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Cited by 40Sexual Differentiation and DisordersAdrenal Hormones and DisordersMetabolism and Genetic Disorders

Decreased adrenomedullary function in infants with classical congenital adrenal hyperplasia.

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Kim, Mimi S., Ryabets-Lienhard, Anna, Bali, Bhavna, Lane, Christianne J., Park, Ashley H., Hall, Sandra, Geffner, Mitchell E.·2014·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jc.2014-1274PMC PMC4121032
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Abstract

CONTEXT: Classical congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency can cause life-threatening adrenal crises as well as severe hypoglycemia, especially in very young children. Studies of CAH patients 4 years old or older have found abnormal morphology and function of the adrenal medulla and lower levels of epinephrine and glucose in response to stress than in controls. However, it is unknown whether such adrenomedullary abnormalities develop in utero and/or exist during the clinically high-risk period of infancy and early childhood. OBJECTIVE: The objective of the study was to characterize adrenomedullary function in infants with CAH by comparing their catecholamine levels with controls. Design/Settings: This was a prospective cross-sectional study in a pediatric tertiary care center. MAIN OUTCOME MEASURES: Plasma epinephrine and norepinephrine levels were measured by HPLC. RESULTS: Infants with CAH (n = 9, aged 9.6 ± 11.4 d) had significantly lower epinephrine levels than controls [n = 12, aged 7.2 ± 3.2 d: median 84 [(25th; 75th) 51; 87] vs 114.5 (86; 175.8) pg/mL, respectively (P = .02)]. Norepinephrine to epinephrine ratios were also significantly higher in CAH patients than controls (P = .01). The control infants had primary hypothyroidism, but pre- and posttreatment analyses revealed no confounding effects on catecholamine levels. CONCLUSIONS: This study demonstrates for the first time that infants with classical CAH due to 21-hydroxylase deficiency have significantly lower plasma epinephrine levels than controls, indicating that impaired adrenomedullary function may occur during fetal development and be present from birth. A longitudinal study of adrenomedullary function in CAH patients from infancy through early childhood is warranted.

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Crossref · 10.1210/jc.2014-1274

Cites

25 of 25 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

9 of 35 cited sources checked · 4 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    When subjected to moderate-to-high intensity exercise, CAH adolescents with partial epinephrine deficiency show lower epinephrine and glucose levels than controls.

    “When subjected to the stress of moderate-to highintensity exercise, CAH adolescents with a partial epinephrine deficiency show lower epinephrine and glucose levels as a physiological response than controls (9,10).”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [9] Weise, 2004, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glucose elevation in response to high-intensity exercise, J Clin Endocrinol Metab source
    • cites [10] Green-Golan, 2007, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glycemic control during prolonged moderate-intensity exercise, J Clin Endocrinol Metab source

      The Results report lower epinephrine throughout exercise and lower glucose in adolescents with classic CAH at 60, 75, and 90 minutes than in controls. The study tested prolonged moderate-intensity exercise, not moderate-to-high-intensity exercise, and glucose was not lower at every time point. Page numbers were unavailable in our copy. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • Findingown data

    In CAH subjects, subanalysis before and after hydrocortisone treatment showed no difference in catecholamines.

    “However, our subanalysis of subjects before and after treatment showed no difference in catecholamines (data not shown).”
    Quote in the paperSubstantial claim
  • Findingown data

    Infants with classical CAH due to 21-hydroxylase deficiency have significantly lower plasma epinephrine levels than age-matched controls.

