Purpose: To obtain information about preorchiectomy gonadal function in pat
ients with testicular germ cell cancer to improve the clinical management o
f fertility and other andrologic aspects in these men.
Patients and Methods: in group 1, a group of 83 consecutive patients with t
esticular germ cell cancer (TGCC) investigated before orchiectomy, semen an
alysis was carried out in 63 patients and hormonal investigations, includin
g measurement of follicle-stimulating hormone, luteinizing hormone (LH), te
stosterone, estradiol, sex hormone-binding globulin (SHBG), inhibin B, and
human chorionic gonadotropin (hCG), in 71 patients. Hormone levels in patie
nts with elevated hCG (n = 41) were analyzed separately. To discriminate be
tween general cancer effects and specific effects associated with TGCC, the
same analyses were carried out in a group of 45 consecutive male patients
with malignant lymphoma (group 2). Group 3 comprised 141 men employed in a
Danish company who served as controls in the comparison of semen parameters
. As a control group in hormone investigations, 193 men were selected rando
mly from the Danish National Personal Register to make up group 4.
Results: We found significantly lower sperm concentration (median, 15 x 10(
6)/mL; range, 0 to 128 x 10(6)/mL) and total sperm count (median, 29 x 10(6
)/mL; range, 0 to 589 x 10(6)) in patients with testicular cancer than in p
atients with malignant lymphomas (sperm concentration: median, 48 x 10(6)/m
L; range, 0.04 to 250 x 10(6)/mL; sperm count: median, 146 x 10(6); range,
0.05 to 418 x 10(6)) (P <.001 and P <.001) and healthy men (sperm concentra
tion: median, 48 x 10(6)/mL; range, 0 to 402 x 10(6)/mL; sperm count: media
n, 162 x 10(6); range, 0 to 1253 x 10(6)) (P <.001 and P <.001). FSH levels
were increased in men with testicular cancer (median, 5.7 IU/L; range, 2.0
to 27 IU/L) compared with both men with malignant lymphomas (median, 3.3 I
U/L; range, 1.01 to 12.0 IU/L) and healthy controls (median, 4.1 IU/L; rang
e, 1.04 to 21 IU/L) (P =.001 and p =.007, respectively). Surprisingly, we f
ound significantly lower LH in the group of men with TGCC (median, 3.6 IU/L
; range, 1.12 to 11.9 lU/L) than in healthy men (median, 4.7 IU/L; range, 1
.3 to 11.9 IU/L) (p =.01). We could not defect any differences between men
with testicular cancer and men with malignant lymphomas and healthy men wit
h regard to serum levels of testosterane, SHBG, and estradiol. Men with tes
ticular cancer who herd increased hCG levels had significantly lower LH and
significantly higher testosterone and estradiol than those without detecta
ble hCG levels.
Conclusion: Spermatogenesis is already impaired in men with testicular canc
er before orchiectomy. Neither local suppression of spermatogenesis by tumo
r pressure nor a general cancer effect seems to fully explain this impairme
nt. The most likely explanation is preexisting impairment of spermatogenesi
s in the contralateral test is in men with testicular cancer. The question
of whether also a pre-existing Leydig cell dysfunction is present in men wi
th testicular cancer could not be answered in this study because the tumor
seems to have a direct effect on the Leydig cells. Men with testicular canc
er had low LH values as compared with controls. We speculate that increased
intratesticular level of hCG also in men without measurable serum hCG may
play a role by exerting LH-like effects on the Leydig cells, causing increa
sed testosterone and estrogen levels and low LH values in the blood. (C) 19
99 by American Society of Clinical Oncology.