Plasma dexamethasone and the dexamethasone suppression test

Journal o/ 4//ecrrw

Drsorders

IS (1988)

9?-100

El>eXler

JAD

00554

Plasma dexamethasone

and the dexamethasone

Irutlal and follow-up tests In depressed Gordon

F Johnson

suppression patients

‘, Glenn E Hunt ’ and Ian Caterson

i Rews~on

recel\ed

(Accepled

28 Januan

9 Fehruan

test

’

1988)

1988)

Plasma dexamethasone concentrations FoUowlng oral dexamethasone adnumstratlon v.ere exammed In 78 patients with major depression pnor to and dunng treatment The test-retest stablhty of plasma dexamethasone levels wltlun patients aas satlsfacton Hlth an overall slgruflcant posltlve correlation between tests for each patient However slgruflcant \anability was noted in lndlvldual patients Change in pre-DST cortlsol and plasma dexamethasone levels were the tHo vanables m that order of importance contnbutlng to change m DST status In studies exanunmg the cluucal utlhty of senal dexamethasone suppression tests as a guide to recolen from depresslon. the effect of banabilIty m plasma desamethasone concentrations should be taken into account

Key nsords

Dexamethasone

suppression

test, Test-retest

Introduction

In patients with depression, falure to adequately suppress plasma cortlsol followmg a dexamethasone suppression test (DST) has been advocated as 3 laboratory ad m the diagnosis, and

Address for correspondence fcssor ne\

Department

N S W 2006 Prebmmarv

of Psyclua~n

G F Johnson Um\erslty

-

0165-0327/88/$03

Shd-

Auslraha

results of ISIS study were presented al the 4th

World Congress on B~oloncai Pstch~atn _ 1985

4sscx1a1e Proof S\dne\

Phtladelphta

U S 4

stablhty,

hl;?lor depression

normahsdtlon of cortlsol response during treatment. as a guide to chmcal outcome (Carroll et al . 1981, Greden et al. 1983) The mechamsms underlymg abnormal cortlsol response to dexamethasone m depressed patients are complex but major determmants of non-suppresslon are cortlsol hypersecretion dnd the a\h~lablhty of plasma deuimethasone (Poland et al 1987) Wide lntra-lndl\ldual vanablhtb in plasma dexamethasone concentrdtlons occurs followmg dexamethasone adrrurustration and there IS an mberse cunlhnear relatlonskp between plasma cortlsol and plasma dexamethasone with slgmflcant differences In plasma dexamethasone levels

50 I 1988 Elsewer Science Pubhshers B V (Blomedul

Dlklslon)

94

between suppressors and non-suppressors dt alI samplmg times (Holsboer et al 1984 Johnson et al 1984 Arana et al 1985 Carr et al. 1986) Therefore failure to suppress plasma cortlsol ma\ result from altered hypothalanuc-pltultarqadrenal (HPA) aus function associated mlth depre5slon hut It ma\ also be deternuned by lo\i plabma dexamethasone levels Moreover. dose-response studies suggest that \ahd categonsatlon of de\amethasone huppresston status can best he made u hen plasma delamethasone levels he ~lth~n a defmed range or mmdob Tlus detects patlent> Hhohe plasma dexamethasone levels are too Ion or too hqJ~ leadlng to false-posltlbe or false-negatl\e result5 respectIveI> (Johnson et al 1987) Recently. test-retest \ranablllt> of plasma dekamethahone concentrations has been reported (Johnson et al. 1986 Berger et al 1985 Baumgartner et al 1986, Holshoer et al 1986 Carson and Halbrerch. 1987) Where change In DST 3tatus ulth benal testing IS to be used to monitor cluucal recovery. changes In plasma dexamethasone levels may confound the slgruflcance of change m DST status particularly normahsatlon The follobmg report exanunes the stablhty of plasma dexamethasone concentrations hetkbeen tests m 78 patients with major depresslon and evaluates the contnbutlon of change m dekamethasone concentratlonb and change m predexamethasone plasma cortlsol levels to altered DST status Methods

