Pulsatile Luteinizing Hormone Secretion in Patients with Addison’s Disease. Impact of Glucocorticoid Substitution1
J. Hangaard,
M. Andersen,
E. Grodum,
O. Koldkjær and
C. Hagen
Department of Endocrinology, Odense University Hospital (J.H.,
M.A., E.G., C.H.), DK-5000 Odense C; and the Department of Clinical
Chemistry, Sønderborg Hospital (O.K.), DK-6400 Sønderborg,
Denmark
Address all correspondence and requests for reprints to: Jørgen Hangaard, M.D., Department of Endocrinology, Odense University Hospital, DK-5000 Odense C, Denmark.
The physiological and pathophysiological role of cortisol inpulsatile
LH release was investigated in 14 patients (5 men,6 premenopausal
women, and 3 postmenopausal women) with Addison’sdisease. The
explicit effect of cortisol in relation to theeffect of
corticotropin-releasing factor (CRF), ACTH, and opioidswas ensured by
hypo-, normo-, and hypercortisolism. Hypocortisolismwas obtained by
24-h discontinuation of hydrocortisone (HC)followed by 23-h saline
infusion. Eucortisolism was securedby infusion of HC (0.5 mg/kg) over
23 h. Stress-appropriatehypercortisolism was obtained by infusion
of HC (2.0 mg/kg)over 23 h, preceded by treatment for 5 days with
dexamethasone(1.5 mg/day). To imitate the normal diurnal rhythm for
serumcortisol, HC was infused in graduated doses. Blood samplingwas
performed every 10 min during the last 10 h of the studyperiod,
followed by a LH-releasing hormone test (5 µg,iv) and a TRH test (10
µg, iv). In pre- and postmenopausalwomen, the mean LH level and the
LH pulsatility pattern weresimilar on the 3 occasions. In contrast,
the mean LH level inmen was significantly reduced during
hypocortisolism comparedto that during eucortisolism (3.26 ±
0.68 vs. 4.49 ±0.83 U/L; P <
0.05) and was associated with a clear decreasein LH pulse amplitude
(1.09 ± 0.33 vs. 1.96 ±0.53 U/L;
P < 0.05). During high doses of glucocorticoids,
themean LH level in men was significantly lower than that during
eucortisolism(3.81 ± 0.88 vs. 4.49 ± 0.83
U/L; P < 0.05).In both men and women, the mean
PRL levels increased significantly(P < 0.05)
during hypocortisolism, whereas high glucocorticoiddoses suppressed
the mean PRL level (P < 0.05). The LH andPRL
responses to LH-releasing hormone and TRH were, however,similar during
low, medium, and high cortisol levels in bothmen and women. In
conclusion, our data suggest that the attenuationof pulsatile LH
secretion in men during hypo- and hypercortisolismis due to variations
in the hypothalamic opioid activity secondaryto alterations in serum
cortisol levels. A higher level of opioidreceptor activity in men than
in low estrogen women may explainthe gender differences.
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