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Letters to the Editor |
1 Departments of Clinical Chemistry and 2 Oncology, Helsinki University Central Hospital, Helsinki University, Helsinki, Finland
aAddress correspondence to this author at: Ulf-Håkan Stenman, Helsinki University Central Hospital, Biomedicum Helsinki, Rm. A423a, Haartmaninkatu 8, P.O. Box 700, FIN-00029 Helsinki, Finland. Fax 358-9-47171737; e-mail ulf-hakan.stenman@hus.fi.
| The first 20% of the full text of this article appears below. |
To the Editor:
Alfa-fetoprotein (AFP) and serum human chorionic gonadotropin (hCG) are reliable markers of testicular cancer, and treatment of a relapse is often initiated on the basis of marker increase alone. Slightly increased hCG concentrations have occasionally been misinterpreted to indicate a relapse, leading to inappropriate chemotherapy (1). We describe a seminoma patient in whom a relapse was suspected 10 years after therapy because the patient had increased hCG concentrations found to be caused by hypogonadism-induced pituitary hCG secretion.
A 27-year-old man underwent left radical orchiectomy and adjuvant radiotherapy for stage I testicular seminoma in the early 1990s at Helsinki University Central Hospital. The patient had a preoperative serum hCG of 0.5 IU/L (upper reference limit 0.7 IU/L) and AFP <1 IU/L (upper reference limit 9 IU/L). Atrophy of the nonmalignant testicle was suspected on the basis of preoperative ultrasound findings, but the serum testosterone concentration, 10.2 nmol/L, was within the reference interval (10–38 nmol/L), whereas follicle-stimulating hormone (FSH) concentration was increased, at 28
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U.-H. Stenman Commentary Clin. Chem., January 1, 2008; 54(1): 213 - 214. [Full Text] [PDF] |
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