Normal Hypothalamic-Pituitary-Adrenal Axis by High-Dose Cosyntropin Testing in Patients with Abnormal Response to Low-Dose Cosyntropin Stimulation: A Retrospective Review

Fleseriu, Maria; Gassner, Marika; Yedinak, Christine G.; Chicea, Liana; Delashaw, Johnny B.; Loriaux, D. Lynn

doi:10.4158/ep09153.or

Cited by 19 publications

(2 citation statements)

References 23 publications

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“…Finally, because the concentration of plasma ACTH achieved is optimally in the middle of the ACTH-cortisol dose response curve, any change in the Km (shifting in the dose-response curve to the left or right) will clearly confound the results. For these and other reasons, the low-dose ACTH stimulation test has not achieved its goal of minimizing false-negative responses and has, rather, increased the number of falsely low (abnormal) results (false positives) (84, 247). …”

Section: Adrenal Insufficiencymentioning

confidence: 99%

Physiological Basis for the Etiology, Diagnosis, and Treatment of Adrenal Disorders: Cushing's Syndrome, Adrenal Insufficiency, and Congenital Adrenal Hyperplasia

Raff

Sharma

Nieman

2014

Comprehensive Physiology

122

105

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The hypothalamic-pituitary-adrenal (HPA) axis is a classic neuroendocrine system. One of the best ways to understand the HPA axis is to appreciate its dynamics in the variety of diseases and syndromes that affect it. Excess glucocorticoid activity can be due to endogenous cortisol overproduction (spontaneous Cushing’s syndrome) or exogenous glucocorticoid therapy (iatrogenic Cushing’s syndrome). Endogenous Cushing’s syndrome can be subdivided into ACTH-dependent and ACTH-independent, the latter of which is usually due to autonomous adrenal overproduction. The former can be due to a pituitary corticotroph tumor (usually benign) or ectopic ACTH production from tumors outside the pituitary; both of these tumor types overexpress the proopiomelanocortin gene. The converse of Cushing’s syndrome is the lack of normal cortisol secretion and is usually due to adrenal destruction (primary adrenal insufficiency) or hypopituitarism (secondary adrenal insufficiency). Secondary adrenal insufficiency can also result from a rapid discontinuation of long-term, pharmacological glucocorticoid therapy because of HPA axis suppression and adrenal atrophy. Finally, mutations in the steroidogenic enzymes of the adrenal cortex can lead to congenital adrenal hyperplasia and an increase in precursor steroids, particularly androgens. When present in utero, this can lead to masculinization of a female fetus. An understanding of the dynamics of the HPA axis is necessary to master the diagnosis and differential diagnosis of pituitary-adrenal diseases. Furthermore, understanding the pathophysiology of the HPA axis gives great insight into its normal control.

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Section: Adrenal Insufficiencymentioning

confidence: 99%

Physiological Basis for the Etiology, Diagnosis, and Treatment of Adrenal Disorders: Cushing's Syndrome, Adrenal Insufficiency, and Congenital Adrenal Hyperplasia

Raff

Sharma

Nieman

2014

Comprehensive Physiology

122

105

View full text Add to dashboard Cite

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“…(1, 20) Low dose (1 μg) cortrosyn (21) elicits similar cortisol responses (20, 22) with inconsistent reliability. (23) Importantly, as this test has not been rigorously validated in hospitalized acutely ill patients often with multiple co-morbidities, the accuracy by which this test validly diagnoses adrenal-cortisol insufficiency is unclear. We therefore chose to use the term biochemical adrenal-cortisol insufficiency or sufficiency in this study.…”

Section: Introductionmentioning

confidence: 99%

Clinical Factors Associated with Biochemical Adrenal-cortisol Insufficiency in Hospitalized Patients

Ben-Shlomo

Mirocha

Gwin

et al. 2014

The American Journal of Medicine

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Background Diagnosis of adrenal-cortisol insufficiency is often misleading in hospitalized patients as clinical and biochemical features overlap with co-morbidities. We analyzed clinical determinants associated with a biochemical diagnosis of adrenal-cortisol insufficiency in non-ICU hospitalized patients. Methods In a retrospective cohort study we reviewed 4668 inpatients with random morning cortisol levels ≤15 μg/dL hospitalized in our center between 2003 and 2010. Using serum cortisol threshold level of 18 μg/dL 30 and/or 60 minutes after cortrosyn (250 μg) injection to define biochemical adrenal-cortisol status, we characterized and compared insufficient (n=108, serum cortisol ≤18 μg/dL) and sufficient ( n=394; serum cortisol >18 μg/dL) non-ICU hospitalized patients. Results Commonly reported clinical and routine biochemical adrenal-cortisol insufficiency features were similar between insufficient and sufficient inpatients. Biochemical adrenal-cortisol insufficiency was associated with increased frequency of liver disease, specifically hepatitis C (p=0.01) and prior orthotopic liver transplantation (p<0.001), HIV (p=0.005) and reported preexisting male hypogonadism (p<0.001) as compared to biochemical adrenal-cortisol sufficiency group. Forty percent of insufficient inpatients were not treated with glucocorticoids after diagnosis. Multivariable logistic analysis demonstrated that inpatients with higher cortisol levels (p=0.0001), higher diastolic blood pressure (p=0.05) and females (p=0.009) were more likely not to be treated, while those with previous short-term glucocorticoid treatment (p=0.002), had other co-existing endocrine diseases (p=0.005) or received an inhospital endocrinology consultation (p<0.0001) were more likely to be replaced with glucocorticoids. Conclusions Commonly reported adrenal-cortisol insufficiency features do not reliably identify hospitalized patients biochemically confirmed to have this disorder. Co-morbidities including hepatitis C, prior orthotopic liver transplantation, HIV, and reported pre-existing male hypogonadism may help identify hospitalized non-ICU patients for more rigorous adrenal insufficiency assessment.

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Dynamic Tests in Clinical Endocrinology

2023

Endocrinology

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Normal Hypothalamic-Pituitary-Adrenal Axis by High-Dose Cosyntropin Testing in Patients with Abnormal Response to Low-Dose Cosyntropin Stimulation: A Retrospective Review

Cited by 19 publications

References 23 publications

Physiological Basis for the Etiology, Diagnosis, and Treatment of Adrenal Disorders: Cushing's Syndrome, Adrenal Insufficiency, and Congenital Adrenal Hyperplasia

Physiological Basis for the Etiology, Diagnosis, and Treatment of Adrenal Disorders: Cushing's Syndrome, Adrenal Insufficiency, and Congenital Adrenal Hyperplasia

Clinical Factors Associated with Biochemical Adrenal-cortisol Insufficiency in Hospitalized Patients

Dynamic Tests in Clinical Endocrinology

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