Document Detail

Transient anomalies in genital appearance in some extremely preterm female infants may be the result of foetal programming causing a surge in LH and the over activation of the pituitary-gonadal axis.
MedLine Citation:
PMID:  18466346     Owner:  NLM     Status:  MEDLINE    
AIM: Animal studies have linked foetal programming with the development of the polycystic ovarian syndrome, and metabolic syndrome, in adulthood. The objective is to describe the investigation of four extreme-premature female infants born between 25 and 29 weeks' gestation with apparent genital abnormalities in association with unusually high androgens and gonadotrophins, to postulate a cause and to raise awareness of pitfalls in assessment of these infants. METHODS: Clinical examination and biochemical evaluation of four infants referred for apparent congenital ambiguity. RESULTS: Female gender was assigned at birth. Chromosome analysis confirmed 46XX, urine steroid profiles demonstrated no evidence of congenital adrenal hyperplasia and only the expected levels of foetal adrenal steroids. Elevated LH (up to 162 IU/l), testosterone (up to 2.6 nmol/l), Delta(4 )androstenedione (up to > 35 nmol/l) and dehydro-epiandrosterone sulphate (DHEAS) (up to 26.6 micromol/l) were seen in all four infants. These decreased over time but were significantly different from a control population of premature infants of similar gestational age. CONCLUSIONS: We postulate that the clinical pattern of apparent clitoral enlargement in some extremely premature infants may reflect true temporary virilization due to an unusually high (or excessive) LH surge, in turn causing high foetal androgens. Foetal programming of gonadotrophin excess is probably the primary cause of androgen increase, in turn causing virilization, in some extreme-premature infants. These may potentially be a group at future risk of polycystic ovary or metabolic syndrome, however, further work needs to be conducted to substantiate this hypothesis.
Ronda Greaves; Rodney W Hunt; Margaret Zacharin
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Publication Detail:
Type:  Case Reports; Journal Article; Multicenter Study     Date:  2008-05-08
Journal Detail:
Title:  Clinical endocrinology     Volume:  69     ISSN:  1365-2265     ISO Abbreviation:  Clin. Endocrinol. (Oxf)     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-05     Completed Date:  2009-08-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0346653     Medline TA:  Clin Endocrinol (Oxf)     Country:  England    
Other Details:
Languages:  eng     Pagination:  763-8     Citation Subset:  IM    
Complex Biochemistry Department, The Royal Children's Hospital, Parkville, Victoria, Australia.
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MeSH Terms
Fetal Development / physiology*
Genitalia, Female / abnormalities*,  anatomy & histology
Gonads / metabolism,  physiology*
Infant, Extremely Low Birth Weight / blood,  physiology
Infant, Newborn
Infant, Premature / blood,  physiology*
Luteinizing Hormone / blood*
Pilot Projects
Pituitary Gland / metabolism,  physiology*
Sex Determination (Analysis)
Time Factors
Reg. No./Substance:
9002-67-9/Luteinizing Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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