Patients mlth maJor depression uere selected from consecutl\‘e adrmsslons to the Affective DISorders LJtut. Royal Prince Alfred Hospital Dlagnoses were made Independently hq two psychsatnsts usmg DSM-III cntena (Amencan Psycluatnc Association 1980) A 2-5-day basehne stahlhsatron penod was obsened pnor to the Imteal DST Patients were rated on a 21-Item Hamilton Rating Scale for Depression (Harrulton 1960) Routine laboratory tests Included h\er and thyroid function tests and the usual exclusion cntcna nere applied as detailed elseuhere (Carroll et al 1981. Johnson et al 1984) During treatment and pnor to discharge cluucal ratings and a repeat DST aere obtained In 78

patients out of 145 consecutlbe adrru~~lons \\lth m.qor depresblon Special effort> were taken to obtain a follow-up DST In patients who were non-suppressor> on the lmtlal test Flfti-se\en ot the 145 consecutl\e admIssIons Here non-supprebsors on rrutlal testing of which 37 had a repeat DST The other 41 patients that had a repeat DST Here suppresborb on the mltlal tebt T\\entb-se\en of the Inltlal patient3 sampled \\ere part of a pre\ IOUS report In\ esttgatlng plasma dekamethasone and plasma cortlsol and DST (Johnson et al 1984) Patients recelred chmclan’b choice of treatment such as electrocon\ulsr\e thrrapq (ECT) or antrdeprebsant< Adequac! of antldepressant drug treatment was morutored by routine plasma Ir~el ashay Pm edures

The DST procedure has the same on adnusslon and dl.scharge Blood for plasma cortlsol teas collected at 4 p m on day 1 and tbo 0 5mg tablet5 of deuamethasone \\ere adnutustered orally at 11 p m On da> 2 blood \\as collected for corttsol and dexamethasone assay at 8 a m and 4 p m The cntenon for non-suppression \\a5 a plasma cortisol concentrdtlon greater than 139 nmoljl (5 pg/dl) Plasma cortlsol was measured hq radlolmmunoassaq (RIA) (Chmcal Assaks Cambndge. hlA) The Intra- and Interassav coefflclents of Lanatlons uere less than 105 Dexamethabone was also measured by RIA. the standard used was 9n-fluor-lip 17 21-trlhvdrouh-16n-methyl-l 4pregnadlen-3.20-dlone (Stcralolds WIlton, NH) and the tracer \\as [6 7(n)- ‘Hjdevamethasone (New England Nuclear Boston MA) The antiserum to deramethasone was from RIA-Labor (Prof Vecsel Pharmakologrsches lnstltut der Unrversltat Heidelberg) The mtra- and Interassaq coefflclents of lanatlon \\erre less than 100; and the assay \\as sen>ltl\e to less than 0 3 nmol,#l Several btudles have reported the cross-reactlrlty betueen dexamethasone and cortlsol to be less than 25 (Hlchenb and Hogans 1974 Enghsh et al 1975 Kaaal et al 1985) and the cross-reactlon between devamethasone and its maJor metabohtes, h-hqdroxy-deuamethasone and 20-dlh>drodexamethasone to be less than 14 (English et al 1975)

The data were analyed using chl-sqtwe Imear regresslon analysis of vanance nlth repeated measures and multtple regression analysis usmg a standard statlsttcal package (Not-us15 1985) The results In tables and text are eupresbed ~5 mean f SD Results Details of the 78 patients studled and thetr DST status (suppressor or non-suppressor) on adnuwon and pnor to discharge are shown m Table 1 DST status did not change m 44 patients hho uere either suppressors (group 1 II = 32) or nonon both test5 (group 4. 11= 12) suppressors Change from non-suppresston to suppresslon occurred In 25 patients (group 3) and con\ersel> from suppresston to non-suppresslon m rune patlents (group 2) There Here no slgmftcnnt dlfferences bet\\een the four DST groups and age Height. gender. duratton of hospltahsatlon or proportlon of pattents Hlth melanchoha (Table 1) Seventy of depresslon as measured by the 21-Item Harrulton Depresston Rating Scale Has not stgtuflcantI! drfferent between suppressors and non-suppressors on mltlal rutmg or pnor to discharge Furthermore. none of the subfactor scores on the Hanulton scale were slgruflcantly dtfferent be-

