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THE PITUITARY‐LEYDIG CELL AXIS IN MEN WITH SEVERE DAMAGE TO THE GERMINAL EPITHELIUM
Author(s) -
TSATSOULIS A.,
WHITEHEAD E.,
JOHN J. ST.,
SHALET S. M.,
ROBERTSON W. R.
Publication year - 1987
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1987.tb02952.x
Subject(s) - medicine , endocrinology , germinal epithelium , leydig cell , epithelium , biology , hormone , luteinizing hormone , spermatogenesis , genetics
SUMMARY Eighteen men (mean age 27, range 18‐30 years) treated for Hodgkin's disease with 6‐8 courses of MVPP (Mustine, Vinblastine, Procarbazine and Prednisolone) have had Leydig cell function assessed by their steroidogenic responses to stimulation by a single bolus dose of HCG (1000 units intramuscularly). Normal age‐matched men ( n = 16) acted as controls. Baseline immunoreactive FSH was markedly raised in the patients (mean 18.1 ± SD 6‐9 vs 2.0 ± 1.5 IU/1, P < 0‐0001) reflecting damage to the germinal epithelium. Immunoreactive LH was also greater in patients (10‐3 + 3‐9 IU/1) than in controls (3‐9+1‐9 IU/1, P <00001). There were no differences between the baseline testosterone, androstenedione, oestradiol, oestrone and sex hormone binding globulin (SHBG) concentrations. The testosterone/SHBG ratios were similar in the two groups and there was no correlation between baseline LH and testosterone concentrations or testosterone/SHBG ratios. Testosterone, androstenedione, oestradiol and oestrone secretion in response to HCG stimulation were similar at 24 h and 96 h in both groups. In order to explain the paradox of elevated immunoreactive LH in the face of normal testicular steroidogenesis in such patients, LH biological activity (B) as well as LH immunoreactivity (I) and FSH and testosterone were estimated in a second similar group of patients ( n = 17, mean age 27, range 17‐43 years) and in a further age‐matched control group ( n = 17). Bioactive and immunoreactive LH levels were significantly increased (P< 0‐005 and P < 0‐001, respectively) in the patient group. However, the biological: immunological (B:I) LH ratios were found to be similar in the patients (2.7 ± 0.6, mean ± SD) and controls (2.8 ± 0.7). There was a significant correlation between immunoreactive LH and FSH concentrations in the patient group (r = 0‐65, P <001), but not in the controls. In conclusion Leydig cell function, as judged by the steroidogenic responses to HCG stimulation, is normal in patients with chemotherapy‐induced spermatogenic damage. The biological activity of LH is not changed, but there is a resetting of the LHLeydig cell axis