amenorrhea and abnormal vaginal bleeding. The three patients, whose lesions were confined to the uterus, were treated by total hysterectomy and their follow-up has been uneventful. Review of the literature showed that 62 patients with PSTT were alive and 15 had died, two as a complication of treatment. The diagnosis of PSTT may be difficult on a dilatation and currettage specimen. Metastases are a powerful indicator of adverse outcome. Prognosis, as assessed on pathologic criteria, is unreliable; however, a mitotic count of more than five mitoses per 10 high power fields is significant. Surgery is the mainstay of treatment. Hysterectomy is generally indicated, but young patients who wish to remain fertile may be treated by conservative surgery. In a few cases of progressive disease, chemotherapy has achieved remission, but generally chemotherapy and radiotherapy are ineffective. Long-term follow-up is essential as PSTT may progress after years of remission. Serum human chorionic gonadotrophin (hCG) levels are the best available marker of disease, but the disease may still progress even if hCG levels are not raised.

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