CHORIOCARCINOMA...

CEREBROVASULAR EMBOLIZATION OForiocarcinoma - I don't have time to die! - what happened to me November 4th 1994.

My story of how Choriocarcinoma affected my life m

Links to sites by people I have met who also beat choriocarcinomaetastas

Peter G. Rose, MD

Bagshawe and Brooks(1) first reported that choriocarcinoma could be found at autopsy in the pulmonary tree of patients who died with pulmonary hypertension. More recently, Seckl et al(2) reported the successful chemotherapeutic treatment of three patients with pulmonary emboli or pulmonary hypertension and elevated HCG levels. In the current report, a case of an acute and progressive neurologic event associated with cerebrovascular occlusion and an elevating HCG is presented. Case A 31-year-old woman, gravida 1, para 0-0-1-0, was admitted to the Neurology Department on November 5, 1994, for altered mental status. A complete blood count, chemistries, toxic screen, and coagulation studies were within normal limits. A cerebrospinal fluid analysis, including chemistries, immunoelectrophoresis, Gram stain, and culture, was negative. Sedimentation rate, C-reactive protein, antinuclear and anticardiac antibodies, serum electrophoresis, and VDRL were negative. A urine pregnancy test was positive, and a quantitative HCG was 3100 U/L. The patient had a complete molar pregnancy 2 years earlier, which was evacuated by D&C. At that time, her HCG was 58,000 U/L. She had sporadic follow- up, and in March 1993, the HCG was less than 5 U/L. During her hospitalization, she had progressive disorientation, diplopia, and dysarthria. A magnetic resonance imaging study-demonstrated infarction involving the thalamus bilaterally, right occipital pole, left cerebella hemisphere, and, to a lesser extent, the left occipital pole. A cerebral angiogram demonstrated occlusion of the distal calcarine branches of the right posterior cerebral artery. There was no evidence of vasculitis. A cardiac ultrasound scan was normal, with no vegetations or septal defects. A repeat spinal tap showed a ratio of cerebrospinal fluid to serum HCG of less than 1:100, which was not consistent with metastatic central nervous system gestational trophoblastic disease. Computed tomographic (Ct) scans of the chest, abdomen, and pelvis were normal. Serum alpha-fetoprotein was negative, excluding a mixed germ cell tumor. Serial HCG levels rose from 3020 to 6610 U/L from November 6 to November 11. A pelvic examination, vaginal ultrasound with Doppler flow, and an endometrial biopsy were performed; results were unremarkable. On November 12, the patient developed a severe headache -- and CT scan evidence of intracranial bleeding. An emergency craniotomy and hematoma evacuation was performed. Her HCG level on November 14 was 9050 U/L. Pathology from the craniotomy demonstrated no evidence of trophoblastic tissue. By November 16, the patient re-bled and underwent re-operation for hematoma evacuation. On November 17, the HCG level was elevated to 11,600 U/L, and a second spinal tap demonstrated a cerebrospinal fluid to serum HCG ratio greater than 1:60. It was unclear whether this was related to intracranial trophoblastic disease or to blood that crossed the blood brain barrier following surgery. On November 19, while intubated in the Intensive Care Unit, the patient was started on etoposide, actinomycin D, methotrexate, cyclophosphamide, and vincristine therapy. The patient's mental status improved quickly, and she was extubated 2 days after chemo- therapy initiation. The HCG level fell from 9630 to 179 U/L from November 21 to December 2. She continued to receive chemotherapy on a biweekly basis. Her HCG normalized after three Cycles of actinomycin D, methotrexate, cyclophosphamide, and vincristine. She received a total of six cycles of therapy and remains fully functional and disease-free 23 months later. Comment If untreated, choriocarcinoma is a rapidly fatal tumor of women of reproductive age. The clinical, biochemical, and radiologic findings as well as the dramatic response to chemotherapy in the current case provide support to the diagnosis of cerebrovascular embolic disease. More definite proof of this diagnosis would require an autopsy.

References 1. Bagshawe KD, Brooks WOW. Subacute pulmonary hypertension due to chorionepithelioma. Lancet 1959;i:653-8. 2. Seckl MI, Rustin GIS. Newlands ES. Gwyther Sj. Bomamji J. Pulmonary embolism, pulmonary hypertension, and choriocarcinoma. Lancet 1991;338:1313-5. Received March 4. 1996. Received in revised form Apri19, 1996. Accepted April 10, 1996. Copyright 1996 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc. \ \ Obstetrics & Gynecology From the Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University MacDonald Women's Hospital, University Hospitals of Cleveland, Case Western Reserve University, Cleveland, Ohio.

MY STORY, CHORIOCARCINOMA AND I