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Gonadal dysgenesis with X‐monosomy in a cynomolgus monkey ( Macaca fascicularis )
Author(s) -
Reyes Francisco I.,
Osborn Russell G.,
Fuller Gene B.,
Hobson William C.,
Greenberg Cheryl R.,
Ray Manoranjan,
Thliveris James A.,
Faiman Charles
Publication year - 1990
Publication title -
american journal of primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 81
eISSN - 1098-2345
pISSN - 0275-2565
DOI - 10.1002/ajp.1350220103
Subject(s) - endocrinology , medicine , biology , gonadotropin , luteinizing hormone , follicle stimulating hormone , gonadal dysgenesis , virilization , aneuploidy , hormone , chromosome , androgen , genetics , gene
A 3‐year‐old female cynomolgus monkey ( Macaca fascicularis ) was found to have inappropriately high circulating immunoassayable follicle‐stimulating hormone (FSH) and luteinizing hormone (LH) levels compatible with primary gonadal failure. Hypergonadotropic hypogonadism was confirmed by the findings of persistently high serum gonadotropin levels by both LH bioassay and FSH and LH radioimmunoassays and low levels of serum estradiol. In addition, circhoral gonadotropin pulsatility and an exaggerated response to a gonadotropin‐releasing hormone challenge were demonstrated. Both FSH and LH coeluted in a single peak on gel filtration column chromatography. Clinically, the animal showed the following features of Turner syndrome: small body size, sexual underdevelopment, gonadal streaks with absent follicles, and a chromosomal constitution of 41,X. A similar case has been reported previously in a rhesus monkey ( Macaca mulatta ). Considering the fetal and live birth prevalences in humans of aneuploidy in general and X‐monosomy in particular, one would predict that this chromosomal aberration underlies a high number of pregnancy failures in nonhuman primates.