(Chest. 2005;128:619S-620S.)
© 2005
American College of Chest Physicians
Metastatic Cancer While Receiving Continuous Prostacyclin Therapy*
Karen A. Fagan, MD;
Todd M. Bull, MD;
David B. Badesch, MD, FCCP and
Norbert F. Voelkel, MD
* From the Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, University of Colorado Health Sciences Center, Denver, CO.
Correspondence to: Karen Fagan, MD, 4200 East Ninth Ave, C-272, Denver, CO 80262; e-mail: karen.fagan{at}uchsc.edu
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Introduction
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Prostacyclin and its derivatives are reported to decrease tumor metastases in several animal models. Potential mechanisms include the modulation of endothelial cell adhesion molecule expression, decreased adhesion of tumor cells to the subendothelial matrix, decreased tumor cell-platelet aggregation, decreased tumor cell-induced endothelial cell retraction, and decreased growth of micrometastases. The inhibition of cyclooxygenase-2 has been demonstrated to decrease the formation of colon adenomas and the development of colon carcinoma. Cancer chemoprevention trials using prostacyclin are underway. Thus, we hypothesized that patients receiving prostacyclin treatment are relatively protected from the development of metastatic malignancy.
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Methods and Results
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Six patients (approximately 6% of the current group of patients at the University of Colorado Health Sciences Center who are receiving prostacyclin treatment) received diagnoses of metastatic malignancy during prostacyclin treatment. Primary tumors, age, gender, prostacyclin initiation date, and most recent or terminal dose of prostacyclin are summarized in Table 1
. Two patients have died of metastatic disease.
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Table 1.. Summary of Primary Tumors, Age, Gender, Prostacyclin Initiation Date, and Most Recent or Terminal Dose of Prostacyclin*
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Conclusions
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In this small group of patients, prostacyclin therapy did not protect the patient from the development of metastatic cancer. Possible explanations include observations in which the intermittent administration of cicaprost was protective in rats from metastases while continuous administration was not. Additionally, prostacyclin has been shown to induce vascular endothelial growth factor expression, which plays an important role in the growth of tumors and metastases. Interestingly, all patients are women and half of have ovarian cancer. Further studies are necessary to determine whether continuously infused prostacyclin may increase the metastatic rate and/or the potential for the growth of tumors, or the development of specific tumors.
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Introduction
Methods and Results