    “Infants with CAH (n ϭ 9, aged 9.6 Ϯ 11.4 d) had significantly lower epinephrine levels than controls [n ϭ 12, aged 7.2 Ϯ 3.2 d: median 84 [(25th; 75th) 51; 87] vs 114.5 (86; 175.8) pg/mL, respectively (P ϭ .02)].”
    • Also stated in: § Results · plain
      “The main finding of this study was significantly lower plasma epinephrine levels in CAH infants than controls [Figure 1A; 84 (51; 87) vs 114.5 (86; 175.8) pg/mL, respectively, P ϭ .02].”
    • Also stated in: § Discussion · boosted
      “This study demonstrates that infants with CAH have significantly lower plasma epinephrine levels than agematched controls, which carries significance for prediction of disease severity at an early stage in life (18).”
    Quote in the paperSubstantial claim
  • Findingown data

    In control infants with congenital hypothyroidism, plasma catecholamine levels do not differ between the hypothyroid state before LT4 treatment and the euthyroid state after LT4 treatment.

    “In our controls with congenital hypothyroidism, there were no differences in catecholamine levels between the hypo-and euthyroid states, thus eliminating a potential confounding effect of hypothyroidism on catecholamine levels.”
    Quote in the paperSubstantial claim
  • Findingown data

    Plasma norepinephrine levels do not differ significantly between infants with CAH and controls.

    “Plasma norepinephrine levels did not differ between groups [Figure 1B; CAH 1031 (719; 1187) vs controls 836 (774; 1145) pg/mL, P ϭ .6]”
    Quote in the paperSubstantial claim
  • May combine two claims. 12
  • Classified as probably not a substantial claim. 15

  • May combine two claims.

    Premisecitation

    In CAH, plasma epinephrine levels are low but norepinephrine is not affected.

    “We and others have found that, although plasma epinephrine levels are low in CAH, norepinephrine is not affected (2, 9, 10), likely due to reduced phenylethanolamine N-methyltransferase activity in the adrenal medulla (7,8), but also because norepinephrine is primarily derived from sympathetic nerve endings (9).”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [2] Merke, 2000, Adrenomedullary dysplasia and hypofunction in patients with classic 21-hydroxylase deficiency, N Engl J Med source
    • cites [9] Weise, 2004, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glucose elevation in response to high-intensity exercise, J Clin Endocrinol Metab source
    • cites [10] Green-Golan, 2007, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glycemic control during prolonged moderate-intensity exercise, J Clin Endocrinol Metab source

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Older patients with CAH have an adrenal medulla that is morphologically and functionally abnormal.

    “A normal adrenal cortex is necessary for adrenomedullary development and function in the fetus (5-8), and although older patients with CAH have an adrenal medulla that is morphologically and functionally abnormal (2, 9, 10), it is not known when this adrenomedullary disruption begins.”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [2] Merke, 2000, Adrenomedullary dysplasia and hypofunction in patients with classic 21-hydroxylase deficiency, N Engl J Med source
    • cites [9] Weise, 2004, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glucose elevation in response to high-intensity exercise, J Clin Endocrinol Metab source
    • cites [10] Green-Golan, 2007, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glycemic control during prolonged moderate-intensity exercise, J Clin Endocrinol Metab source

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Children with CAH are at greater risk for seizures, cognitive impairment, and increased mortality due to severe hypoglycemia associated with illness.

    “Further studies are needed to understand adrenomedullary morphology and function in very young children, especially those with CAH, who are at greater risk for seizures, cognitive impairment (13-15), and increased mortality (16) due to severe hypoglycemia associated with illness.”
    Quote in the paperSubstantial claim3 of 4 sources checked
    • cites [13] Hinde, 1984, Hypoglycaemia during illness in children with congenital adrenal hyperplasia, Br Med J (Clin Res Ed) source
    • cites [14] Mackinnon, 1977, Hypoglycaemia in congenital adrenal hyperplasia, Arch Dis Child source

      The case reports describe profound hypoglycaemia during illness, and the discussion calls hypoglycaemia in children with CAH a 'potentially lethal complication.' That supports a risk of death, but the paper does not establish increased mortality from illness-associated hypoglycaemia. The seizure and cognitive-impairment portions are attached to other citations, not this source. (LLM, conf=0.82)

      Experimental — accuracy not yet measured
    • cites [15] Donaldson, 1994, Presentation, acute illness, and learning difficulties in salt wasting 21-hydroxylase deficiency, Arch Dis Child source

