Increase in first morning voided urinary luteinizing hormone levels precedes the physical onset of puberty.

Demir, And; Voutilainen, Raimo; Juul, Anders; Dunkel, Leo; Alfthan, Henrik; Skakkebæk, Niels E.; Stenman, Ulf‐Hǎkan

doi:10.1210/jcem.81.8.8768859

Cited by 28 publications

(40 citation statements)

References 12 publications

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“…Measurement of first-voided ULH to detect pubertal changes was suggested over a decade ago (12,13,23,24), but was not adopted in the clinical practice of pediatric endocrinology. Apparently, lack of normative data for normal and disordered puberty prevented the implementation of this measure so far.…”

Section: Discussionmentioning

confidence: 99%

“…More than a decade ago, along with the development of high-sensitive immunoassay for gonadotropins that replaced the RIA, Demir et al (11) have shown that urinary gonadotropins are age related and significantly increased during puberty (12). It has been suggested that urinary gonadotropins measurements can be used for differential diagnosis of pubertal disorders (13).…”

Section: Introductionmentioning

confidence: 99%

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The diagnostic value of first-voided urinary LH compared with GNRH-stimulated gonadotropins in differentiating slowly progressive from rapidly progressive precocious puberty in girls

Zung¹,

Burundukov

Ulman

et al. 2014

European Journal of Endocrinology

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Objective: Characterization of pubertal progression is required to prevent unnecessary intervention in unsustained or slowly progressive (SP) precocious puberty (PP), while delivering hormonal suppression in rapidly progressive (RP) PP. We aimed to assess the diagnostic value of first-voided urinary LH (ULH) compared with GNRH-stimulated gonadotropins in differentiating these forms of PP. Methods: A total of 62 girls with PP underwent both GNRH stimulation and ULH assay. Fifteen girls with peak LH R10 IU/l started treatment immediately, whereas the other 47 girls were evaluated after 6 months for pubertal advancement, height acceleration, and bone-age maturation. Based on these criteria, the participants were assigned to five subgroups: pubertal regression, no progression or progression by one, two or three criteria. The first three subgroups were defined as SP-PP (nZ29), while the other two subgroups were defined as RP-PP (nZ18). An additional 23 prepubertal girls were evaluated for ULH. Results: ULH but not serum gonadotropins could distinguish girls with two and three criteria from less progressive subgroups. By comparison with SP-PP (i.e. regression group and groups 0 and 1), those with RP-PP (group 2C3) had lower peak FSH (9.28G2.51 vs 12.57G4.30; PZ0.007) and higher peak LH:FSH ratio (0.42G0.30 vs 0.22G0.12; PZ0.022) and ULH (1.63G0.65 vs 1.05G0.26 IU/l; P!0.001). Based on receiver operating characteristics analysis, a ULH cutoff of 1.16 IU/l had a better sensitivity (83%) and positive and negative predictive values (65 and 88% respectively) than the other two parameters, with a specificity of 72%. Conclusions: ULH assay is a noninvasive, reliable method that can assist in the distinction between SP-and RP-PP.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The diagnostic value of first-voided urinary LH compared with GNRH-stimulated gonadotropins in differentiating slowly progressive from rapidly progressive precocious puberty in girls

Zung¹,

Burundukov

Ulman

et al. 2014

European Journal of Endocrinology

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“…34 The uncertainty can be overcome by measuring urinary secretion of luteinizing hormone, which increases before physical signs of puberty are evident. 90 During early puberty in boys, testosterone measures are most reliable when blood sampling is done in the morning, when testosterone levels are expected to be highest. 91 There are a few available assays for steroid receptor levels in humans that are limited in their validity and still under additional development.…”

Section: Physiologic Markersmentioning

confidence: 99%

Examination of US Puberty-Timing Data from 1940 to 1994 for Secular Trends: Panel Findings

