Hair cortisol content was not associated with a cumulative disease severity index.

Hair cortisol was positively related to eosinophil levels.

Hair cortisol was negatively related to HbS.

Hair cortisol content was not associated with Hb level, white blood cell count, mean corpuscular volume, differential lymphocytes, differential monocytes, platelets, reticulocytes, blood urea nitrogen, creatinine, uric acid, total bilirubin, aspartate aminotransferase, alkaline phosphatase, albumin, or fetal Hb.

Hair cortisol was positively associated with serum cortisol, corticosterone, and progesterone.

Morning saliva cortisol and diurnal cortisol ratio were not significantly different among participants with SCD relative to the control group.

Cortisol profiles

Participants with SCD displayed either normal cortisol profiles (n = 8) or flat cortisol profiles (n = 13).

Morning saliva cortisol was lower in participants with flat cortisol profile relative to participants with a normal cortisol profile.

Diurnal saliva cortisol was higher in participants with flat cortisol profile relative to participants with a normal cortisol profile.

Morning saliva cortisol was negatively correlated with wake time for participants with SCD.

Participants with a flat saliva cortisol profile had a later wake time and higher central phase relative to participants with a normal cortisol profile.

Comparisons across cortisol profiles were not statistically significant for total sleep time, bedtime, sleep onset latency, night waking, wake bouts mobile minutes, or fragmentation index.

Comparisons across cortisol profiles were not statistically significant for full scale IQ, verbal comprehension index, perceptual reasoning index, working memory index, and processing speed index; however, each index was lower in participants with a flat cortisol level (not statistically significant).

Serum cortisol was significantly lower among participants with SCD (total sample and steady state) relative to the control group.

Serum cortisol was not significantly different among participants with SCD during VOC relative to the control group.

Serum cortisol was significantly higher in participants with SCD during VOC relative to participants with SCD in steady state.

Serum cortisol in participants with SCD during VOC was not associated with verbal pain scores upon admission or number of days spent in the hospital.

Serum cortisol was significantly higher in participants with severe SCA compared with patients with mild SCA.

Cortisol-to-copeptin ratio was higher in subjects with severe SCA compared with those with moderate SCA.

Cortisol-to-CRP ratio was not significantly different across disease severity groups.

Plasma cortisol was significantly lower among patients with SCD relative to the control group.

Plasma cortisol was not significantly different among participants with SCD relative to the control group.

Plasma cortisol was not significantly different among participants with SCD receiving hydroxyurea relative to participants with SCD not receiving hydroxyurea.

Plasma cortisol was not significantly related to VOC frequency during the year before blood draw.

Plasma cortisol was not significantly related to age, gender, melatonin level, weight, height, or body mass index.

Serum cortisol was significantly lower among participants with SCD relative to the control group.

4.8% of participants with SCD (4/82) displayed low cortisol (defined as morning cortisol of <190 nmol/L).

Serum cortisol was not associated with ferritin level.

Of 9 participants with SCD, 1 (11%) displayed elevated serum cortisol level (defined as cortisol range of 44-1030 nmol/L).

Morning serum cortisol was significantly lower among participants with SCD relative to the control group.

ACTH-stimulated cortisol level 60 minutes after stimulation was not significantly different among participants with SCD relative to the control group.

Morning serum cortisol was inversely correlated with serum iron levels, and it was positively correlated with total iron binding capacity.

Morning serum cortisol was inversely correlated with ferritin level.

Basal plasma cortisol was not significantly different among participants with SCD relative to the control group.

ACTH-stimulated cortisol level 60 minutes after stimulation was not significantly different among participants with SCD relative to the control group.

Basal plasma cortisol was not significantly different among participants with SCD relative to the control group.

Peak ACTH-stimulated cortisol level was not significantly different among participants with SCD relative to the control group during the 180-minute test.

Of 38 participants with SCD, 24 (63%) displayed low serum cortisol (defined as <7 μg/dL) on at least 1 occasion.

When only morning cortisol values were considered (4 AM to 8 AM), 13 of 20 (65%) of participants with valid samples displayed low serum cortisol

Of 16 participants with low cortisol (defined as <7 μg/dL on at least 1 occasion), 10 (63%) showed cosyntropin-stimulated cortisol increases to ≥18 μg/dL after 1 hour.

Of 36 participants with SCD, 7 (20%) displayed suppressed plasma cortisol (defined as cortisol of <100 IU/L)

Plasma cortisol was not correlated with opioid dose.

Plasma cortisol was significantly lower among male and female participants with SCD relative to male and female controls, respectively.

Plasma cortisol was not significantly different among male participants with SCD relative to female participants with SCD.

Plasma cortisol was not significantly different across disease severity groups (measured using a cumulative disease severity index) among male and female participants.

Plasma cortisol was significantly lower among participants with SCD relative to the control group.

Plasma cortisol was not significantly correlated with luteinizing hormone, follicle stimulating, and testosterone.

Plasma cortisol among participants with SCD was positively correlated with pain intensity (measured using the visual pain analog pain scale)

Plasma cortisol was positively correlated with oxytocin.

Plasma cortisol was significantly lower in participants with SCD relative to healthy controls (HbAA).

Plasma cortisol was not significantly different in participants with SCD relative to participants with sickle cell trait (HbAS).

Plasma cortisol was significantly lower than the normal range (defined as 165-825 nmol/L) in 9 of 36 participants with SCD.

Plasma cortisol was significantly higher in participants with SCD during VOC relative to participants with SCD during routine clinic appointment.

Baseline plasma cortisol was not significantly different among participants with SCD during steady state relative to the control group.

Baseline plasma cortisol was significantly lower in participants with SCD during VOC relative to the control group.

Plasma cortisol was not significantly different among participants with SCD during VOC relative to repeated measures plasma cortisol among the same participants in steady state.

Plasma cortisol was not significantly different among participants with SCD during VOC relative to participants with SCD in steady state 60 minutes after ACTH stimulation.

Plasma cortisol was not significantly different among participants with SCD during VOC and in steady state relative to the control group at 30 or 60 minutes after insulin stimulation.

Plasma cortisol was significantly lower in participants with SCD during VOC relative to the control group at 90 minutes after insulin stimulation.

Plasma cortisol was not significantly different among participants with SCD without VOC relative to the control group at 90 minutes after insulin stimulation.

Basal plasma cortisol was not significantly different among participants with SCD relative to the control group.

ACTH-stimulated cortisol level was not significantly different among participants with SCD relative to the control group at 30, 60, and 120 minutes after stimulation.

Basal plasma cortisol was not significantly different among participants with SCD relative to the control group.

Plasma cortisol was not significantly different among participants with SCD relative to the control group 60 minutes after tetracosactide stimulation.

The change in plasma cortisol from baseline to after tetracosactide stimulation was significantly lower among participants with SCD relative to the control group.

Of 10 participants with SCD, 5 (50%) did not achieve “optimal adrenal stimulation” (defined as reaching a twofold increase of basal plasma cortisol) after tetracosactide stimulation.