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Secondary Treatment Failure without Anti‐human Chorionic Gonadotropin Antibody in a Patient with Kallmann Syndrome
Author(s) -
Kitahara Satoshi,
Yoshida Kenichiro,
Ishizaka Kazuhiro,
Higashi Yotsuo,
Takagi Kentaro,
Oshima Hiroyuki
Publication year - 1998
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.1998.tb00378.x
Subject(s) - azoospermia , medicine , human chorionic gonadotropin , gonadotropin , luteinizing hormone , endocrinology , testosterone (patch) , spermatogenesis , follicle stimulating hormone , hormone , infertility , pregnancy , biology , genetics
A 29‐year‐old man with Kallmann syndrome suddenly developed decreased semen volume, azoospermia, and facial hair loss after 11 years of successful human chorionic gonadotropin (hCG) and human menopausal gonadotropin (hMG) treatment. Anti‐hCG antibody was not detected in the patient's serum. A high serum level of luteinizing hormone (LH) with nasal LH‐releasing hormone analogue administration failed to increase serum testosterone to a sufficient level. Testosterone injection after cessation of hCG and hMG therapy was able to improve semen volume, but not azoospermia. Resumption of hCG and hMG therapy after 6 months cessation partially restored spermatogenesis. The secondary failure of hCG and hMG therapy suggests a decrease of testicular sensitivity to LH as well as hCG.