      The ACUTE ILLNESS section (page unavailable) documents hypoglycaemic convulsions and finds lower presenting blood glucose and more hypoglycaemic convulsions among children with learning difficulties. It does not establish that hypoglycaemia caused the learning difficulties; the authors discuss several possible causes. Increased mortality is separately cited to reference 16 in the citing sentence, so it is not assessed as an attribution to this paper. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [16] Swerdlow, 1998, Mortality in patients with congenital adrenal hyperplasia: a cohort study, J Pediatr source

  • May combine two claims.

    Premisecitation

    When stressed, infants and toddlers with CAH are at high risk for morbidity and mortality from adrenal crises and severe hypoglycemia, with epinephrine deficiency possibly contributing to further risk.

    “When stressed, infants and toddlers with CAH are at high risk for morbidity and mortality from adrenal crises and severe hypoglycemia, with epinephrine deficiency possibly contributing to further risk (19).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [19] Keil, 2010, Hypoglycemia during acute illness in children with classic congenital adrenal hyperplasia, J Pediatr Nurs source

      The Introduction and Discussion say that young children with classic CAH are at risk of hypoglycemia during illness, that stress-dose hydrocortisone helps prevent adrenal crisis, and that epinephrine deficiency may contribute. But the study enrolled children aged 3–10, not infants and toddlers; it measured significant glucose lowering rather than specifically severe hypoglycemia and did not establish a high risk of mortality. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Study design and conductcitation

    The small cohort size is a limitation, but catecholamine studies in older CAH children have used similar sample sizes and show similarly significant findings, implying sufficient power with these sample sizes.

    “Although the small cohort size is an obvious limitation, catecholamine studies in older CAH children have used similar sample sizes (9, 10) and show similarly significant findings, implying sufficient power with these sample sizes.”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [9] Weise, 2004, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glucose elevation in response to high-intensity exercise, J Clin Endocrinol Metab source
    • cites [10] Green-Golan, 2007, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glycemic control during prolonged moderate-intensity exercise, J Clin Endocrinol Metab source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationcitation

    The 18% difference in basal epinephrine levels between CAH and control infants would become increasingly relevant during times of high metabolic stress, such as severe illness.

    “We surmise that the 18% difference in basal epinephrine levels between CAH and control infants would become increasingly relevant during times of high metabolic stress, such as severe illness (10).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [10] Green-Golan, 2007, Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glycemic control during prolonged moderate-intensity exercise, J Clin Endocrinol Metab source

      The Discussion (page unavailable) says epinephrine is thought to be especially important during high metabolic stress, including severe illness, and links low epinephrine to hypoglycemic crises in some patients with CAH. It does not report an 18% basal epinephrine difference in infants; the study's participants were substantially older. Thus it supports the proposed relevance of stress, but not the infant-specific measurement. (LLM, conf=0.87)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    Control infants with congenital hypothyroidism were no longer hypothyroid by visit 2 after LT4 treatment.

    “and were no longer hypothyroid by visit 2 on LT4 treatment [visit 1: free T 4 0.8 ng/dL (0.2; 2.0) (reference 2.2-5.3) and TSH 160 U/mL (75.2; 230.5) (reference 3.2-35); visit 2: free T 4 4.0 ng/dL (1.4; 4.7) (reference 1.6 -3.8 Ͻ 2 wk, 0.9 -2.2 ng/dL Ͼ 2 wk), and TSH 1.2 IU/mL (0.5; 10.8) (reference 1.70 -9.10 Ͻ 1 mo, 0.80 -8.20 Ն 1 mo); SI unit conversion ϫ 12.87 ϭ picomoles per liter].”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    In older patients, hypothyroidism increases norepinephrine levels.