et al. 2008

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Whether children, especially girls, are entering and progressing through puberty earlier today than in the mid-1900s has been debated. Secular trend analysis, based on available data, is limited by data comparability among studies in different populations, in different periods of time, and using different methods. As a result, conclusions from data comparisons have not been consistent. An expert panel was asked to evaluate the weight of evidence for whether the data, collected from 1940 to 1994, are sufficient to suggest or establish a secular trend in the timing of puberty markers in US boys or girls. A majority of the panelists agreed that data are sufficient to suggest a trend toward an earlier breast development onset and menarche in girls but not for other female pubertal markers. A minority of panelists concluded that the current data on girls' puberty timing for any marker are insufficient. Almost all panelists concluded, on the basis of few studies and reliability issues of some male puberty markers, that current data for boys are insufficient to evaluate secular trends in male pubertal development. The panel agreed that altered puberty timing should be considered an adverse effect, although the magnitude of change considered adverse was not assessed. The panel recommended (1) additional analyses of existing puberty-timing data to examine secular trends and trends in the temporal sequence of pubertal events; (2) the development of biomarkers for pubertal timing and methods to discriminate fat versus breast tissue, and (3) establishment of cohorts to examine pubertal markers longitudinally within the same individuals.

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“…This is a crucial distinction as expectative ('watch-and-wait') management is inappropriate in the context of teenage CHH. For the differential diagnosis of the two conditions, a variety of physiological and stimulation tests have been proposed, such as assessment of LH pulsatility by frequent sampling (14), prolactin response to various provocations (15), gonadotrophin response to GNRH (16), testosterone response to human chorionic gonadotrophin (hCG) (17,18,19) and first morning-voided urine FSH and LH (20). Most recently, a single measurement of inhibin B level has been shown to discriminate complete CHH from CDGP with specificity of 100% at inhibin B concentration of 35 pg/ml in pre-pubertal boys (21).…”

Section: Evaluation Of Delayed Pubertymentioning

confidence: 99%

TRANSITION IN ENDOCRINOLOGY: Induction of puberty

Dunkel

Quinton

2014

European Journal of Endocrinology

117

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Puberty is the period during which we attain adult secondary sexual characteristics and reproductive capability. Its onset depends upon reactivation of pulsative GNRH, secretion from its relative quiescence during childhood, on the background of intact potential for pituitary-gonadal function. This review is intended: to highlight those current practices in diagnosis and management that are evidence based and those that are not; to help clinicians deal with areas of uncertainty with reference to physiologic first principles; by sign-posting relevant data arising from other patient groups with shared issues; to illustrate how recent scientific advances are (or should be) altering clinician perceptions of pubertal delay; and finally, to emphasise that the management of men and women presenting in advanced adult life with absent puberty cannot simply be extrapolated from paediatric practice. There is a broad spectrum of pubertal timing that varies among different populations, separated in time and space. Delayed puberty usually represents an extreme of the normal, a developmental pattern referred to as constitutional delay of growth and puberty (CDGP), but organic defects of the hypothalamo-pituitary-gonadal axis predisposing to hypogonadism may not always be initially distinguishable from it. CDGP and organic, or congenital hypogonadotrophic hypogonadism are both significantly more common in boys than girls. Moreover, around 1/3 of adults with organic hypogonadotrophic hypogonadism had evidence of partial puberty at presentation and, confusingly, some 5-10% of these subsequently may exhibit recovery of endogenous gonadotrophin secretion, including men with Kallmann syndrome. However, the distinction is crucial as expectative ('watch-and-wait') management is inappropriate in the context of hypogonadism. The probability of pubertal delay being caused by organic hypogonadism rises exponentially both with increasing age at presentation and the presence of associated 'red flag' clinical features. These 'red flags' comprise findings indicating lack of prior 'mini-puberty' (such as cryptorchidism or micropenis), or the presence of non-reproductive congenital defects known to be associated with specific hypogonadal syndromes, e.g. anosmia, deafness, mirror movements, renal agenesis, dental/digital anomalies, clefting or coloboma would be compatible with Kallmann (or perhaps CHARGE) syndrome. In children, interventions (whether in the form or treatment or simple reassurance) have been historically

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Increase in first morning voided urinary luteinizing hormone levels precedes the physical onset of puberty.

Cited by 28 publications

References 12 publications

The diagnostic value of first-voided urinary LH compared with GNRH-stimulated gonadotropins in differentiating slowly progressive from rapidly progressive precocious puberty in girls

The diagnostic value of first-voided urinary LH compared with GNRH-stimulated gonadotropins in differentiating slowly progressive from rapidly progressive precocious puberty in girls

Examination of US Puberty-Timing Data from 1940 to 1994 for Secular Trends: Panel Findings

TRANSITION IN ENDOCRINOLOGY: Induction of puberty

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