Gonadotrophin-secretion in adrenocortical insufficiency: impact of glucocorticoid substitution

1982 ◽  
Vol 101 (4) ◽  
pp. 580-585 ◽  
Author(s):  
H. Vierhapper ◽  
W. Waldhäusl ◽  
P. Nowotny

Abstract. In patients with deficient endogenous glucocorticoid production due to primary adrenal insufficiency (n = 4) or bilateral adrenalectomy (n = 2) a rise in LRH-stimulated concentrations of LH was seen following withdrawal of substitution therapy for 84 h. Consecutive re-administration of glucocorticoids (dexamethasone 2.0 mg/day for 3 days) resulted in increased basal concentrations of LH and FSH and a diminished secretory response of LH upon iv LRH (100 μg). Five patients substituted with glucocorticoids because of adrenocortical insufficiency presented upon the administration of exogenous ACTH1-24 with unchanged basal and LRH-stimulated concentrations of LH and FSH as compared to a placebo experiment. These data suggest that the withdrawal and subsequent re-administration of glucocorticoid substitution alters basal and stimulated concentrations of gonadotrophins in patients with adrenocortical insufficiency, thus providing evidence for the importance of adequate glucocorticoid supply in the regulation of gonadotrophin secretion.

1992 ◽  
Vol 126 (4) ◽  
pp. 319-324 ◽  
Author(s):  
Ronald Comtois ◽  
Josée Hébert ◽  
Jean-Paul Soucy

The clinical and biochemical manifestations of secondary adrenocortical insufficiency are not well defined in the medical literature. This study was designed to determine the clinical and laboratory features suggesting the diagnosis of adrenal insufficiency in 15 chronic ACTH deficiency patients during low and normal cortisol states. Except for fatigue and weakness, the characteristic clinical manifestations of primary adrenal insufficiency occurred rarely. ACTH deficiency did not significantly modify blood glucose, serum calcium, sodium, potassium and differential white blood cell count. However, serum T4 was lower (65±19 vs 95±21 nmol/l, p< 0.001) during cortisol deficiency, while T3 was higher (2.4±0.67 vs 2.0±0.60 nmol/l, p<0.001). Furthermore, rT3 decreased significantly during hypocorticism (0.27±0.07 vs 0.18±0.07 nmol/l, p<0.001). TheT4/T3 ratio was significantly lower than the normal in 15 out of the 17 episodes of ACTH deficiency (29±12.5 vs 57±9.4, p<0.0001). We conclude that the increase in T3 and decrease in T4 levels are associated with chronic secondary adrenocortical insufficiency. This laboratory feature could be due, at least in part, to the increased peripheral conversion of T4 to T3 during cortisol deficiency.


1996 ◽  
Vol 24 (2) ◽  
pp. 221-227 ◽  
Author(s):  
G Akçay ◽  
F Aral ◽  
N Özbey ◽  
A Azezli ◽  
Y Orhan ◽  
...  

Long-standing primary failure of pituitary-dependent endocrine glands may lead to hyperplasia of the pituitary cells. These changes in the pituitary gland may be correlated with the severity and duration of target-endocrine gland insufficiency. Production of adrenocorticotrophic hormone by the pituitary tumour and modest hyperprolactinaemia may develop due to adrenocortical insufficiency, but production of prolactin by the pituitary tumour due to primary adrenal insufficiency is rare. A case study is presented, with primary adrenal insufficiency associated with hyperprolactinaemia and pituitary macroadenoma (most probably prolactinoma). Plasma levels of prolactin were found to decrease after glucocorticoid, mineralocorticoid and bromocriptine therapy.


Author(s):  
Julia R. Broussard ◽  
Naim Mitre

AbstractWe report the use of continuous subcutaneous hydrocortisone infusion in an adolescent patient with primary adrenal insufficiency. This novel hydrocortisone delivery method proved to be a feasible, well-tolerated and safe option for selected patients with poor response to conventional therapy.


2017 ◽  
Vol 23 ◽  
pp. 23-24
Author(s):  
Moses Ko ◽  
Timothy Quek ◽  
Yin Kon ◽  
Daniel Ek Kwang Chew

2018 ◽  
Author(s):  
Peter Wolf ◽  
Johanna Mayr ◽  
Marko Poglitsch ◽  
Alois Gessl ◽  
Anton Luger ◽  
...  

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