Publications by authors named "A Chryssikopoulos"

In young members of a large family from a Greek island with a closed society, clinical and hormonal symptoms of 21-OH deficiency (CAH) were present. To discriminate those affected from those unaffected, we measured the basal and ACTH stimulated 30 values of 17-hydroxyprogesterone (17-0HP) progesterone (P) and cortisol (F) in combination with HLA-phenotypes in 25 out of 40 members of this family. The indices of the Gutai30-min assessment (17-0HP+P response to ACTH testing at 30 min), GF (F response at 30 min) and the ratio GF30/Guai30 named the Marina index were evaluated.

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Unlabelled: The study was aimed to find out the prevalence of non-classical congenital adrenal hyperplasia (NC-CAH) due to 21-hydroxylase deficiency (21-OHdef) among Greek women with hirsutism and polycystic ovary syndrome (PCOS) and to compare the results of ACTH stimulated 17-hydroxyprogesterone 60 min (17-OHP60) values, with human leukocyte antigens (HLA) phenotypes, in any patient diagnosed as having NC-CAH. One hundred and seven women with hirsutism and PCOS were included in the study. All were presented at the Reproductive Endocrinology Outpatient Clinic with hirsutism and PCOS.

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Objective: The purpose of this study was to evaluate thyroid function and TSH and cortisol (F) secretion in hyperandrogenemic women with nonclassical congenital adrenal hyperplasia (NC-CAH) due to 21-hydroxylase deficiency (Group A) when compared with women with hyperandrogenemic symptoms (menstrual irregularities, hirsutism, acne, seborrhea and sterility) of other etiologies (Group B).

Methods: Seventy-two women were subjected to stimulation of the adrenal cortex with i.v.

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The circuit of gonadotropins (FSH, LH) and ovaries (theca and granulosa cells) in ovarian estrogen and androgen production is well established. Recent research has revealed an intraovarian network that may ultimately prove relevant to the understanding of ovarian hyperandrogenism. Most of these substances, such as growth factors and cytokines, do not have independent effects on basal androgen production, but exhibit their regulatory potential by modulating hCG- or LH-stimulated steroid production.

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