ADENOHYPOPHYSEAL-GONADAL DYSFUNCTION IN MALE HEMODIALYZED PATIENTS BEFORE AND AFTER SUBTOTAL PARATHYROIDECTOMY

Citation
I. Zofkova et al., ADENOHYPOPHYSEAL-GONADAL DYSFUNCTION IN MALE HEMODIALYZED PATIENTS BEFORE AND AFTER SUBTOTAL PARATHYROIDECTOMY, Nephron, 74(3), 1996, pp. 536-540
Citations number
26
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00282766
Volume
74
Issue
3
Year of publication
1996
Pages
536 - 540
Database
ISI
SICI code
0028-2766(1996)74:3<536:ADIMHP>2.0.ZU;2-7
Abstract
The function of the adenohypophyseal-gonadal axis in haemodialyzed mal e patients is modified: the serum testosterone level is low, and the g onadotropin levels are increased. The pathogenetic role of secondary h yperparathyroidism in this disorder has not previously been defined. T he area under the curve (AUG) and the secretion kinetics of testostero ne, luteinizing hormone (LH), and follicle-stimulating hormone after a dministration of LH-releasing hormone were examined in 7 dialyzed men with secondary hyperparathyroidism (mean age 36.2, range 20-47 years) before and 3 and 6 months after parathyroidectomy (PTX). The operation was successful in all 7 patients, as intact parathyroid hormone decli ned markedly during both postoperative periods as compared with the va lues before PTX: 81 +/- (SEM) 34 and 138 +/- 57 ng/l versus 965 +/- 11 6 ng/l (p < 0.01 and p < 0.01). The testosterone AUC prior to PTX (63 +/- 115 nmol/l x min) and 3 months(-4 +/- 36 nmol/l x min) and 6 month s after PTX (-62 +/- 69) did not differ significantly, as was the case with LH AUC(1,110 +/- 223 and 1,214 +/- 331 and 1,020 +/- 314 U/l x m in, respectively) and follicle-stimulating hormone AUC (525 +/- 334 an d 634 +/- 347 and 533 +/- 264 U/l x min, respectively). The secretion kinetics of all three hormones was atypical as compared with healthy m en of similar age, but it did not change after PTX. There were no corr elations between the sexual indicators and parathyroid hormone, 1,25(O H)(2)D-3, calcium, or phosphate during the individual periods. These f indings indicate that secondary hyperparathyroidism is probably not in volved in the dysfunction of the adenohypophyseal-gonadal axis in dial yzed men.