Child DevelopmentCPHMINIPUBNCT02784184
COPENHAGEN Minipuberty Study
An observational study of Child Development and Disorders of Sex Development, run by Copenhagen University Hospital, Rigshospitalet at 1 site in Denmark.
Trial summary
Minipuberty is a term used to describe the transient activation of the pituitary-gonadal axis 2-3 months after birth in both boys and girls. It is, however, not known why infants reach adult levels of reproductive hormones in early life, nor is the exact timing of the peak known. Read more about this study
- Who is it for?
- Ages Up to 12 months
- Conditions the study is for
- Child Development, Disorders of Sex Development
- How many people
- 280 participants
- Where
- 1 siteDenmark
- Study dates
- Aug 2016to 31 Dec 2019
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Up to 12 months
- All sexes
- No healthy volunteers
- Child
Study population: Pregnant women, meeting the inclusion criteria, and the fathers-to-be followed at the Department of Obstetrics, Rigshospitalet. Further, parents and infants with disordered sexual development (DSD). These patients will be recruited via The Department of Growth and Reproduction, Rigshospitalet. Parents whose fetuses have been diagnosed prenatally with any DSD diagnosis or during the first 6 months of life will be invited to participate. Three groups of participants in this study: 1. A group of healthy infants 2. All infant patients diagnosed with or under evaluation for DSD 3. The parents of the healthy infants and DSD patients Number (approximately) of participants: 1. 200 healthy infants (100 boys and 100 girls) 2. unknown number of DSD infants that will be referred within a year to the Department of Growth and Reproduction; estimation: 15 DSD infants. 3. 400 parents of healthy infants (200 fathers and 200 mothers) - unknown number of parents of DSD patients
Who may be able to join
- Singleton pregnancy
- Maternal and paternal Caucasian origin
- Maternal pre-pregnancy BMI between 18 and 35 kg/m2
- No serious maternal illness, including no pre-existing maternal diabetes nor thyroid gland diseases
- Term pregnancy (week 37+0 to 41+7)
- No gestational diabetes
Show all 9Show fewer
- No fetal malformations or chromosomal disorders
- Birth weight of child between 3rd and 97th percentile
- Only healthy infants born at term will be included in the study which all prospective participants will be informed of.
Who cannot join
- -
Trial locations and contacts
1 site in 1 country.
Denmark1 site
Department of Growth and Reproduction, Rigshospitalet
Copenhagen, 2100
About this study
Minipuberty is a term used to describe the transient activation of the pituitary-gonadal axis 2-3 months after birth in both boys and girls. It is, however, not known why infants reach adult levels of reproductive hormones in early life, nor is the exact timing of the peak known. Furthermore, what determines the timing of peaks and suppressions of reproductive hormones from infancy throughout childhood and into adolescence remains to be elucidated.
The study aims to described and evaluate dynamic changes in the hypothalamic-pituitary- gonadal axis in early postnatal life.
Read the detailed description
Minipuberty is a term used to describe the transient activation of the pituitary-gonadal axis 2-3 months after birth in both boys and girls. It is, however, not known why infants reach adult levels of reproductive hormones in early life, nor is the exact timing of the peak known. Furthermore, what determines the timing of peaks and suppressions of reproductive hormones from infancy throughout childhood and into adolescence remains to be elucidated.
Few studies have investigated minipuberty and one, for example, found that it is affected in premature infants (before gestation week 37). However, no studies on normative data throughout minipuberty in infants exist.
Furthermore, using minipuberty as a window for diagnosis of endocrine disorders and future reproductive function has been suggested. Defining minipuberty, both in terms of circulating hormone levels and urinary metabolites, in healthy infants is therefore essential in order to utilize this window. Studies using patients with Disorders of Sex Development during minipuberty have been carried out, but they are hampered by small sample sizes and lack of control groups.
