I-125-labelled human chorionic gonadotrophin (hCG) as an elimination marker in the evaluation of hCG decline during chemotherapy in patients with testicular cancer

Citation
Tb. Christensen et al., I-125-labelled human chorionic gonadotrophin (hCG) as an elimination marker in the evaluation of hCG decline during chemotherapy in patients with testicular cancer, BR J CANC, 80(10), 1999, pp. 1577-1581
Citations number
16
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
BRITISH JOURNAL OF CANCER
ISSN journal
00070920 → ACNP
Volume
80
Issue
10
Year of publication
1999
Pages
1577 - 1581
Database
ISI
SICI code
0007-0920(199907)80:10<1577:IHCG(A>2.0.ZU;2-J
Abstract
The rate of reduction in the concentration of serum human chorionic gonadot rophin (hCG) following chemotherapy for germ cell tumours may follow a comp lex pattern, with longer apparent half-life during later stages of chemothe rapy, even in patients treated successfully. The commonly used half-life of less than 3 days for hCG to monitor the effect of chemotherapy in patients with germ cell tumours of the testis may represent too simple a model. I-1 25-labelled hCG was injected intravenously in 27 patients with germ cell tu mours and elevated hCG during chemotherapy. The plasma radioactivity and hC G concentrations were followed. During chemotherapy, the plasma disappearan ce of hCG showed a biphasic pattern, with an initial fast and a later slow component in all patients. Using the steep part of the hCG plasma disappear ance curve, five patients who achieved long-term remission had half-lives l onger than 3 days (3.6-6.8 days), whereas four out of five patients not ach ieving long-term remission had half-lives shorter than 3 days. After the th ird treatment cycle, eight patients who achieved long-term remission had hC G half-lives longer than 3 days (7.4-17.0 days). In these patients, the pla sma disappearance of [I-125]hCG was equivalent to that of hCG. Thus, the sl ow decline of hCG represented a slow plasma disappearance rather than a hCG production from vital tumour cells and could, consequently, not be used to select patients for additional or intensified chemotherapy. The concept of a fixed half-life for plasma hCG during treatment of hCG-producing germ ce ll tumours is inappropriate and should be revised. Difficulties in interpre ting a slow decline of hCG may be overcome by comparing the plasma disappea rance of total hCG with the plasma disappearance of [I-125]hCG.