Late Night Salivary Cortisol in the diagnosis of neoplastic hypercortisolism (including cyclic Cushing’s syndrome)

Raff, Hershel

doi:10.1007/s11102-022-01214-2

Cited by 9 publications

(7 citation statements)

References 17 publications

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“…Salivary cortisol is an index of the free, bioactive cortisol in the blood. [38][39][40] As such, what appear to be small changes in salivary cortisol…”

Section: Discussionmentioning

confidence: 98%

“…Although this effect appeared slightly smaller at 1 month than 1 week post-injury, the nonsignificant group × time interaction implied that this elevation in cortisol persisted in the mTBI group throughout the 1-month follow-up period. Salivary cortisol is an index of the free, bioactive cortisol in the blood 38–40. As such, what appear to be small changes in salivary cortisol are translated into pathophysiologically significant changes in glucocorticoid receptor-mediated activity 41.…”

Section: Discussionmentioning

confidence: 99%

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Salivary Cortisol Dynamics After Mild Traumatic Brain Injury

Musacchio

Kallenbach

Huber

et al. 2023

Journal of Head Trauma Rehabilitation

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Objective: To assess mild traumatic brain injury (mTBI)-related alterations in baseline (resting) salivary cortisol and cortisol reactivity to cognitive and exercise stressors, which are frequently encountered during mTBI rehabilitation and recovery. Setting: Persons with mTBI were recruited from a level 1 trauma center emergency department. Uninjured controls (UCs) were recruited from the community. Participants: Participants were 37 individuals with mTBI and 24 UCs. All patients with mTBI were enrolled at 7 ± 3 days post-injury, met the American Congress of Rehabilitation Medicine definition of mTBI, and had no acute intracranial findings on clinical neuroimaging (if performed). Design: A prospective cohort study design was used. All participants provided saliva samples 10 times during each of 2 visits spaced 3 weeks apart (1 week and 1 month post-injury for the mTBI group). Each visit included baseline saliva sampling and sampling to evaluate reactivity to a cognitive stressor (Paced Auditory Serial Addition Test) and physical stressor (Buffalo Concussion Treadmill Test [BCTT]). Main Outcome Measure: Natural log-transformed salivary cortisol was measured by enzyme immunoassay. Cortisol was predicted using a linear mixed-effects model by group (mTBI and UC), visit (1 week and 1 month), and saliva sample. Results: Mean salivary cortisol was higher in the mTBI group (1.67 nmol/L [95% CI 1.42-1.72]) than in controls (1.30 nmol/L [1.12-1.47]), without an mTBI × time interaction. At 1 week, the mTBI group had greater cortisol reactivity in response to the BCTT. Conclusions: Higher cortisol in individuals with mTBI at 1 week and 1 month post-injury extends previous findings into the subacute recovery period. Furthermore, the mTBI group demonstrated a greater cortisol response to mild-to-moderate aerobic exercise (BCTT) at 1 week post-injury. Given the increasing role of exercise in mTBI rehabilitation, further research is warranted to replicate these findings and identify the clinical implications, if any, of enhanced hypothalamic-pituitary-adrenal axis responses to exercise in civilians with recent mTBI.

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“…Salivary cortisol is an index of the free, bioactive cortisol in the blood. [38][39][40] As such, what appear to be small changes in salivary cortisol…”

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Salivary Cortisol Dynamics After Mild Traumatic Brain Injury

Musacchio

Kallenbach

Huber

et al. 2023

Journal of Head Trauma Rehabilitation

Self Cite

View full text Add to dashboard Cite

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“…Diagnostic test selection may be country or center specific based on individual experience, local test performance, and patient-specific considerations. A 24-hour urinary free cortisol test, 1-mg overnight dexamethasone test, and late-night salivary cortisol measurement may all be used for initial diagnosis of suspected endogenous Cushing syndrome (Figure 2 and Table 3). In patients with an adrenal adenoma, dexamethasone suppression is the preferred initial test .…”

Section: Diagnosis Of Cushing Syndromementioning

confidence: 99%

“…For example, diagnostic biochemical thresholds established for immunoassays cannot be applied to liquid chromatography mass spectrometry because reference ranges are method and assay dependent. Oral biotin supplementation can interfere with test results when a biotin-avidin separation method is used …”

Section: Diagnosis Of Cushing Syndromementioning

confidence: 99%

Cushing Syndrome

Reincke

Fleseriu

2023

JAMA

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ImportanceCushing syndrome is defined as a prolonged increase in plasma cortisol levels that is not due to a physiological etiology. Although the most frequent cause of Cushing syndrome is exogenous steroid use, the estimated incidence of Cushing syndrome due to endogenous overproduction of cortisol ranges from 2 to 8 per million people annually. Cushing syndrome is associated with hyperglycemia, protein catabolism, immunosuppression, hypertension, weight gain, neurocognitive changes, and mood disorders.ObservationsCushing syndrome characteristically presents with skin changes such as facial plethora, easy bruising, and purple striae and with metabolic manifestations such as hyperglycemia, hypertension, and excess fat deposition in the face, back of the neck, and visceral organs. Cushing disease, in which corticotropin excess is produced by a benign pituitary tumor, occurs in approximately 60% to 70% of patients with Cushing syndrome due to endogenous cortisol production. Evaluation of patients with possible Cushing syndrome begins with ruling out exogenous steroid use. Screening for elevated cortisol is performed with a 24-hour urinary free cortisol test or late-night salivary cortisol test or by evaluating whether cortisol is suppressed the morning after an evening dexamethasone dose. Plasma corticotropin levels can help distinguish between adrenal causes of hypercortisolism (suppressed corticotropin) and corticotropin-dependent forms of hypercortisolism (midnormal to elevated corticotropin levels). Pituitary magnetic resonance imaging, bilateral inferior petrosal sinus sampling, and adrenal or whole-body imaging can help identify tumor sources of hypercortisolism. Management of Cushing syndrome begins with surgery to remove the source of excess endogenous cortisol production followed by medication that includes adrenal steroidogenesis inhibitors, pituitary-targeted drugs, or glucocorticoid receptor blockers. For patients not responsive to surgery and medication, radiation therapy and bilateral adrenalectomy may be appropriate.Conclusions and RelevanceThe incidence of Cushing syndrome due to endogenous overproduction of cortisol is 2 to 8 people per million annually. First-line therapy for Cushing syndrome due to endogenous overproduction of cortisol is surgery to remove the causative tumor. Many patients will require additional treatment with medications, radiation, or bilateral adrenalectomy.

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“…Screening for CS includes measuring salivary cortisol [2], urinary free cortisol and performing an overnight Dexamethasone suppression test [3], each with specific caveats. Excluding non-tumoral hypercortisolemia is also paramount in many patients [4].…”

mentioning

confidence: 99%

Special issue: Cushing's disease update

Fleseriu

2022

Pituitary

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Late Night Salivary Cortisol in the diagnosis of neoplastic hypercortisolism (including cyclic Cushing’s syndrome)

Cited by 9 publications

References 17 publications

Salivary Cortisol Dynamics After Mild Traumatic Brain Injury

Salivary Cortisol Dynamics After Mild Traumatic Brain Injury

Cushing Syndrome

Special issue: Cushing's disease update

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