Tc. Friedman et al., DECREASED DELTA-SLEEP AND PLASMA DELTA-SLEEP-INDUCING PEPTIDE IN PATIENTS WITH CUSHING SYNDROME, Neuroendocrinology, 60(6), 1994, pp. 626-634
To evaluate the sleep disturbances of patients with Cushing syndrome a
nd to examine the relationship between the sleep disturbances and plas
ma levels of delta-sleep-inducing peptide-like immunoreactivity (DSIP-
LI), we performed three polysomnographic/endocrinological studies in p
atients with Cushing syndrome. In study 1, polysomnography was studied
in 12 patients and 12 matched normal volunteers. In addition, DSIP-LI
was measured every 30 min for 24 h in 9 patients with Cushing syndrom
e and 12 normal volunteers. The percentage of time spent in delta slee
p (stages 3 and 4) was significantly reduced in patients with Cushing
syndrome(5.8 +/- 1.4%; mean +/- SEM) compared to normal volunteers (14
.0 +/- 2.5%) (p < 0.01). REM sleep indices, however, were not signific
antly different between the two groups. There was a significant negati
ve correlation between amount of delta sleep and 08.00 h DSIP-LI (r =
-0.43, p < 0.05), which is against the notion of a causal relationship
between DSIP-LI and delta sleep. The circadian rhythm of plasma DSIP-
LI was found to be similar in Cushing patients and normal volunteers.
In study 2, we measured plasma levels of delta-sleep-inducing peptide-
like immunoreactivity (DSIP-LI) at 08.00 h in 65 patients with Cushing
syndrome and 49 normal volunteers. The 08.00 h DSIP-LI concentrations
of 797 +/- 57 pmol/l (mean +/- SEM) in the patients with Cushing synd
rome were significantly reduced compared to the level of 1,062 +/- 99
pmol/l found in the normal volunteers (p < 0.05). In study 3, plasma w
as drawn simultaneously from the petrosal sinuses and peripheral veins
of Cushing patients. No central-toperipheral gradient for plasma DSIP
-LI was noted and neither peripheral, nor central plasma DSIP-LI was a
ffected by administration of intravenous ovine CRH. We conclude that p
atients with Cushing syndrome have less delta sleep and lower plasma c
oncentrations of DSIP-LI than normal controls, however a causal relati
onship between the two appears to be unlikely. The pituitary does not
appear to be the site of synthesis of plasma DSIP, whose source remain
s unknown.