Testicular steroid sulfatase overexpression is associated with Leydig cell dysfunction in primary spermatogenic failure

Andrology ◽  
2020 ◽  
Author(s):  
Maria C. Lardone ◽  
Ian N. Reyes ◽  
Eliana Ortiz ◽  
Antonio Piottante ◽  
Cristián Palma ◽  
...  
2019 ◽  
Vol 10 ◽  
Author(s):  
Yiyan Wang ◽  
Chaobo Ni ◽  
Xiaoheng Li ◽  
Zhenkun Lin ◽  
Qiqi Zhu ◽  
...  

1999 ◽  
Vol 17 (5) ◽  
pp. 1493-1493 ◽  
Author(s):  
S. J. Howell ◽  
J. A. Radford ◽  
W.D.J. Ryder ◽  
S. M. Shalet

PURPOSE: To evaluate testicular function in men after treatment with cytotoxic chemotherapy. PATIENTS AND METHODS: We measured testosterone, sex hormone–binding globulin (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels in 209 men after treatment with mechlorethamine, vinblastine, procarbazine, and prednisone, hybrid chemotherapy, or high-dose chemotherapy and in 54 healthy age-matched controls. RESULTS: The mean age of the patients was 38 years (range, 19 to 68 years), and all patients had received chemotherapy between 1 and 22 years previously. Patients had significantly higher mean LH (7.9 v 4.1 IU/L; P < .0001) and FSH levels (18.8 v 3.1 IU/L; P < .0001) than controls. There was no significant difference in mean total testosterone level between the patients and controls, but there was a trend toward a lower mean testosterone/SHBG ratio in the patients (0.63 v 0.7; P = .08). Analysis of the hormonal parameters using a model that allowed for the effects of increasing age on testicular function showed evidence of significant recovery of gonadal function in the first 10 years after treatment. Fifty-two percent of patients had LH levels at or above the upper limit of normal, and 32% of patients had increased LH with testosterone levels in the lower half of the normal range, suggesting a degree of Leydig cell impairment. CONCLUSION: In a significant proportion of men, there is good evidence of Leydig cell dysfunction after cytotoxic chemotherapy. The clinical significance of this Leydig cell dysfunction is not clear, but some of these men may benefit from testosterone replacement. Further studies are warranted.


2016 ◽  
Vol 8 (10) ◽  
pp. 306 ◽  
Author(s):  
Taylor C Peak ◽  
Nora M Haney ◽  
William Wang ◽  
Kenneth J DeLay ◽  
Wayne J Hellstrom

1987 ◽  
Vol 64 (6) ◽  
pp. 1194-1198 ◽  
Author(s):  
JOHN D. BOOTH ◽  
GEORGE R. MERRIAM ◽  
RICHARD V. CLARK ◽  
D. LYNN LORIAUX ◽  
RICHARD J. SHERINS

The Lancet ◽  
1981 ◽  
Vol 318 (8245) ◽  
pp. 529
Author(s):  
Christina Wang ◽  
RonaldP. Ng ◽  
T.K. Chan ◽  
David Todd

1980 ◽  
Vol 1 (3) ◽  
pp. 127-132 ◽  
Author(s):  
LUIS J. RODRIGUEZ-RIGAU ◽  
KEITH D. SMITH ◽  
EMIL STEINBERGER
Keyword(s):  

2006 ◽  
Vol 91 (11) ◽  
pp. 4705-4708 ◽  
Author(s):  
Anne M. Wikström ◽  
Katrine Bay ◽  
Matti Hero ◽  
Anna-Maria Andersson ◽  
Leo Dunkel

Abstract Context: Levels of the Leydig cell-specific hormone insulin-like factor 3 (INSL3) are incompletely characterized in boys during pubertal development. Objective: The objective of the study was to characterize changes in INSL3 levels during spontaneous puberty in healthy boys, boys with aromatase inhibitor-induced hypergonadotropic hyperandrogenism, and boys with Leydig cell dysfunction. Design: This was a prospective clinical study. Setting: The study was conducted at a university hospital pediatric endocrinology outpatient clinic. Patients: Patients included 30 healthy boys with idiopathic short stature (ISS) aged 9.0–14.5 yr and 14 boys with Klinefelter syndrome (KS) aged 10–13.9 yr. Intervention: In ISS boys, intervention included aromatase inhibitor letrozole or placebo for 24 months. Main Outcome Measures: Serum INSL3 levels in relation to bone age, Tanner pubertal stages, and LH and testosterone levels were measured. Results: Onset of puberty was associated with a significant increase in INSL3 levels from 0.06 ± 0.01 ng/ml at Tanner G1 to 0.32 ± 0.16 ng/ml at G2 (P &lt; 0.0001). Adult INSL3 levels (≥0.55 ng/ml) were attained at bone age 13–14 yr. ISS boys with letrozole-induced hypergonadotropic hyperandrogenism had, after 12 months of therapy, higher INSL3 levels than did placebo treated (0.85 ± 0.54 vs. 0.26 ± 0.17 ng/ml, P &lt; 0.01). In KS boys during spontaneous puberty, after an initial increase similar to that in healthy boys, INSL3 concentrations leveled off despite hyperstimulation by LH. Positive correlations occurred between serum INSL3 and LH and between INSL3 and testosterone levels in all three groups (P &lt; 0.0001). Conclusions: In boys, the Leydig cell-specific hormone INSL3 may serve as a new marker for onset and progression of puberty. Pubertal increase in INSL3 levels seems to depend on LH. In KS subjects, INSL3 concentrations indicate Leydig cell dysfunction from midpuberty onward.


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