Alberto Janni

Increased DHEAs levels in PCO syndrome: evidence for the existence of two subgroups of patients

In 49 patients affected by PCO syndrome the serum levels of dehydroepiandroster-one-sulphate (DHEAs) were determined and correlated with the cfinical presentation and the endocrine pattern. Twenty-three patients (47%) had high DHEAs levels (h-DHEAs patients). They presented a milder clinical presentation (low incidence of amenorrhea) than PCO patients with normal DHEAs levels (n-DHEAs patients). In h-DHEAs patients the finding of a normal DHEAs. response to ACTH and of slightly increased 17OHP serum levels suggested that the elevation of serum DHEAs was not due to an adrenal enzymatic deficiency but to a tonic hyperstimulation of the adrenals. Two subgroups of h-DHEAs patients were identified: in the first subgroup, PRL and estrone levels were increased and probably explained the DHEAs hypersecretion; in the second subgroup, the endocrine pattern was very similar to that observed in n-DHEAs.patients and a clear explanation for DHEAs increase was not found, although the possibility of an exaggerated secretion of some pituitary hormones with adrenal androgen stimulating activity must be considered.

Increased circulating levels of immunoreactive β-endorphin in polycystic ovary syndrome is not caused by increased pituitary secretion

Abstract OBJECTIVE: Our purpose was to investigate the source and role of elevated levels of immunoreactive β-endorphin in polycystic ovary syndrome. We wished to determine whether immunoreactive β-endorphin secretion in patients with polycystic ovary syndrome is influenced by body weight and whether the pituitary release of immunoreactive β-endorphin with corticotropin-releasing hormone is related to luteinizing hormone levels or adrenal androgen secretion. STUDY DESIGN: Eighteen patients with polycystic ovary syndrome and 10 ovulatory controls were studied. Each subject received 1 μg/kg intravenous corticotropin-releasing hormone and an oral glucose tolerance test on alternate days. Levels of plasma immunoreactive β-endorphin, corticotropin, luteinizing hormone, cortisol, adrenal androgens, and insulin were measured. RESULTS: Although immunoreactive β-endorphin levels were elevated in patients with polycystic ovary syndrome ( p \lt 0.01), incremental responses after corticotropin-releasing hormone were similar to controls and were not influenced by body weight. Serum luteinizing hormone levels were not affected by corticotropin-releasing hormone and did not correlate with immunoreactive β-endorphin levels. Adrenal androgen responses after corticotropin-releasing hormone were increased in patients with polycystic ovary syndrome ( p \lt 0.01) but were not correlated with immunoreactive β-endorphin secretion. After oral glucose was given, elevated fasting insulin levels increased significantly in patients with polycystic ovary syndrome ( p \lt 0.01), as did immunoreactive β-endorphin levels ( p \lt 0.05). The increases in insulin and immunoreactive β-endorphin levels were correlated ( p \lt 0.05). CONCLUSIONS: Pituitary secretion of immunoreactive β-endorphin is normal in patients with polycystic ovary syndrome, and pancreatic secretion appears to be increased. Corticotropin-releasing hormone does not influence luteinizing hormone levels, and adrenal androgen sensitivity is not influenced by immunoreactive β-endorphin secretion. (AM J OBSTET GYNECOL 1992;167:1819-24.)

Prevalence of late-onset 11 β-hydroxylase-deficiency in hirsute patients

Serum levels of 11-deoxycortisol were determined in 182 hirsute women. Three patients presented high basal 11-deoxycortisol levels and an exaggerated response of this steroid to ACTH stimulation. A fourth patient had normal basal 11-deoxycortisol but was hyperresponsive to ACTH stimulation. Therefore diagnosis of late-onset 11 β-hydroxylase deficiency was made in 4 out of 182 hirsute women with a prevalence of 2.2% in the group studied. In these patients, clinical findings and other hormonal patterns were not different from those of other women suffering from hirsutism.

The endocrine pattern of late onset adrenal hyperplasia (21-hydroxylase deficiency)

We describe 5 adult women with severe hirsutism due to late onset 21-hydroxylase deficiency. Diagnosis was performed on the finding of high serum 17-hydroxyprogesterone (170HP) levels with a marked hyperresponse to an ACTH test. The endocrine study showed in most patients a gonadotropin behaviorsimilarto that observed inclassical polycystic ovary (PCO) syndrome. Prolactin levels were slightly increased in basal conditions and presented an exaggerated response to TRH stimulation.

Hypothalamic-pituitary-thyroid axis in acromegaly

To evaluate the hypothalamic-pituitary-thyroid axis in acromegaly, total and free thyroid hormones and TSH response to TRH were determined in 36 acromegalic patients. In 10 patients, rT3 and thyroxine binding globulin (TBG) were also assayed by radioimmunoassay. In 15 patients the TSH response to TRH was also studied after medical or surgical therapy of the acromegaly. In 34 patients total thyroid hormones were in the normal range whereas two patients had low serum levels of free thyroid hormones. Thirty-two of the acromegalic patients were euthyroid. However, only 43.7% of the euthyroid patients had a normal TSH response to TRH. Nine patients had a reduced TSH rise after TRH, whereas in 4 patients the response was exaggerated and in 5 delayed. In all patients studied rT3 and TBG were in the normal range. After medical or surgical therapy of the acromegaly we observed improvement or normalization of the TSH response to TRH. In conclusion, the TSH response to TRH is frequently altered in acromegaly, whereas thyroid function is generally normal. Hypothalamic effects of GH hyperproduction may explain the alterations of TSH secretion in many cases in view of the normalization of TSH secretion after therapy of acromegaly.