Epinephrine Deficiency in Hypocorticotropic Hypopituitary Children*

Rudman, Daniel; Moffitt, Steven D.; Fernhoff, Paul M.; Blackston, R. Dwain; Faraj, Bahjat A.

doi:10.1210/jcem-53-4-722

Cited by 40 publications

(16 citation statements)

References 37 publications

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“…They found no difference between groups in either the resting or stimulated levels of norepinephrine. They suggested that the lower epinephrine levels in hypocorticotropic hypopituitary patients may have been the result of impaired adrenomedullary enzymatic synthesis of epinephrine (20). In the present study we found the basal mean epinephrine level of GH-NORM patients was above the mean epinephrine concentration of GHND, which was in turn above the mean level of epinephrine in G H D type 1 and type 2.…”

Section: Glucose Img/ol)contrasting

confidence: 43%

“…(20) reported a 80-90% reduction of epinephrine levels both at rest and in response to exercise stimulation only in patients with hypocorticotropic hypopituitarism. They found no difference between groups in either the resting or stimulated levels of norepinephrine.…”

Section: Glucose Img/ol)mentioning

confidence: 98%

“…Although the differences in epinephrine levels between groups did not attain statistical significance in our analysis, the trend in the data agrees with the findings of Rudman et ul. (20).…”

Section: Glucose Img/ol)mentioning

confidence: 99%

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The Catecholamine Response to Hypoglycemia in Children with Isolated Growth Hormone Deficiency Syndromes and Multiple Pituitary Hormone Defects

Chalew

Kowarski

1986

Pediatr Res

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ABSTRACT. We examined the catecholamine response to insulin-induced hypoglycemia in 46 short children evaluated for growth hormone (GH) deficiency by both pharmacologic stimulation and integrated concentration of GH. Twelve patients had quantitatively normal GH secretion by both pharmacologic stimulation and integrated concentration of GH (GHNORM). Twenty-two patients had normal GH to pharmacologic stimulation but subnormal integrated concentration of GH (GHND). Twelve patients had GH deficiency by both tests (GHD): six had isolated GH deficiency (GHD type 1) and six had multiple hormone deficiencies (GHD type 2). There was no significant difference between the peak epinephrine, norepinephrine, and cortisol responses of GH-NORM, GHND, and GHD type 1 patients. The mean peak epinephrine response of GHD type 2 patients was significantly lower (564 f 561 pg/ml, p < 0.03) compared to the other patient groups. There was no significant difference between the peak norepinephrine levels between GHD type 2 patients and the remaining groups. There was no correlation between decrease in blood glucose and either increase in growth hormone, catecholamine, or cortisol concentrations. There was a significant correlation between log peak epinephrine and peak cortisol response (r = 0.53, p < 0.0002) of the 46 subjects. Neither the basal nor stimulated catecholamine levels correlated with the integrated concentration of cortisol. We conclude that 1) isolated GH deficiency is not associated with impairment of the catecholamine response to hypoglycemia; 2) impairment of the epinephrine response to hypoglycemia is only associated with multiple pituitary hormone deficiencies; 3) in children, the degree of glucose lowering is not correlated with the magnitude of peak GH, catecholamine, or cortisol responses. (Pediatr Res 20: 1097-1101, 1986 Abbreviations GH-NORM, patients with normal quantitative growth hormone levels by stimulation and IC-GH

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Section: Glucose Img/ol)contrasting

confidence: 43%

Section: Glucose Img/ol)mentioning

confidence: 98%

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The Catecholamine Response to Hypoglycemia in Children with Isolated Growth Hormone Deficiency Syndromes and Multiple Pituitary Hormone Defects

Chalew

Kowarski

1986

Pediatr Res

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“…The finding, therefore, of blunted epinephrine in the patient group is plausibly explained by reduced adrenal PNMT activity in these individuals. Supporting this view are three previous studies in ACTHand cortisol-deficient children that have reported blunted epinephrine responses (reduced by 70-90%) to hypoglycemia and exercise (34)(35)(36). It is therefore pertinent to assess other markers of ANS activity in the patient group to determine if day 1 hypoglycemia had any effects on subsequent counterregulatory responses.…”

Section: Discussionmentioning

confidence: 93%

Prevention of an increase in plasma cortisol during hypoglycemia preserves subsequent counterregulatory responses.

Shavers¹,

Davis²,

Costa³

1997

J. Clin. Invest.

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The aim of this study was to determine whether preventing increases in plasma cortisol during antecedent hypoglycemia preserves autonomic nervous system counterregulatory responses during subsequent hypoglycemia. Experiments were carried out on 15 (8 male/7 female) healthy, overnightfasted subjects and 8 (4 male/4 female) age-and weightmatched patients with primary adrenocortical failure. 5 d before a study, patients had their usual glucocorticoid therapy replaced with a continuous subcutaneous infusion of cortisol programmed to produce normal daily circadian levels. Both groups underwent identical 2-d experiments. On day 1, insulin was infused at a rate of 1.5 mU/kg per min, and 2-h clamped hypoglycemia (53 Ϯ 2 mg/dl) was obtained during the morning and afternoon. The next morning, subjects underwent an additional 2-h hypoglycemic (53 Ϯ 2 mg/ dl) hyperinsulinemic clamp. In controls, day 2 steady state epinephrine, norepinephrine, pancreatic polypeptide, glucagon, growth hormone, and muscle sympathetic nerve activity were significantly blunted ( P Ͻ 0.01) compared with day 1 hypoglycemia. In marked contrast, when increases of plasma cortisol were prevented in the patient group, day 2 neuroendocrine, muscle sympathetic nerve activity, hypoglycemic symptoms, and metabolic counterregulatory responses were equivalent with day 1 results. We conclude that ( a ) prevention of increases of cortisol during antecedent hypoglycemia preserves many critical autonomic nervous system counterregulatory responses to subsequent hypoglycemia; ( b ) hypoglycemia-induced increases in plasma cortisol levels are a major mechanism responsible for causing subsequent hypoglycemic counterregulatory failure; and ( c ) our results suggest that other mechanisms, apart from cortisol, do not play a major role in causing hypoglycemia-associated autonomic failure. ( J. Clin. Invest. 1997. 100:429-438.)

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“…Adrenomedullary dysfunction was characterized by incomplete formation of the adrenal medulla and a depletion of secretory vesicles in chromaffin cells (24). Basal and post-exercise plasma epinephrine levels were also found to be reduced in children with ACTH deficiency (27). In our study, peak epinephrine levels at ITT were correlated with peak cortisol levels, but not with peak GH levels.…”

Section: Discussionmentioning

confidence: 38%

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

Morita¹,

Otsuki²,

Izumi³

et al. 2007

eur j endocrinol

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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 ACTHadrenal 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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Epinephrine Deficiency in Hypocorticotropic Hypopituitary Children*

Cited by 40 publications

References 37 publications

The Catecholamine Response to Hypoglycemia in Children with Isolated Growth Hormone Deficiency Syndromes and Multiple Pituitary Hormone Defects

The Catecholamine Response to Hypoglycemia in Children with Isolated Growth Hormone Deficiency Syndromes and Multiple Pituitary Hormone Defects

Prevention of an increase in plasma cortisol during hypoglycemia preserves subsequent counterregulatory responses.

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

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