In addition, little is known about the genetic and epigenetic factors that drive the onset, progression and termination of minipuberty as well as the actual puberty, i.e. the factors responsible for the quiescence of the HPG axis during childhood and the dis-inhibition responsible for pubertal onset. Therefore, much attention was drawn on the study performing whole exome sequencing in patients and relatives with central precocious puberty (CPP). For the first time, MKRN3 was suggested as the primary factor responsible for HPG inhibition during mid-childhood. A number of studies support that MKRN3 mutations cause CPP, and genetic variation of MKRN3 affect pubertal timing in healthy girls. Our findings of declining serum levels of MKRN3 prior to pubertal onset in healthy girls support MKRN3 as a regulator of pubertal onset. The exact mechanism through which MRKN3 exceeds its effect remains to be elucidated; however, its zink-finger structure indicates regulation of superior cellular processes such as epigenetic regulation of DNA transcription.
Twin studies suggest that 60% of the inter-individual variation is caused by genetic factors. However, genome wide association (GWA) studies only explain a fraction of the variation in age at puberty. Recently, our research group has revealed the largest effect of a single SNP on age at pubertal onset in girls. The location of the SNPs in genes regulating FSH action emphasizes the need of a wide focus including downstream processes in the HPG axis when evaluating factors regulating puberty.
In general, the abovementioned studies have led to a spark in the interest in epigenetic studies, i.e. studies of genetic changes that are not caused by changes in the DNA sequences themselves, but rather regulatory mechanisms of DNA expression. Generally, this is thought to include DNA methylation, histone modifications and small RNAs. Epi-mutations (improper epigenetic regulation) possibly account for more of the variation in puberty than genetic factors. Previously, both gene-specific and genome-wide DNA methylation patterns have been studied. Genome-wide hypomethylation seen in peripheral leukocytes has been shown to be linked with an array of cancers, including colorectal cancers. As multiple histone modifications exist and analysis requires special sample treatment procedures, DNA methylation is the most appropriate epigenetic marker to analyze. A study of rats found that specific gene hypomethylation was accountable for lack of pubertal onset, but the link between epigenetics and mini- and pubertal timing and progression has, however, only scarcely been studied. Understanding this link would greatly add to our knowledge of reproductive function and normal sex development.
Disorders of Sex Development (DSD) is an umbrella term covering conditions with congenital disordered development of chromosomal, gonadal or anatomical sex. Genital abnormalities may include as many as up to 4-6 in 1000 births, although individual disorders are much rarer, e.g. 45,X/46,XY mosaicism is seen in about 1 in 15000 live births. Previously DSD diagnoses were labeled with different and often imprecise terms such as 'intersex', 'sex reversal' and 'hermaphroditism' etc. In 2006, DSD nomenclature was renamed and grouped according to genetic sex into sex chromosome DSD, 46,XY DSD and 46,XX DSD.
DSD patients are diagnosed at different periods in life depending on their diagnosis, phenotype and primary and secondary sexual development. Patients with sex chromosome DSD can be diagnosed at prenatal screenings, patients with affected external genitalia at birth, some during childhood due to growth abnormalities, some during adolescence due to abnormal pubertal progression and lastly, some in adulthood due to infertility.
Understanding normal sex development is therefore the key to identifying and optimizing diagnosis and treatment of patients with DSD. A project, as the present, that seeks to investigate normal minipuberty while comparing to minipuberty in patients with DSD is therefore of great importance. Furthermore, knowledge of the genetic and epigenetic control mechanisms of minipuberty will aid the understanding of reproductive physiology and in particular DSD pathology.
- Conditions
- Child Development, Disorders of Sex Development
- Keywords
- Hypothalamic-pituitary-gonadal axis
- Medical subject headings
- Disorders of Sex Development
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| 1 year follow-up group | 1 year follow-up group including 6 measurements | |
| 40 days diaper study subgroup | Subgroup of the "1 year follow-up group" including 15 girls undergoing daily measurement of urinary hormone excretion |
What is being measured
The primary outcome is the main question the study is designed to answer.
