ISSN:
1432-0711
Keywords:
Polycystic ovarian disease
;
Differentiation of types
;
Growth factors
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary 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 17α-hydroxyprogesterone (17α OHP) and the estrone/androstendione (E1/Δ4A) ratio. Patients in group I (n=18) had an elevated T level (〉1.0 ng/ml) and a 17α OHP level under 4.0 ng/ml. This type of POCD was called the “androgen” type. Patients in group II (n=7) had normal T- and 17α OHP levels under 4.0 ng/ml and an elevated (E1/Δ4A) ratio. This type of PCOD was called the “estrogen” type. Group III (n=8) comprised patients with 17α OHP levels over 4.0 ng/ml. This type of PCOD was called the “adrenocortical” type. In two patients of this group, a modified ACTH test revealed late-onset congenital hyperplasia. The endocrine parameters of the patients with PCOD were compared with those of 17 adult without signs of PCOD. Statistical evaluation was done by variance analysis. Women with acromegaly often show signs of androgenism as well as menstrual cycle abnormalities. This may indicate an association between the growth factors human growth hormone (HGH) and somatomedin-C (Sm−C) and the biosynthese and metabolism of steroid hormone. Recent experiments have demonstrated such associations. Our study showed an association between the HGH and Sm−C levels and abnormal steroid hormone concentrations in women with androgen type PCOD (group I). These patients had a significantly decreased HGH level, a significantly decreased HGH/Sm−C ratio, and an increased average Sm−C level. These data suggest that elevated Sm−C levels can, by a negative-feedback mechanism, inhibit pituitary HGH production. We discuss the possible mechanisms causing elevation of plasma Sm−C, HGH, steroid hormones, excessive food intake, and possibly prolactin seem responsible for the clinical manifestation of increased Sm−C production in adolescence and for its level in the fertile years of patients.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00931548
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