Diagnosis of secondary adrenal insufficiency: evaluation of the standard dose short synacthen test in comparison to the insulin tolerance test in patients with hypothalamic-pituitary disease

2005 ◽  
Vol 113 (S 1) ◽  
Author(s):  
T Deutschbein ◽  
N Unger ◽  
H Wiedemayer ◽  
D Stolke ◽  
A Yuece ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Standard Dose ◽  
Tolerance Test ◽  
Insulin Tolerance Test ◽  
Secondary Adrenal Insufficiency ◽  
Pituitary Disease ◽  
Insulin Tolerance ◽  
Synacthen Test ◽  
Short Synacthen Test

scholarly journals Response of Cortisol Metabolites in the Insulin Tolerance Test and Synacthen Tests

2015 ◽  
pp. S237-S246 ◽  
Author(s):  
K. SIMUNKOVA ◽  
M. DUSKOVA ◽  
M. KOSAK ◽  
M. KRSEK ◽  
V. HANA ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Tolerance Test ◽  
Insulin Tolerance Test ◽  
Similar Response ◽  
Strongly Correlated ◽  
Insulin Tolerance ◽  
Stimulation Tests ◽  
Synacthen Test ◽  
Short Synacthen Test ◽  
Cortisol Metabolites

Determination of response of cortisol and its metabolites to different stimuli may be important for adrenal gland disorders. To date, only one metabolite, cortisone, has been followed in stimulation tests of the adrenal gland. We aimed to describe a response of cortisol metabolites to the standard short Synacthen test (HDST), insulin tolerance test (ITT), low dose Synacthen test (LDST) and medium dose Synacthen test (MDST). Sixty healthy subjects were investigated: 30 men and 30 women. Plasma for measurements of cortisol and its metabolites was obtained before and 30th and 60th min after Synacthen and insulin administration. The cut-off 500 nmol/l of cortisol was reached after stimulation in all of tests, the maximal stimulation level was reached in 60th min in all of the tests except for LDST. The response of cortisol and its metabolites at 30th and 60th min strongly correlated in all of the tests except for LDST. Cortisol and its metabolites increased after stimulation; in contrast, cortisone and its metabolites decreased. We showed that the response of the cortisol metabolites during the Synacthen tests and ITT well correlated, and the MDST showed similar response compared to HDST. The decrease in cortisone metabolites may correspond to the regeneration of cortisol from cortisone in response to stimulation test.

scholarly journals Reduced epinephrine reserve in response to insulin-induced hypoglycemia in patients with pituitary adenoma

2007 ◽  
Vol 157 (3) ◽  
pp. 265-270 ◽  
Author(s):  
Shinya Morita ◽  
Michio Otsuki ◽  
Maki Izumi ◽  
Nobuyuki Asanuma ◽  
Shuichi Izumoto ◽  
...  
Keyword(s):  
Pituitary Adenoma ◽  
Adrenal Insufficiency ◽  
Serum Cortisol ◽  
Tolerance Test ◽  
Secondary Adrenal Insufficiency ◽  
Counterregulatory Hormones ◽  
Insulin Tolerance ◽  
Secondary Hypothyroidism ◽  
Severe Impairment ◽  
Plasma Gh

Objective: Hypoglycemia induces rapid secretion of counterregulatory hormones such as catecholamine, glucagon, cortisol, and GH. Insulin-induced hypoglycemia is used for evaluating GH–IGF-I and ACTH–adrenal axes in patients with pituitary disorders. The aim of this study was to determine whether the response of catecholamine secretion to hypoglycemia is disrupted in patients with pituitary adenoma. Methods: The study population comprised 23 patients with pituitary adenoma (non-functioning adenoma or prolactinoma). An insulin tolerance test was performed and serum catecholamines as well as plasma GH and serum cortisol were measured. Results: The study patients showed diminished response of plasma epinephrine to insulin-induced hypoglycemia. With the cutoff level of peak epinephrine for defining severe impairment set at 400 pg/ml, more patients with secondary adrenal insufficiency showed severe impairment of the epinephrine response than did those without it. Peak epinephrine levels to insulin-induced hypoglycemia were significantly correlated with peak cortisol levels. In patients with secondary hypothyroidism, secondary hypogonadism, GH deficiency, or diabetes insipidus, the prevalence of severe impairment of the epinephrine response was similar to that in patients without these deficiencies. Conclusions: Impaired epinephrine secretion in response to insulin-induced hypoglycemia was frequently observed in patients with pituitary adenoma. This disorder was especially severe in patients with secondary adrenal insufficiency.

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