Testicular microlithiasis and leydig cell proliferation in wistar rats underwent fowler-stephens procedure

Gougoudi, Evagelia; Zachariou, Zacharias; Kogia, Eleni; Zavitsanakis, Athanasios

doi:10.4081/pmc.2012.73

Cited by 3 publications

(3 citation statements)

References 16 publications

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“…It is noted that testicular microliths do not typically affect Leydig cells, and maybe associated with Sertoli cell dysfunction ( 19 ). However, there is some evidence that microliths are associated with Leydig cell hyperplasia in rats ( 22 ). They are seen more frequently in children with Down syndrome and associated with testicular torsion, varicocele, retractile testes, cryptorchidism, inguinal hernias, and testicular neoplasms, though there is no evidence that they are premalignant ( 19 , 20 ).…”

Section: Discussionmentioning

confidence: 99%

A Case of Familial Male-limited Precocious Puberty with a Novel Mutation

Gurnurkar¹,

DiLillo²,

Carakushansky³

2021

Jcrpe

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Familial male-limited precocious puberty (FMPP), also known as testotoxicosis, is a rare cause of precocious puberty in males. It is caused by a mutation in the luteinizing hormone/chorionic gonadotropin receptor ( LHCGR ) gene, resulting in the receptor being constitutively activated. This causes excessive production of testosterone, leading to precocious puberty in males. Generally, boys present with signs of puberty, such as pubic hair growth, acne, and increased height velocity around the age of 2-4 years old. Like any other cause of precocious puberty, the goal of treatment is to prevent virilization and also delay closure of the epiphyseal plates to maintain adult height potential. Treatment, therefore, is aimed at decreasing the effects of testosterone, as well as stopping the conversion of testosterone to estrogen. Little is known about the long-term effects of treatment because the disorder is so rare. However, studies using bicalutamide and anastrozole have been promising. In this report, we present a boy with FMPP with a novel mutation in the LHCGR gene, who has been responding well to therapy using both drugs.

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Section: Discussionmentioning

confidence: 99%

A Case of Familial Male-limited Precocious Puberty with a Novel Mutation

Gurnurkar¹,

DiLillo²,

Carakushansky³

2021

Jcrpe

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“…Gougoudi et al 20 show microlithiasis on testicular ultrasound examination of Wistar rats underwent Fowler-Stephens procedure.…”

Section: Discussionmentioning

confidence: 99%

Measurement of testicular volume in Wistar rats using a caliper and ultrasonography in experimental surgery

et al. 2016

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PURPOSE:To compare the measurement of the testicular volume of Wistar rats using a caliper and ultrasonography. METHODS:Forty Wistar rats were randomly assigned into four groups. A tensile force of 1.6 Newton (N) and 1.0 N was applied to the right spermatic cord in group I and group II, respectively. Group III was the sham group, and group IV served as a control. The initial and final testicular volumes were measured using a caliper and ultrasonography and compared. A significance level of 5% was used. RESULTS:The Kappa coefficient was equal to 0.292 (p = 0.006). The Pearson correlation coefficient obtained for the percent reduction in the right testicular volume using ultrasonography and a caliper was equal to 0.696 (p < 0.001). CONCLUSION:There was reasonable agreement and a significant positive correlation between the percent reduction in the right testicular volume using ultrasonography and a caliper.

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“…While observed in some cases ( 25 , 26 ), hydrocele is not a common cause of testicular microlithiasis ( 27 ). Microlithiasis has also not been reported in patients with LH-activating mutations; Gougoudi et al ( 28 ) reported that testicular microlithiasis co-existed with Leydig cell hyperplasia in Wistar rats. Thus, whether Leydig cell hyperstimulation in our patient is the cause of microlithiasis or not is not known.…”

Section: Discussionmentioning

confidence: 99%

Testotoxicosis: Report of Two Cases, One with a Novel Mutation in LHCGR Gene

Evliyaoğlu

2015

Jcrpe

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Testotoxicosis is a rare disorder which presents as isosexual peripheral precocious puberty in males. Despite the pattern of autosomal dominant inheritance, sporadic cases also may occur. Due to activating mutation in luteinizing hormone (LH))/choriogonadotropin receptor (LHCGR) gene, early virilization and advancement in bone age are common with increased serum testosterone levels above adult ranges, despite low LH and follicular-stimulating hormone (FSH) levels. There are different treatment regimens, such as combination of bicalutamide (antiandrogen agent) and a third-generation aromatase inhibitor, that are reported to be well-tolerated and successful in slowing bone age advancement and preventing progression of virilization. We report here two patients who presented with peripheral precocious puberty and an activating mutation in the LHCGR gene: one with a family history and previously determined mutation and the other without family history and with a novel mutation (c.830G>T). Combination of bicalutamide+anastrozole was ineffective in slowing pubertal progression and bone age. Short-term results were better with ketoconazole.

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Testicular microlithiasis and leydig cell proliferation in wistar rats underwent fowler-stephens procedure

Abstract: Microlithiasis and Leydig cell hyperplasia seem to have causative relation in operated undescended testis and present serious postoperative complications, with a review in the literature.

Cited by 3 publications

References 16 publications

A Case of Familial Male-limited Precocious Puberty with a Novel Mutation

A Case of Familial Male-limited Precocious Puberty with a Novel Mutation

Measurement of testicular volume in Wistar rats using a caliper and ultrasonography in experimental surgery

Testotoxicosis: Report of Two Cases, One with a Novel Mutation in LHCGR Gene

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