Serum and urinary metabolites of reproductive hormones (e.g. steroid hormone metabolites and gonadotropins) (newborn)
change/course serum and urinary metabolites
Measured: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth plus 40 days daily measurement (urine, female 40 days diaper study subgroup)
Urinary metabolites of endocrine disrupting chemicals (e.g. phthalates, phenols, perfluorinated compounds and parabens) (newborn)
change/course urinary metabolites
Measured: 3-7d, & 1,3,5,7,12m or 2,4,6,8,12m after birth plus 40 days daily measurement (urine, female 40 days diaper study subgroup)
Basic clinical examination (newborn) (size and proportions)
change/course: measurements of length, weight, skin folds and hip-waist ratio
Measured: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Basic clinical examination (newborn) (pubertal staging)
change/course: pubertal staging using Tanners classification (including testicular size in boys assessed by Prader's orchidometer and ultrasound
Measured: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Basic clinical examination (newborn) (genitalia)
change/course: classification of external genitalia (classification of genital tubercle, location of gonads, position of urethra, labia/scrotal fusion)
Measured: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Basic clinical examination (newborn) (penile measurement)
change/course: penile measurement with a ruler (in boys)
Measured: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Basic clinical examination (newborn) (AGD)
change/course: ano-genital distance (AGD) measured with a ruler
Measured: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Genetic profiling
Genotyping of different genetic loci (genetic variation of loci regulating hormone signalling, e.g. FSHB, etc.)
Measured: single determination or 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Epigenetic profiling
change/course: epigenetic variation of loci regulating hormone signalling
Measured: single determination or 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Secondary outcomes (8)
Basic clinical examination (parents) (height)
Height
Measured: postpartal (within first 3 months)
Basic clinical examination (parents) (weight)
self-reported pre-pregnancy weight for the mother and postpartal weight of the father
Measured: postpartal (within first 3 months)
Basic clinical examination (parents)
Skinfolds measured above the biceps, triceps, at the flank, and below the scapula
Measured: postpartal (within first 3 months)
Pregnancy and perinatal outcome (newborn and mother)
Perinatal outcome including birth weight, -length, partus mode, adverse events/complications, pre- and perinatal drug intake, pregnancy outcomes including gestational age, pregnancy complications, IVF Treatment etc.
Measured: before birth and perinatal phase
Medical history and exposure (parents) (basic)
Basic medical history (parents) (questionaire / journal)
Measured: postpartal (within first year)
Medical history and exposure (parents) (obstetrical)
Obstetrical history including outcomes of previous pregnancies and births (mother), smoking and drug intake during pregnancy (mother) (questionaire / journal)
Measured: postpartal (within first year)
Medical history and exposure (parents) (puberty)
Pubertal history (parents) including age at menarche, pubertal timing with regard to peers, age at menopause of the mother of the parents etc. (questionaire)
Measured: postpartal (within first year)
Breastfeeding and food intake (newborn)
change/course: breastfeeding and food intake of the newborn during the course of the first year (questionaire)
Measured: first year of life
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted27 May 2016 (estimated)
- Study startAug 2016
- Primary completion31 Dec 2019 (estimated)
- Study completion31 Dec 2019 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (3)Papers the sponsor has linked to this study.
- Other trials for Child DevelopmentStudies of the same condition, open and under way.
- More trials run by Copenhagen University Hospital, RigshospitaletThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 280 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Copenhagen University Hospital, Rigshospitalet
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Anders Juul, Copenhagen University Hospital, Rigshospitalet
- Investigators
- Anders Juul, Prof., Study chair, Copenhagen University Hospital, RigshospitaletAlexander S Busch, MD, Principal investigator, Copenhagen University Hospital, Rigshospitalet
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02784184
- Sponsor's protocol ID
- RH-H-15014876
- Other IDs
- RH-2015-210-04146
- Acronym
- CPHMINIPUB
- Status last verified
- Feb 2019
- First submitted
- 17 May 2016
- Last updated
- 15 Feb 2019
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- No
Publications
Pridik C, Juul A, Busch AS. Free testosterone and IGF-I mediate sex-specific linear growth during minipuberty. Endocr Connect. 2026 Apr 15;15(4):e250930. doi: 10.1530/EC-25-0930. Print 2026 Apr 1.
