1988
DOI: 10.1007/bf00931548
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Polycystic ovarian disease: Endocrinological parameters with specific reference to growth hormone and somatomedin-C

Abstract: Thirty-three women (22-38 years old) with polycystic ovarian disease (PCOD) were included in this study. The criteria for diagnosis were: an LH/FSH ratio greater than 2.0; polycystic ovaries, diagnosed by means of palpation and ultrasound; androgenism and menstrual cycle abnormalities. Using endocrine parameters, we attempted to define distinct forms of PCOD. The patients were placed in three groups according to serum levels of testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha OHP) and the estrone/an… Show more

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Cited by 30 publications
(6 citation statements)
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“…Our patient's basal and post‐glucose GH concentrations were not elevated, excluding GH excess as the cause of the radiological findings. Indeed GH was undetectable in her fasting sample, consistent with the finding of GH hyposecretion in women with PCOD (Urdl 1988).…”
Section: Discussionsupporting
confidence: 87%
“…Our patient's basal and post‐glucose GH concentrations were not elevated, excluding GH excess as the cause of the radiological findings. Indeed GH was undetectable in her fasting sample, consistent with the finding of GH hyposecretion in women with PCOD (Urdl 1988).…”
Section: Discussionsupporting
confidence: 87%
“…Urdl [20] recently reported that PCOS patients with elevated testosterone had signifi cantly decreased GH levels with decreased GH/IGF-I ratio. Although IGF-I levels were not significantly higher in these patients, these results indicated that elevated IGF-I levels inhibited pituitary GH production by nega tive feedback.…”
Section: Discussionmentioning
confidence: 99%
“…In one view, insulin resistance is the primary defect, and leads to increased IGF-I action upon target tissues by directly binding to IGF-I receptors (to which insulin can bind with low affinity via specificity spillover) or by suppressing serum IGFBP-1 levels (Suikkari et al, 1989;Barbieri et al, 1988;Nestler et al, 1989b). Alternatively, a developmental abnormality in the establishment of the "setpoint" for IGF-I activity in various tissues, possibly related to nutritional factors early in life, has been proposed (Urdl, 1988;Kazer, 1989). Such an abnormality could be characterized by increased availability of IGF-I (in either an endocrine or paracrine context), increased target tissue sensitivity to IGF-I, an increase in the size of various IGF-I-dependent tissue compartments, or some combination of the three.…”
Section: Polycystic Ovary Syndromementioning
confidence: 99%