Naslov
LHbeta response to insulin-induced hypoglycemia in patients with non-functioning pituitary adenomas

Autori
Škorić, Tanja ; Breskovac, Ljiljana ; Plavšić, Vesna ; Koršić, Mirko ; Tomašić, Jelka ; Aganović, Izet ; Giljević, Zlatko ; Perković, Zdravko ; Kaštelan, Darko

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Abstracts PB-42 / - Odense, 1999, 127-127

Skup
9th Meeting of the European Neuroendocrine Association

Mjesto i datum
Odense, Danska, 03.09.1999. - 07.09.1999

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
insulin-induced hypoglycemia; nonfunctioning pituitary adenomas; LHbeta

Sažetak
Insulin-induced hypoglicemia (IIH) profoundly inhibits the activity of the hypothalamic GnRH pulse generator and decreases mean serum LH concentration. Several factors (CRF, PRL, endogenous opioid peptides, vasopressin, estradiol) have been proposed to have a certain role in this response. The absent response of gonadotrophins to IIH was found in pathological condition like non-functioning pituitary adenoma (NFA). A patient with pure alpha-subunit secreting pituitary adenoma and significant serum alpha-subunit increase in response to IIH has been previously described. Therefore, the effect of IIH on LHbeta secretion in patients with NFA was investigated. Nineteen patients (male:female=9:10, mean age 50.210.6 years) with NFA were examined. The increase of serum LHbeta to IIH was found in 10/19 patients - group I of patients- (the average increase was 62.7  5.9 percent, min. 14 percent max. 124 percent). The remaining 9 patients responded to IIH with decrease of serum LH concentration - group II of patients - (the average decrease was 38.9  15.3 percent). The concomitant increase of LH to IIH was found only in 4/10 patients of group I, and, surprisingly, in 2/9 patients of group II. Basal levels of LHbeta as well as LHbeta response to LHRH stimulation were not significantly different between the groups. On the contrary, serum basal LH levels were significantly higher in the patients of group I in comparison to the patients of group II. Decreased basal LH levels were found in 3/10 patients of group I and 8/9 patients of group II, while absent or impaired responsivity of LH to LHRH was found in 3/10 and in 4/9, respectively. Basal serum PRL, ACTH and cortisol levels did not differ between the groups. Impaired responses of ACTH and cortisol to IIH were shown in 4/10 patients of group I and in 6/9 patients of group II. Although the underlying mechanism of LHbeta response to insulin still remains unclear and confirmation in a larger number of patients is mandatory, the finding of abnormal or nonspecific LHbeta increase might be of diagnostic value in patients with NFA.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

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