Differentiating true precocious puberty and puberty variants in consecutive 275 girls: a single center experience.

Objectives: This study aimed to identify clinical features of girls referred to a pediatric endocrinology clinic for suspected precocious puberty, differentiate true precocious puberty from other variants, evaluate treatment status, and identify distinguishing factors between patient groups.

Methods: We retrospectively evaluated the records of 275 consecutive girls aged 0-10 years referred for suspected precocious puberty.

Results: Among the patients, 30 (10.

Evaluation of androgen receptor and androgen receptor splice-variant 7 in bladder cancer; a novel approach into an ancient topic.

Purpose: The contribution of androgen receptors (AR) on bladder cancer has been demonstrated in pre-clinical studies, however in clinical studies, only the canonical AR (AR-FL) protein was measured by immunohistochemistry and conflicting results were obtained. To get better insight into the alterations of AR signalling, we used western blotting (WB) method and simultaneously measured both mRNA and protein levels of AR-FL and AR-V7.

Methods: 23 naive non-muscle invasive bladder cancer patients and 12 healthy individuals were included.

Low-cord orchidectomy for testicular cancer: what would be different?

Introduction: High cord radical orchidectomy (HRCO) is accepted as the standard surgical approach in testicular cancer, however low cord orchidectomy (LCRO) can reduce the morbidity of operation without worsening the oncological outcomes.

Methods: We retrospectively re-examined the specimens of men to determine the level of spermatic cord invasion (SCI). Men who had proximal SCI with negative surgical margins after HRCO were assumed to have de-novo residual tumour if LCRO was performed.

Congenital Adrenal Hyperplasia with Combined 21-hydroxylase deficiency and 17α-hydroxylase/17,20-lyase deficiency: An undervirilized male.

21-hydroxylase deficiency stands as the most prevalent form of congenital adrenal hyperplasia, primarily resulting from mutations in the CYP21A2 gene. On the other hand, mutations within the CYP17A1 gene lead to 17α-hydroxylase/17,20-lyase enzyme deficiencies. The scarcity of 17-OH deficiency is noteworthy, accounting for less than 1% of all congenital adrenal hyperplasia cases.