PubMed 41921027Ljubicic ML, Busch AS, Upners EN, Fischer MB, Petersen JH, Raket LL, Frederiksen H, Johannsen TH, Juul A, Hagen CP. A Biphasic Pattern of Reproductive Hormones in Healthy Female Infants: The COPENHAGEN Minipuberty Study. J Clin Endocrinol Metab. 2022 Aug 18;107(9):2598-2605. doi: 10.1210/clinem/dgac363.
PubMed 35704034Ljubicic ML, Busch AS, Upners EN, Fischer MB, Main KM, Andersson AM, Johannsen TH, Hagen CP, Juul A. Dynamic changes in LH/FSH ratios in infants with normal sex development. Eur J Endocrinol. 2022 Jun 1;187(1):135-142. doi: 10.1530/EJE-21-0999.
PubMed 35521767
Study at a glance
From the registry record, last updated by the sponsor on 15 Feb 2019. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- COPENHAGEN Minipuberty Study
- ClinicalTrials.gov ID
- NCT02784184
- Acronym / sponsor ID
- CPHMINIPUB / RH-H-15014876
- Conditions
- Child Development, Disorders of Sex Development
- Keywords
- Hypothalamic-pituitary-gonadal axis
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 280 participants (estimated)
- Lead sponsor
- Copenhagen University Hospital, RigshospitaletUniversity, hospital or other
- Study start
- Aug 2016
- Primary completion
- 31 Dec 2019 (estimated)
- Study completion
- 31 Dec 2019 (estimated)
- First posted
- 27 May 2016 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Minipuberty is a term used to describe the transient activation of the pituitary-gonadal axis 2-3 months after birth in both boys and girls. It is, however, not known why infants reach adult levels of reproductive hormones in early life, nor is the exact timing of the peak known. Furthermore, what determines the timing of peaks and suppressions of reproductive hormones from infancy throughout childhood and into adolescence remains to be elucidated.
The study aims to described and evaluate dynamic changes in the hypothalamic-pituitary- gonadal axis in early postnatal life.
Detailed description
Minipuberty is a term used to describe the transient activation of the pituitary-gonadal axis 2-3 months after birth in both boys and girls. It is, however, not known why infants reach adult levels of reproductive hormones in early life, nor is the exact timing of the peak known. Furthermore, what determines the timing of peaks and suppressions of reproductive hormones from infancy throughout childhood and into adolescence remains to be elucidated.
Few studies have investigated minipuberty and one, for example, found that it is affected in premature infants (before gestation week 37). However, no studies on normative data throughout minipuberty in infants exist.
Furthermore, using minipuberty as a window for diagnosis of endocrine disorders and future reproductive function has been suggested. Defining minipuberty, both in terms of circulating hormone levels and urinary metabolites, in healthy infants is therefore essential in order to utilize this window. Studies using patients with Disorders of Sex Development during minipuberty have been carried out, but they are hampered by small sample sizes and lack of control groups.
In addition, little is known about the genetic and epigenetic factors that drive the onset, progression and termination of minipuberty as well as the actual puberty, i.e. the factors responsible for the quiescence of the HPG axis during childhood and the dis-inhibition responsible for pubertal onset. Therefore, much attention was drawn on the study performing whole exome sequencing in patients and relatives with central precocious puberty (CPP). For the first time, MKRN3 was suggested as the primary factor responsible for HPG inhibition during mid-childhood. A number of studies support that MKRN3 mutations cause CPP, and genetic variation of MKRN3 affect pubertal timing in healthy girls. Our findings of declining serum levels of MKRN3 prior to pubertal onset in healthy girls support MKRN3 as a regulator of pubertal onset. The exact mechanism through which MRKN3 exceeds its effect remains to be elucidated; however, its zink-finger structure indicates regulation of superior cellular processes such as epigenetic regulation of DNA transcription.
Twin studies suggest that 60% of the inter-individual variation is caused by genetic factors. However, genome wide association (GWA) studies only explain a fraction of the variation in age at puberty. Recently, our research group has revealed the largest effect of a single SNP on age at pubertal onset in girls. The location of the SNPs in genes regulating FSH action emphasizes the need of a wide focus including downstream processes in the HPG axis when evaluating factors regulating puberty.
