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Hypogonadotropic hypogonadism(HH) and constitutional delay in growth and puberty (CDGP) account for the underlying aetiology of delayed puberty with overlapping clinical and hormonal features. The present study aims to evaluate the pubertal development and final height(FH) outcome in patients presenting with delayed puberty due to HH and CDGP. The hospital files of 1654 boys older than 14 years of age who were evaluated for delayed puberty between 01.01.2002 and 01.04.2022 in Hacettepe University İhsan Doğramacı Children's Hospital Pediatric Endocrinology Department were reviewed retrospectively. 191 patients who met the inclusion criteria were included in the study. The mean age of admission was 14.6 ± 0.9 years. Of those, 149 patients had CDGP and 42 patients had HH. The mean FH-SDS of patients with HH (- 0.09 ± 1.0) was higher than those with CDGP (- 0.64 ± 0.91) (p = 0.003). In total, 118 out of 128 patients (92.2%) with CDGP and 36 out of 39 patients (92.3%) with HH had reached an FH consistent with their target height(TH). There was no statistically significant difference between the FH-SDS of patients with CDGP who received testosterone therapy for induction of puberty and those who did not receive (- 0.46 ± 0.97 SD vs. - 0.74 ± 0.87 SD; p = 0.094). Conclusion: Individuals presented with delayed puberty due to both CDGP and HH have reached an FH consistent with their TH to a large extent. Patients with HH had a higher presenting and final height than those with CDGP, which was attributed to the higher TH. Induction of puberty with testosterone in boys with CDGP seems not to have a clinically meaningful impact on the FH and long-term pubertal progression.
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http://dx.doi.org/10.1007/s00431-025-06374-4 | DOI Listing |
Pediatr Ann
September 2025
Reproductive Medicine Associates of New Jersey, IVIRMA Global, Basking Ridge, New Jersey.
Puberty marks the development of secondary sexual characteristics and reproductive capacity, with normal onset ranging from age 8 to 13 years in female children. Precocious puberty (ie, the onset of secondary sexual characteristics before age 8 years in female children) can result from central or peripheral mechanisms, requiring tailored diagnostic and therapeutic approaches. Delayed puberty (ie, the absence of sexual development beyond expected age ranges) often stems from primary or secondary hypogonadism.
View Article and Find Full Text PDFBMJ Case Rep
September 2025
Obstetrics and Gynaecology, King George's Medical University, Lucknow, Uttar Pradesh, India.
The rare endocrine condition known as Van Wyk-Grumbach syndrome (VWGS) is typified by delayed bone age, multicystic ovaries, isosexual precocious puberty and increased, untreated primary hypothyroidism. It typically presents in paediatric patients but can occasionally be missed until adulthood. We report an unusual adult presentation of VWGS in a short-statured woman in her early 20s who presented with menorrhagia-induced severe anaemia, hypothyroid features and multicystic ovaries.
View Article and Find Full Text PDFPsychoneuroendocrinology
August 2025
Department of Psychology, Stanford University, Stanford, CA, USA.
Childhood exposure to pollution has been associated with elevated levels of depressive symptoms during adolescence. Epidemiological studies have related exposure to pollution to altered pubertal timing; however, the effects of pollution exposure on levels of pubertal hormones and their developmental trajectories (i.e.
View Article and Find Full Text PDFPediatr Diabetes
September 2025
Pediatric Endocrinology Department, Gaafar Ibn Auf Pediatric Tertiary Hospital, Khartoum, Sudan.
Mauriac syndrome (MS) is a rare condition linked to inadequate glycemic control in type 1 diabetes mellitus (T1DM) and has also rarely been reported in patients with neonatal diabetes. MS manifests as growth failure, delayed puberty, cushingoid features, and hepatomegaly. The condition can be associated with complications like dyslipidemia, retinopathy, and nephropathy.
View Article and Find Full Text PDFZhonghua Nei Ke Za Zhi
September 2025
Duchenne muscular dystrophy (DMD) is an X-linked recessive myopathy caused by mutations in the dystrophin gene, which is divided into presymptomatic, early ambulatory, late ambulatory, early non-ambulatory, and late non-ambulatory stages according to its disease progression. Some patients experience non-progressive cognitive developmental delays in the presymptomatic stage. DMD patients gradually develop osteoporosis, cardiomyopathy, decreased respiratory function, delayed puberty, and gastrointestinal symptoms as the disease progresses.
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