TABLE

tHeen the groups Smular chrucal Improvement ds reflected bv decreased Hanulton scores pnor to dtscharge uas observed In all four groups (Table 2) 41~0. there Here no slgmflcant differences In treatment allocatIon such as ECT or sntldepressant medlcatton between the groups (Table 2) Mean plasma dexamethasone concentrations mere slgruftcantI\ different beween suppressors and non-suppressors on both lrutlal and follow-up testmg On Inltlal testing the plasma dewmethdsone concentratlom In suppressors \\ere bgher compared to non-suppressors at 8 J m (11 7 + 5 5 1s 79+31 nmol/l) and 4 pm (43t27 \s 25kl 1 nmol/‘l) (I= (1 76)=1339 and 1383 P < 0 001. re5pectl\el>) Slnular differences \\ere obsened on folloa-up between suppressors and non-suppressors at 8 a m (13 1 f 5 2 ~‘5 9 3 f 6 5 nmol/l) and at 4 p m (4 S f 2 7 15 2 7 f 1 6 nmol,/l) ( F = 7 02 and 8 60. P < 0 005 respectirelb) The 4-p m plasma deuametha\one lebels on first and second testmg (DSTl and DSTZ) are shoHn for each pattent In Fig 1 Overall there WJS a posrtlve correlation between 4-p m plasma dexamethasone levels between tests for all patients (r = 0 62) Hoaeker conslderable differences betHeen tests occurred In some patients Afternoon dexamethasone concentrations waned more than

1

DET4ILS

OF P4TIENTS

WITH

MAJOR

DEPRESSION

ON

suppre\sors

Suppre,bor

on both

non-supprebwr

(group

1)

(group 2)

10

ADh~ISSIOlu

AND

PRIOR

TO DISCHARGE

(n = 78)

Non-

Non-

Total

suppressor

suppressor,

(hfean _+SD)

lo suppresbor

on both

(group 3)

(group 4)

hlales

13

4

9

7

33

Female\

19 -

5 -

16

5

45

37 L

9

25

12

7x

4ge

51

36

48

58

49 & 2

Weight (kg) Da\\ heluecn

66 5

64

59 4

63 1

64 t

32

31

36

35

34+’

Total

1SStS

DSM-Ill Mqor

1

draqnosrs depresslon

with melanchoha ~lth pswhow features onI\ ’ Numbers

”

I6

5

13

4

38

14 (6)

4

10 (3)

5 (31

33

2

0

2

shown m parentheses are Ihe wbset of pauents \slth mel~choha

3 and psvchotlc feaures

7

1

1 7 nmol m 22 patients (1 7 = standard error of the estunate for the lmear regresslon equation). and for ten of these patients the \anahlhtj mas greater than 3 4 nmol/l (Patients 20 25 28 29. 30. 32. 34 50. 66. 75. FIN 1 ) Mean plasma devamethasone levels remalned relatl\ely stable In the tno groups *hose DST status did not change although the absolute concentratmns were h&er m the suppressors on both tests compared to the non-supprebsors (two upper panels Fig 2) Thus IS In contrast to the tugher mean plasma dexamethasone levels on the second test m patrents that changed from non-suppressor to suppressor (lower nght panel Fig 2) Thus Increase was pnmanlq due to SLYpatients H hose dexamethasone levels rose from a range of 2-4 to 4-10 nmol/l (patrents 20 29 32 35. SO and 68 Fig 1) Conversely there was a fall m plahma dexamethasone on the second DST m tao of the rune patients that were suppressors on Irutlal sampling. and non-suppressors on folkw-up testing (patients 1 and 30 Fig 1) In one female patient from group 2 (patient 30). plasma dexamethasone fell from 10 5 to 1 2 nmol/l on retesting Thus patient had a kstory of I v drug abuse and be-

cause she was ldentlfled a5 an outlrcr she nds excluded from the analqsrs The slgmflcant sbfts m plasma drxamethasone that occurred m some patients could not be explamrd b> age wevght. se\ (open and filled circles In Fig 1) or presence of melanchohc feature> (patients 39-71) hloreobrr treatment per se did not explain the dramatlc shfts m dexamethasone concrntratlons between tests The net change In 4-p m plasma dexamethasone from test 1 to test 2 In the three patients treated Hlth loa-dose benzodlazepmes bias 0 2 nmol,‘l. m the 40 patients takmg antidepressants the Increase was 0 5 nmol/l for the >e\en patients takmg antldeprcssants and hthwm there NJS a net Increase of 1 5 nmol/l and for the SLX patients takmg both antidepressants and neuroleptlcs the net glun uas onlb 0 1 nmol/l The effect of ECT on plasma devamethasone levels was slnular to the group @Len antldepressants wth a net gam In deuamethasone of 0 6 nmol/ I on the second DST Pre-DST plasma cortlsol values on mltlal and folk\\-up testing are Illustrated In Fig 2 for each of the four groups Pre-DST plasma cortlsol concentrations uere lugher in non-suppressors (447 +

97

12

10

0

MALES

0

FEMALES

8

8” 8

6

4

2

(I

suppressors on Fig

1 Afternoon

lo discharge

(4 p m

(DSTZ)