In general, the abovementioned studies have led to a spark in the interest in epigenetic studies, i.e. studies of genetic changes that are not caused by changes in the DNA sequences themselves, but rather regulatory mechanisms of DNA expression. Generally, this is thought to include DNA methylation, histone modifications and small RNAs. Epi-mutations (improper epigenetic regulation) possibly account for more of the variation in puberty than genetic factors. Previously, both gene-specific and genome-wide DNA methylation patterns have been studied. Genome-wide hypomethylation seen in peripheral leukocytes has been shown to be linked with an array of cancers, including colorectal cancers. As multiple histone modifications exist and analysis requires special sample treatment procedures, DNA methylation is the most appropriate epigenetic marker to analyze. A study of rats found that specific gene hypomethylation was accountable for lack of pubertal onset, but the link between epigenetics and mini- and pubertal timing and progression has, however, only scarcely been studied. Understanding this link would greatly add to our knowledge of reproductive function and normal sex development.
Disorders of Sex Development (DSD) is an umbrella term covering conditions with congenital disordered development of chromosomal, gonadal or anatomical sex. Genital abnormalities may include as many as up to 4-6 in 1000 births, although individual disorders are much rarer, e.g. 45,X/46,XY mosaicism is seen in about 1 in 15000 live births. Previously DSD diagnoses were labeled with different and often imprecise terms such as 'intersex', 'sex reversal' and 'hermaphroditism' etc. In 2006, DSD nomenclature was renamed and grouped according to genetic sex into sex chromosome DSD, 46,XY DSD and 46,XX DSD.
DSD patients are diagnosed at different periods in life depending on their diagnosis, phenotype and primary and secondary sexual development. Patients with sex chromosome DSD can be diagnosed at prenatal screenings, patients with affected external genitalia at birth, some during childhood due to growth abnormalities, some during adolescence due to abnormal pubertal progression and lastly, some in adulthood due to infertility.
Understanding normal sex development is therefore the key to identifying and optimizing diagnosis and treatment of patients with DSD. A project, as the present, that seeks to investigate normal minipuberty while comparing to minipuberty in patients with DSD is therefore of great importance. Furthermore, knowledge of the genetic and epigenetic control mechanisms of minipuberty will aid the understanding of reproductive physiology and in particular DSD pathology.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| 1 year follow-up group | – | –1 year follow-up group including 6 measurements |
| 40 days diaper study subgroup | – | –Subgroup of the "1 year follow-up group" including 15 girls undergoing daily measurement of urinary hormone excretion |
Who may qualify
- Ages
- Up to 12 months
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child
- Study population
- Pregnant women, meeting the inclusion criteria, and the fathers-to-be followed at the Department of Obstetrics, Rigshospitalet. Further, parents and infants with disordered sexual development (DSD). These patients will be recruited via The Department of Growth and Reproduction, Rigshospitalet. Parents whose fetuses have been diagnosed prenatally with any DSD diagnosis or during the first 6 months of life will be invited to participate. Three groups of participants in this study: 1. A group of healthy infants 2. All infant patients diagnosed with or under evaluation for DSD 3. The parents of the healthy infants and DSD patients Number (approximately) of participants: 1. 200 healthy infants (100 boys and 100 girls) 2. unknown number of DSD infants that will be referred within a year to the Department of Growth and Reproduction; estimation: 15 DSD infants. 3. 400 parents of healthy infants (200 fathers and 200 mothers) - unknown number of parents of DSD patients
Key inclusion criteria (9 listed)
- Singleton pregnancy
- Maternal and paternal Caucasian origin
- Maternal pre-pregnancy BMI between 18 and 35 kg/m2
- No serious maternal illness, including no pre-existing maternal diabetes nor thyroid gland diseases
- Term pregnancy (week 37+0 to 41+7)
Key exclusion criteria (1 listed)
- -
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Serum and urinary metabolites of reproductive hormones (e.g. steroid hormone metabolites and gonadotropins) (newborn)