    “According to studies in older patients, hypothyroidism increased norepinephrine levels (23) but did not significantly affect epinephrine (24,25).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [23] Coulombe, 1977, Catecholamine metabolism in thyroid disease. II. Norepinephrine secretion rate in hyperthyroidism and hypothyroidism, J Clin Endocrinol Metab source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Parents of infants gave written informed consent.

    “Parents of infants gave written informed consent.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The study was approved by the Children's Hospital Los Angeles Institutional Review Board.

    “The study was cross-sectional and approved by the Children's Hospital Los Angeles Institutional Review Board.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Normal development of the adrenal medulla depends on exposure to cortisol produced from the adrenal cortex, with crosstalk between cortical and medullary cells.

    “Normal development of the medulla, the major site of production of epinephrine, depends on exposure to cortisol produced from the cortex, with important crosstalk occurring between cells of the cortex and medulla (5,6).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [5] Ehrhart-Bornstein, 1997, 17α-Hydroxylase and chromogranin A in 6th week human fetal adrenals, Horm Metab Res source
    • cites [6] Schinner, 2005, Cortical-chromaffin cell interactions in the adrenal gland, Endocr Pathol source

  • Classified as probably not a substantial claim.

    Interpretationreasoning

    The higher norepinephrine to epinephrine ratio in CAH infants may reflect decreased epinephrine levels rather than increased norepinephrine.

    “In support of this concept, our study showed a greater norepinephrine to epinephrine ratio in infants with CAH than controls, although it is possible that this is more of a reflection of decreased epinephrine levels.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    The CAH patients were not sick or in distress at their study visit.

    “The CAH patients were not sick or in distress at their study visit and had cortisol 2.1 g/dL (1.2; 5.7) (SI unit conversion ϫ 27.6 ϭ nanomoles per liter).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    The 21-hydroxylase-deficient mouse exhibits severely impaired catecholamine production and structural abnormalities of the medulla and cortex as early as 1 week of age.

    “Like children with CAH, the 21-hydroxylase-deficient mouse exhibits severely impaired catecholamine production, as well as structural abnormalities of the medulla and cortex, as early as 1 week of age (11).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [11] Bornstein, 1999, Adrenomedullary function is severely impaired in 21-hydroxylase-deficient mice, FASEB J source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductreasoning

    Due to limited blood volume, metanephrine and normetanephrine levels and CYP21A2 gene analysis were not performed.

    “Due to the limited amount of blood that could safely be obtained from infants (2 mL/kg), metanephrine and normetanephrine levels, and CYP21A2 gene analysis to assess phenotype-genotype correlation, were not performed.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductreasoning

    Genotyping was not performed due to limitations on blood volume with the clinically indicated blood draw.

    “Genotyping was not performed due to limitations on blood volume (2 mL/kg) with the clinically indicated blood draw.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductown data

    One CAH baby had a congenital heart defect repair at age 2 weeks but was not acutely ill or on medications known to interfere with the catecholamine assay.

    “One CAH baby diagnosed at age 1 week had a congenital heart defect repair at age 2 weeks (3 wk prior to the study visit) but was not acutely ill or on medications known to interfere with the catecholamine assay.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    Impaired adrenomedullary function in CAH may occur during fetal development and be present from birth.

    “indicating that impaired adrenomedullary function may occur during fetal development and be present from birth.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Study design and conductown data

    Both groups consisted of full-term infants (except one 36.3-week CAH baby), appropriate for gestational age, with no statistically significant difference in age, weight, length, head circumference, or vital signs.

    “Both groups consisted of full-term infants (except for one 36.3week old CAH baby), appropriate for gestational age, with no statistically significant difference in age, weight, or length (birth/study visit), head circumference, or vital signs (Table 1).”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductcitation

    Plasma catecholamine levels were quantified by HPLC with interassay and intraassay coefficients of variation less than 5% and limit of detection less than 40 pg/mL.