) plasma

male pallenls

ulth

concentrahons

mayor deprewon

17 h folloamg

Numhers

1-38

on

1 mg dexamethasone Into four group,

both

on adnusslon (DSTl) accordmg

of 139 nmol,‘l

are patients ullh

features

DST2

non suppressors

suppressor

corhsol cnwnon

are pauenls ulth prvchotlc

191 nmol/l) compared to the suppressors (314 f 179 nmol/l F = 9 66. P < 0 005) Seventy-four per cent of the non-suppressors had afternoon (4 p m ) pre-DST cortlsol concentrations abobe 300 nmol/l on the uutlal test. whuzh IS above the 9S? confidence mtenals for normal controls There was a fall m pre-DST cortlsol on folio\\-up testing m patients who suppressed on both tests or whose

DSTl

nonsuppressor to

on borh teals using a posr-dexamelhasone

and numbers 72-78

DSTZ

Pauenrs are dlwded

and fllled Lucles Indicate female patlenls

are pattents ulth melanchoha

DSTl

to

nonsuppressor

dexamethasone

In 78 pauents

DSTZ

suppressor

both

(suppressors or non-suppressors) mdlcate

DSTl

DSTP

DSTl

10 their

(5 pg,,dl)

major depressmn

and pnor DST

EMU\

Open circles

number> 39-71

Mean Lalues for each column appear In Fig 2

DST status changed from non-suppresslon to suppresslon (upper left and lower right panels. Fig 2. respectively) Pre-DST cortlsol values were hqgher on retestmg m the patients that snItched from suppressors to non-suppressors (louer left panel) and remalned elevated throughout hospltahsatlon In the patients that were non-suppressors on both tests (upper r&t panel) Three of the SIX patients

9x

Flp

2 Afternoon

connectmg

(3 p m

groups according rerpecu\el\

cornal

Ths MC) bottom

alrchcd

non-suppresston

plabma sorucol (whd

tDSTlt

and pnor

to thelr DST SIJIU~ on adnuwon

right panels rhow pre-DST SMUI

I pre-DST

cIrcIes) on ndrm,smn

from

and pnor

and dexamethaone IO non-bupprewon

IO supprewon

(loner

quarest

to dwhrlrge

(loser

Isft

right panel) lndute

~+lth rdlsed dexamethasone lebels on follow-up from group 3 (patients 32 35. 68) had elevated pre-DST cortlsols throughout hospltahsatlon Stepwse multlple regresston analysis mdlcated that differences m pre-DST cortlsol values from test 1 to test 2 could explain 195 of the lanablhty In post-DST cortlsol values A further 6% of the vanabthty could be evplalned by changes In plasma dexamethasone levels No other variables such as age. sex, or treatment dunng hospt ahsatlon. had a slgmflcant Influence on predlctlng change In postDST cortlsol values Analysts of the residuals mdlcated no sequential effects ober time of study equahty of vanance and a normal dlstnbutlon A multtple regression analysis of all patients uho here non-suppressors on dt least one test (groups 2, 3 and 4) mdtcated that the drfferences rn preDST cortlsol levels \bere kghly correlated Hlth changes In post-DST corttsol lebels (r = 0 52) and could account for 27% of the kanabrhty As before differences m plasma dexamethasone levels mere negatively correlated v+tth change In postDST cortlsol (r = -0 34) and could explam a further 7’F of the vanabIlIty

and dcxameth~ronr

In 7X depreurd

Lortlwl

pAneI)

patents

concenrr~wn~

Patlent:. uerr

ullng rl cor~~~ol cn~enon of 139 nmol

plasma levels 111wppreaors

panels Illustrrlte the change> In pre-DST

suppressmn

t DST pou~l\e)

bnes connecung

IO discharge (DSTZ)

and

I

an both tests and non-uppres,ora

and plJ\nu In pdtwnt,

dr\ameth~wnr uhose

DST

tdotwd

dl\lded lipper

left and

on both W>I~

In parwnrb uhow SUIU>

The number ot patwnrs In rJLh group 13 g\en

Ilnex

Into four

nornulwd

DST from

In Table 1 T-burl

1 SEhf

Dwuwon

Vanablhty In plasma de\amethasone concentrations was exanuned In 78 patient> nlth major depression pnor to and during antidepressant treatment The test-retebt stablhty of plasma dexamethasone concentrations hlttun patients UJS ~lth an overall slgmflcant posItIke satisfactory correlation between plasma dexamethasone Ielels between test> for each patient However mdt\ldual analysis shoaed wide differences In dexamethasone concentrations m some patients at both 8 a m and 4 p m Ths uas ebldent both m patients whose DST status did not change between tests buch as those \rho Here suppressor5 throughout, and In those In \\horn DST status changed on follow-up testmg The extent of change In plasma dexamethasone concentrations was substantial m some patients hlth 4-p m plasma dexamethasone levels varying by a factor of more than 1 7 nmol/l m 22 patients and In ten of these the difference betbeen tests nas greater than 3 4 nniol/l