Time frame: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth plus 40 days daily measurement (urine, female 40 days diaper study subgroup)
change/course serum and urinary metabolites
Urinary metabolites of endocrine disrupting chemicals (e.g. phthalates, phenols, perfluorinated compounds and parabens) (newborn)
Time frame: 3-7d, & 1,3,5,7,12m or 2,4,6,8,12m after birth plus 40 days daily measurement (urine, female 40 days diaper study subgroup)
change/course urinary metabolites
Basic clinical examination (newborn) (size and proportions)
Time frame: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
change/course: measurements of length, weight, skin folds and hip-waist ratio
Basic clinical examination (newborn) (pubertal staging)
Time frame: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
change/course: pubertal staging using Tanners classification (including testicular size in boys assessed by Prader's orchidometer and ultrasound
Basic clinical examination (newborn) (genitalia)
Time frame: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
change/course: classification of external genitalia (classification of genital tubercle, location of gonads, position of urethra, labia/scrotal fusion)
Basic clinical examination (newborn) (penile measurement)
Time frame: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
change/course: penile measurement with a ruler (in boys)
Basic clinical examination (newborn) (AGD)
Time frame: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
change/course: ano-genital distance (AGD) measured with a ruler
Genetic profiling
Time frame: single determination or 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
Genotyping of different genetic loci (genetic variation of loci regulating hormone signalling, e.g. FSHB, etc.)
Epigenetic profiling
Time frame: single determination or 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth
change/course: epigenetic variation of loci regulating hormone signalling
8 secondary outcomes
Basic clinical examination (parents) (height)
Time frame: postpartal (within first 3 months)
Basic clinical examination (parents) (weight)
Time frame: postpartal (within first 3 months)
Basic clinical examination (parents)
Time frame: postpartal (within first 3 months)
Pregnancy and perinatal outcome (newborn and mother)
Time frame: before birth and perinatal phase
Medical history and exposure (parents) (basic)
Time frame: postpartal (within first year)
Medical history and exposure (parents) (obstetrical)
Time frame: postpartal (within first year)
Medical history and exposure (parents) (puberty)
Time frame: postpartal (within first year)
Breastfeeding and food intake (newborn)
Time frame: first year of life
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 15 Feb 2019.
- Derived from this study: PubMed 41921027Pridik C, Juul A, Busch AS. Free testosterone and IGF-I mediate sex-specific linear growth during minipuberty. Endocr Connect. 2026 Apr 15;15(4):e250930. doi: 10.1530/EC-25-0930. Print 2026 Apr 1.
- Derived from this study: PubMed 35704034Ljubicic ML, Busch AS, Upners EN, Fischer MB, Petersen JH, Raket LL, Frederiksen H, Johannsen TH, Juul A, Hagen CP. A Biphasic Pattern of Reproductive Hormones in Healthy Female Infants: The COPENHAGEN Minipuberty Study. J Clin Endocrinol Metab. 2022 Aug 18;107(9):2598-2605. doi: 10.1210/clinem/dgac363.
- Derived from this study: PubMed 35521767Ljubicic ML, Busch AS, Upners EN, Fischer MB, Main KM, Andersson AM, Johannsen TH, Hagen CP, Juul A. Dynamic changes in LH/FSH ratios in infants with normal sex development. Eur J Endocrinol. 2022 Jun 1;187(1):135-142. doi: 10.1530/EJE-21-0999.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Anders Juul, Prof. study chair
Copenhagen University Hospital, Rigshospitalet
Alexander S Busch, MD principal investigator
Copenhagen University Hospital, Rigshospitalet
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Child Development and Disorders of Sex Development, run by Copenhagen University Hospital, Rigshospitalet at 1 site in Denmark.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 9 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 15 Feb 2019. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Denmark. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Serum and urinary metabolites of reproductive hormones (e.g. steroid hormone metabolites and gonadotropins) (newborn) (time frame: 3-7d, and 1,3,5,7,12m or 2,4,6,8,12m after birth plus 40 days daily measurement (urine, female 40 days diaper study subgroup)). The study lists 9 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02784184, which also lists 3 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 15 Feb 2019.