    “Fractionated plasma catecholamine levels were quantified by HPLC (Quest Diagnostics Nichols Institute).Interassay and intraassay coefficients of variation were less than 5%.The limit of detection was less than 40 pg/mL with normative ranges derived from published data (17).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [17] Candito, 1993, Plasma catecholamine levels in children, J Chromatogr source

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    The institutional review board did not allow blood draws in completely healthy infants unless clinically indicated.

    “Of note, our institutional review board did not allow blood draws in completely healthy infants unless clinically indicated.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    Epinephrine is the major regulator of gluconeogenesis and glycogenolysis in the counterregulatory response to hypoglycemia in newborns.

    “Although the surge consists predominantly of norepinephrine, epinephrine is known to be the major regulator of gluconeogenesis and glycogenolysis in the counterregulatory response to hypoglycemia in newborns (12).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [12] Jackson, 2004, Plasma catecholamines and the counterregulatory responses to hypoglycemia in infants: a critical role for epinephrine and cortisol, J Clin Endocrinol Metab source
22 of 22

  • The authors state this as an assumption.

    There are no published studies on catecholamine levels in infants with CAH.

    “There is a paucity of studies on catecholamine levels in infants, and to our knowledge, there are no published studies on catecholamine levels in infants with CAH.”

  • The authors state this as an assumption.

    It is not known when adrenomedullary disruption begins in CAH.

    “it is not known when this adrenomedullary disruption begins.”

  • The paper relies on this without support.

    Epinephrine and cortisol are counterregulatory hormones that help prevent hypoglycemia.

    “Epinephrine and cortisol are both part of the stress response and, as counterregulatory hormones, also help to prevent hypoglycemia.”

  • The paper relies on this without support.

    Classical CAH due to 21-hydroxylase deficiency can cause life-threatening adrenal crises and severe hypoglycemia, especially in very young children.

    “Classical congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency can cause life-threatening adrenal crises as well as severe hypoglycemia, especially in very young children.”

  • The paper relies on this without support.

    The neonate has a physiological catecholamine surge in response to the stress of normal delivery and exposure to cold.

    “The neonate has a physiological catecholamine surge in response to the stress of normal delivery and exposure to cold.”

  • The paper relies on this without support.

    In CAH, there is deficient cortisol and aldosterone production.

    “In this condition, there is deficient cortisol and aldosterone production, potentially leading to life-threatening adrenal crises.”
6 of 6

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  1. Kim, 2014, Adrenal disorders

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Authors
Kim, M. S., Ryabets-Lienhard, A., Bali, B., Lane, C. J., Park, A. H., Hall, S., & Geffner, M. E.
Affiliations
  • University of Southern California (US)
  • Division of Endocrinology (M.S.K., A.R.-L., B.B., A.H.P., S.H., M.E.G.), Los Angeles, California 90027
Corresponding author
Kim, Mimi S.
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
2014-08-01
Volume
99
Issue
8
Pages
E1597-E1601
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jc.2014-1274
PMC
PMC4121032
OpenAlex
W2046514856
Semantic Scholar
5a72a4e940e584c74f5ae54041161f7e9305a6a6
Cited by
38
References
26
Citations by year
2026: 1 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 8 · 2018: 3 · 2017: 5 · 2016: 3 · 2015: 1
FWCI
1.23
Type
journal article
Language
en
Open access
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Abell Foundation
  • Children's Hospital Los Angeles
  • Quest Diagnostics
  • National Institutes of Health (5ul1rr031986-02, KL2TR000131)
  • National Center for Research Resources (1UL1RR031986, UL1-RR031986)
  • National Center for Advancing Translational Sciences
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
Keywords
classical congenital adrenal hyperplasia, 21-hydroxylase deficiency, adrenomedullary function, epinephrine, norepinephrine, catecholamines, infants, adrenal crisis, hypoglycemia, fetal development
MeSH terms
Adrenal Insufficiency, Adrenal Hyperplasia, Congenital, Adrenal Medulla, Cross-Sectional Studies, Epinephrine, Female, Humans, Infant, Newborn, Male, Norepinephrine, Thyroid Gland, Case-Control Studies

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