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  • 1
    ISSN: 1432-1076
    Keywords: Acute lymphoblastic leukemia ; Hypergonadotropic hypogonadism ; SHBG-deficiency ; Hyperprolatinaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Five pubertal boys (puberty stage Iv–V) and four prepubertal girls with acute lymphoblastic leukemia were treated with a combination of prednisone, vincristine, daunorubicin and l-asparaginase for remission induction. The hypothalamopituitary-gonadal axis was investigated by measuring basal plasma levels of LH, FSH, and PRL in both groups as well as the response to LHRH/TRH stimulation in pubertal boys before, on day 10, 21, and 28 during induction therapy and 23 days after the induction phase (day 51). Furthermore, the binding capacity of sex-hormone-binding globulin (SHBG), plasma levels of testosterone (T) and estradiol (E2) were monitored as well as the testicular volumes of the boys. Within three weeks of induction chemotherapy, plasma T, E2 and the binding capacity of SHBG decreased in both groups, together with a reduction of testicular volumes in the boys. Concommitantly, basal LH, FSH, and PRL values doubled with a normal gonadotrophin response to LHRH. The PRL response to TRH increased at the end of the induction phase, when chemotherapy with vincristine, daunorubicin and l-asparaginase was terminated, but prednisone treatment was continued for 7 another days. During the subsequent prophylactic irradiation of the central nervous system combined with other antileukemic drugs, all hormonal values including testicular volumes in pubertal boys became normal within a period of 3 weeks. Our data clearly demonstrate that an induction chemotherapy regimen such as that employed by the Berlin protocol leads to a transient castrating effect at the gonadal level and to a transient failure of synthesis of SHBG at the hepatic level. Increased prolactin values as well as an increased response to TRH may be related to a decrease in T indicating the existence of a negative feed-back-loop mechanism between T and PRL.
    Type of Medium: Electronic Resource
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