1.Delayed Puberty due to Pituitary Stalk Dysgenesis and Ectopic Neurohypophysis.
Hye Jin YOO ; Kyung Mook CHOI ; Ohk Hyun RYU ; Sang Il SUH ; Nan Hee KIM ; Sei Hyun BAIK ; Dong Seop CHOI
The Korean Journal of Internal Medicine 2006;21(1):68-72
Hypopituitarism is not a common cause of delayed puberty. A 22 year old man was referred to our clinic because of the absence of the development of secondary sexual characteristics. The patient had no complaints of physical discomfort. Random serum testosterone and luteinizing hormone level were obtained and found to be low. The combined pituitary function stimulation test revealed a partial hypopituitarism. A pituitary magnetic resonance imaging (MRI) was obtained and showed decreased pituitary stalk enhancement and ectopic neurohypophysis. Therefore, we conclude that the delayed puberty was a result of hypopituitarism due to pituitary stalk dysgenesis and ectopic neurohypophysis. The patient was started on hormone replacement therapy and gradually developed secondary sexual characteristics.
Time Factors
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Puberty, Delayed/*etiology
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Pituitary Gland, Posterior/*abnormalities
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Male
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Magnetic Resonance Imaging
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Hypopituitarism/*complications/diagnosis
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Humans
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Hormone Replacement Therapy
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Adult
2.Association of prenatal and childhood environment smoking exposure with puberty timing: a systematic review and meta-analysis.
Yiwen CHEN ; Qin LIU ; Wenyan LI ; Xu DENG ; Bo YANG ; Xin HUANG
Environmental Health and Preventive Medicine 2018;23(1):33-33
OBJECTIVES:
Mothers who smoke during pregnancy or while their children are small were common in some populations. Epidemiological studies have tried to detect the effect of prenatal tobacco smoke (PTS), and childhood environmental tobacco smoke (ETS) on puberty timing have not shown a consensus results. We aimed to examine current evidence and estimate the associations between PTS or/and ETS and puberty timing.
METHODS:
Seven databases were searched from inception to May 2017. All the cohort studies examining the associations between PTS and/or ETS and puberty timing were identified. Two reviewers independently screened all studies, evaluated the quality of eligible studies, and extracted the data. The quality assessment of the eligible cohort studies was based on the Newcastle-Ottawa Scale. Risk ratio (RR), standard mean difference (SMD), and 95% confidence intervals (CIs) were calculated and pooled by CMA (Version 2.0, Biostat, Inc., USA).
RESULTS:
Compared with controls, girls with PTS and ETS exposure have an earlier age at menarche (SMD - 0.087, 95% CI 0.174 to - 0.000), and similar results were found in both PTS subgroup (SMD - 0.097, 95% CI - 0.192 to - 0.002) and prospective cohort subgroup (SMD - 0.171, 95% CI - 0.253 to - 0.090). And number of boys with early voice break in PTS group was significantly increasing than non-exposed boys (RR 1.34, 95% CI 1.29 to 1.40).
CONCLUSIONS
PTS exposure possibly decrease age of menarche of girls, and studies on boys were urgent needed. Appropriate and comprehensive outcome measures using unified criteria to classify puberty should be reported in future studies.
Aging
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physiology
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Environmental Exposure
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adverse effects
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Female
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Humans
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Menarche
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physiology
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Pregnancy
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Prenatal Exposure Delayed Effects
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etiology
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Puberty
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physiology
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Smoking
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adverse effects
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Tobacco Smoke Pollution
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adverse effects