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Clinical Chemistry 48: 2289-2290, 2002;
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(Clinical Chemistry. 2002;48:2289-2290.)
© 2002 American Association for Clinical Chemistry, Inc.


Letters

CA-125 Concentrations in Patients Awaiting Cardiac Transplantation

Lorinda Soma1, Michael Allen2, Lynda Tobin2, Colleen Ganster2, Margaret Bulley1, Jennifer Hunt3, Larry J. Kricka1, Marilyn Senior1 and Andrew Kao2a

1 University of Pennsylvania, Medical Center, Department of Pathology, and Laboratory Medicine, 7th Floor, Founders Bldg., 3400 Spruce St., Philadelphia, PA 19104

2 University of Pennsylvania Medical Center, Department of Medicine, Cardiology Division, 6 Penn Tower, 3400 Spruce St., Philadelphia, PA 19104

3 University of Pittsburgh, Department of Pathology, and Laboratory Medicine, 200 Lothrop St., Pittsburgh, PA 15213

aAuthor for correspondence. Fax 215-615-0828; e-mail andrew.kao{at}uphs.upenn.edu.


To the Editor:

CA-125 (cancer antigen or carbohydrate antigen) is a high-molecular weight glycoprotein most appropriately used for monitoring treatment response and recurrence of ovarian carcinoma, with concentrations >35 units/mL indicating residual tumor. Serum concentrations have also been shown to correlate with ovarian tumor mass. Increases, although usually not as marked, have been seen in other conditions such as lung cancer, gastrointestinal cancer, abdominal miliary tuberculosis, endometriosis, pelvic inflammatory disease, and during ovulation in 1–2% of healthy women. Therefore, this serum marker is not recommended as a screening test for ovarian carcinoma (1)(2)(3).

Recently, at the University of Pennsylvania Medical Center, CA-125 was inadvertently ordered on a male heart failure (HF) patient awaiting cardiac transplantation, and was found to be markedly increased at 1060 units/mL. The test was repeated and confirmed the marked increase. The patient was also tested for human anti-mouse antibody (HAMA) to rule out possible interference causing a false-positive result. The results of the HAMA test were negative. The CA-125 concentrations decreased after transplantation with improvement in clinical status (538 units/mL). We analyzed multiple sections of the patient’s explanted native heart by use of immunohistochemical staining for CA-125 (1:50 dilution; positive control = ovarian adenocarcinoma; Dako) to determine the source of CA-125 production. No positive staining was detected in the tissue (cardiac, vascular, and mesothelial cells).

A subsequent literature search revealed one study pertaining to CA-125 in HF patients. That study included 71 patients of all New York Heart Association (NYHA) classes and showed a relationship between advancing HF and progressive increases in CA-125 concentrations [mean CA-125 for NYHA classes: class I = 36 units/mL; class II = 79 units/mL; class III = 210 units/mL; class IV = 502 units/mL (4)].

The authors of this study felt that the elaboration of CA-125 could be from the pericardial mesothelium; however, the exact mechanism is unclear (4)(5)(6)(7). In clinical practice, augmentation of HF therapy is based solely on worsening symptoms and echocardiographic findings. However, on the basis of this initial encouraging report and our experience, this pilot study investigated the possibility of using the CA-125 marker to identify patients with worsening HF before they develop clinical symptomatology.

We analyzed serum CA-125 concentrations using the CENTOCOR CA-125 II RIA from blood obtained during a 6-month period from 35 patients (33 males; 30 Caucasians) with NYHA class III or IV HF awaiting cardiac transplantation. Blood was drawn during their routine clinic visits and while they were hospitalized. This study was approved by the Institutional Review Board, and informed consent was obtained from all patients. Clinical stability was based on examination by a HF cardiologist, as well as invasive hemodynamic measurements. Patients with markedly abnormal hemodynamics, or those with signs of low output failure, were considered unstable. Although many of the patients did show increases in CA-125 concentrations, some being quite marked, there was no correlation between clinical status and the concentration of CA-125 (Table 1 ). There was also no correlation between "confounding" factors, such as pericardial, pleural, or peritoneal effusions.


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Table 1. CA-125 in stable and unstable HF patients.1

We were unable to confirm the published correlation and conclude that CA-125 is not a useful marker in predicting cardiac status or managing pretransplant patients. However, perhaps a larger and longer-term study may be able to show a meaningful relationship.


References

  1. Bast RC, Klug TL, St John E, Jenmison E, Niloff JM, Lazarus H, et al. A radioimmunoassay using a monoclonal antibody to monitor the course of epithelial ovarian cancer. N Engl J Med 1983;309:883-887.[Abstract]
  2. Eerdekens MW, Nouwen EJ, Pollet DE, Briers TW, DeBroe ME. Placental alkaline phosphatase and cancer antigen 125 in sera of patients with benign and malignant diseases. Clin Chem 1985;31:687-690.[Abstract]
  3. Sevinc A, Buyukberber S, Sari R, Kiroglu Y, Turk HM, Ates M. Elevated serum CA-125 levels in hemodialysis patients with peritoneal pleural or pericardial fluids. Gynecol Oncol 2000;77:254-257.[ISI][Medline] [Order article via Infotrieve]
  4. Nagele H, Bahol M, Klapdor R, Schaeperkoetter D, Rodiger W. CA125 and its relation to cardiac function. Am Heart J 1999;137:1044-1049.[Medline] [Order article via Infotrieve]
  5. Kabawat SE, Bast RC, Bahn AK, Welch WR, Knapp RC, Colvin RB. Tissue distribution of a coelomic epithelium related antigen recognized by the monoclonal antibody OC125. Int J Gynecol Pathol 1983;2:275-285.[ISI][Medline] [Order article via Infotrieve]
  6. Zeimet AG, Marth C, Offner FA, Obrist P, Uhl-Steidl M, Geichtinger H, et al. Human peritoneal mesothelial cells are more potent than ovarian cancer cells in producing tumor marker CA-125. Gynecol Oncol 1996;62:384-389.[ISI][Medline] [Order article via Infotrieve]
  7. Carpenter PM, Gamboa GP, Dorion GE, Ramsinghani NS, Aissi AM, Manetta A. Radiation induced CA 125 production by mesothelial cells. Gynecol Oncol 1996;63:328-332.[Medline] [Order article via Infotrieve]




This Article
Right arrow Extract Freely available
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Right arrow Submit an electronic Letter to
the Editor about this paper
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Right arrow Email this article to a friend
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Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
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Google Scholar
Right arrow Articles by Soma, L.
Right arrow Articles by Kao, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Soma, L.
Right arrow Articles by Kao, A.
Related Collections
Right arrow Proteomics and Protein Markers


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