scholarly journals Leydig Cell Tumor-Induced Gonadotropin-Independent Precocious Puberty Progressing to Gonadotropin-Dependent Precocious Puberty Post Orchiectomy: Out of the Frying Pan Into the Fire

Cureus ◽  
2022 ◽  
Author(s):  
Pankaj Singhania ◽  
Rana Bhattacharjee ◽  
Partha Pratim Chakraborty ◽  
Subhankar Chowdhury
Keyword(s):  
Precocious Puberty ◽  
Leydig Cell ◽  
Leydig Cell Tumor ◽  
Cell Tumor

scholarly journals Sertoli-Leydig Cell Tumor of the Ovary, a Rare Cause of Precocious Puberty in a 12-Month-Old Infant

2002 ◽  
Vol 87 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Catherine S. Choong ◽  
Peter J. Fuller ◽  
Simon Chu ◽  
Yvette Jeske ◽  
Francis Bowling ◽  
...  
Keyword(s):  
Precocious Puberty ◽  
Leydig Cell ◽  
Central Precocious Puberty ◽  
Leydig Cell Tumor ◽  
Cell Tumor ◽  
Total Serum ◽  
Surgical Removal ◽  
Mrna Levels ◽  
Lh Receptor ◽  
Early Juvenile Stage

We report a 12-month-old infant who presented with a 4-month history of isosexual precocious puberty secondary to an estrogenizing Sertoli-Leydig cell tumor of the ovary. Total serum immunoreactive inhibin and subunits A and B were markedly elevated before surgical resection and subsequently decreased 7 wk later into the normal prepubertal range. Twenty weeks following surgical removal, the patient presented again with central precocious puberty; inhibin B levels were raised on this occasion, a luteinizing releasing hormone stimulation test confirmed central precocious puberty. This is the youngest reported occurrence of this rare sex cord stromal neoplasm. The prognosis of this extremely rare tumor presenting at this early juvenile stage is uncertain. This report illustrates the usefulness of serum inhibin as a tumor marker during therapeutic suppression with leuprorelin acetate for central precocious puberty. Analysis of genomic and tumor DNA revealed a normal nucleotide sequence for the LH receptor and the Gαs gene. To understand the molecular pathogenesis of this tumor we analyzed mRNA levels for the inhibin A and B subunits, FSH receptor, LH receptor aromatase, steroidogenic factor-1 and the ER β genes. Molecular characterization reveals the presence of genes specific for granulosa and Leydig cells; the relative expression of these genes, in addition to its histologic characteristics, suggests that this tumor may result from a dysdifferentiation of a primordial follicle.

scholarly journals True Precocious Puberty Following Treatment of a Leydig Cell Tumor: Two Case Reports and Literature Review

2015 ◽  
Vol 3 ◽  
Author(s):  
Alberto Verrotti ◽  
Laura Penta ◽  
Letizia Zenzeri ◽  
Laura Lucchetti ◽  
Paolo Giovenali ◽  
...  
Keyword(s):  
Literature Review ◽  
Precocious Puberty ◽  
Leydig Cell ◽  
Case Reports ◽  
Leydig Cell Tumor ◽  
Cell Tumor

scholarly journals Precocious Puberty Associated with Testicular Hormone-secreting Leydig Cell Tumor

Cureus ◽  
2019 ◽  
Author(s):  
Eid Alagha ◽  
Shahd E Kafi ◽  
Mohamed Abdelmaksoud Shazly ◽  
Abdulmoein Al-Agha
Keyword(s):  
Precocious Puberty ◽  
Leydig Cell ◽  
Leydig Cell Tumor ◽  
Cell Tumor

Precocious Puberty in a Child with Unilateral Leydig Cell Tumor of the Testis following Orchiopexy

1993 ◽  
Vol 150 (5 Part 1) ◽  
pp. 1483-1485 ◽  
Author(s):  
Andrew J. Kirsch ◽  
William Bastian ◽  
Harris L. Cohen ◽  
Kenneth I. Glassberg
Keyword(s):  
Precocious Puberty ◽  
Leydig Cell ◽  
Leydig Cell Tumor ◽  
Cell Tumor

scholarly journals A Matter of Time: Delayed Presentation and Rapid Progression from Gonadotropin-Independent to Gonadotropin-Dependent Precocious Puberty following Successful Treatment for a Leydig Cell Tumor

2022 ◽  
Vol 2022 ◽  
pp. 1-4
Author(s):  
C. R. Naotunna ◽  
D. N. Siriwardana ◽  
B. C. Lakmini ◽  
M. Samarasinghe ◽  
N. Atapattu
Keyword(s):  
Precocious Puberty ◽  
Leydig Cell ◽  
Adult Height ◽  
Clinical Signs ◽  
Leydig Cell Tumor ◽  
Cell Tumor ◽  
Rapid Progression ◽  
Delayed Presentation ◽  
The Past ◽  
Hormone Administration

Leydig cell tumors, most often benign, are a rare cause of isosexual gonadotropin-independent precocious puberty in boys due to secretion of testosterone. Very rarely do these tumors produce estrogen, causing gynecomastia. Testicular sparing surgery is the mainstay of treatment currently although radical orchidectomy was the choice in the past. Following surgery, clinical signs improve along with a revision of biochemical changes. Occasionally, it has been reported few children are progressed to gonadotropin-dependent precocious puberty (GDPP) after initial clinical and biochemical recovery. Gonadotropin receptor analogs have been successful on them to halt the progression of puberty, and growth hormone administration has been used to optimize the adult height. Here, we report a case of a 10-year-old boy who presented very late due to failure in recognition of features of puberty due to a Leydig cell tumor. Even though he underwent successful radical orchidectomy, just within 1 month following surgery, he entered GDPP in contrast to the published cases where it was earliest detected at 3 months.

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