Preblous reports habe dlffered on the extent of test-retest stablIlt of plasma dexamethasone and Its chrucal slgruflcance Carroll et al (1980) reported only nunor banablhty rn plasma dexamethasone concentrations m four patients studied dunng Illness and after recovery despite change in DST status from non-suppression to suppression Honever. Berger et al (1985) reported substantial vdnatlon rn plasma dexamethasone levels at 9 a m In 12 patients Hlth at least three senal DSTs dunng hosprtahsatlon They concluded that there was a hnuted mtra-mdlbldual stablhty of dexamethasone pharrnacokmetlcs Smularly. Baumgartner et al (1986) reported wide mtra-lndl\ldual vanatlon In dexamethasone concentrations dunng senal testing m 26 patients with major depressl\e disorder A progressive fall m mean post-dexamethasone cortlsol concentrations over 5 weeks however \\as not accompamed by any slgmficant changes In mean dexamethasone concentrations It was concluded that tlus has not a slgmflcant factor m change m DST status Holsboer et al (1986) reported a slgmflcant nse In plasma dexamethasone concentration In 31 depressed patients who showed lrutral non-suppresslon of cortrsol. but Bho became suppressors dunng treatment. whrle 14 patients uho were suppressors on both tests sho\hed no slgruflcant difference In deKamethasone concentratrons In contrast. Carson and Halbrelch (1987) reported no slgmflcant change overall In plasma dexamethasone concentrations m 15 patients with major depression pnor to and durmg treatment mcludlng those whose DST status changed from non-suppresslon to suppresslon However. slgmfrcant banability was noticed In mdlvldual patients. particularly those v. ho remained suppressors throughout. suggesting an effect of treatment or change In chrucal status, on dexamethasone pharmacokmetlcs The mecharusms underlying vanablhty m dexamethasone concentrations are uncertam but may result from changes m absorption. metabohsm or ehmmatron of dexamethasone Holsboer suggested that a ION plasma dexamethasone level In nonsuppressors ts a state-dependent phenomenon resulting from accelerated metabohsm of dexamethasone wluch normabses on chrucal recovery Whle such a general trend was not observed m thrs study tbs mecharusm cannot be excluded m

the SIX patients who showed marked increases in dexamethasone levels associated ulth change in DST status from non-suppression to suppression Test-retest differences did not appear to be dssoelated with treatment allocatlon. either ECT or antidepressants or the presence of other psychotropic drugs The slgmflcance of althm-patient Lananon in plasma dexamethasone levels depends on the extent and direction of the change m plasma levels lrutlal DST status, and concurrent changes in predexamethasone plasma cortlsol A nse m plasma dexamethasone levels m patients who are uutlal suppressors or a fall m patients Hho are uutlal non-suppressors IS hkely to be of less slgmflcance than a nse m plasma dexamethasone m mltlal non-suppressors or a fall m uutlal suppressors that may contnbute to change m DST status Thus IS Illustrated m three of the SIX patients with railsed plasma dexamethasone levels on follow-up whose change In DST status from non-suppressor to suppressor occurred despite elevated pre-DST cortlsols throughout hospltahsatlon Recent studies by Holsboer et al (1986) and Wledemann and Holsboer (1987) report that early blophase lunetlcs of dexamethasone are rndlstmgulshable among DST suppressors and nonsuppressors, raising doubt as to the Importance of actual plasma dexamethasone levels 9-17 h following adnumstratlon In deternunmg DST response Studies to examme the relatlonsbp between early blophase kmetlcs and plasma levels 9-17 h followmg and the relatlonshrp to plasma ACTH-cortlsol response are currently under day In our laboratory Whole change m plasma dexamethasone levels was a slgmflcant deternunant of change m DST status m some patients difference In pre-DST plasma cortlsol levels between tests uas the most Important deternunant of change In post-DST cortlsol lebels Thus IS consistent with other studies showing cortlsol hqpersecretlon to be a slgmflcant detemunant of non-suppresslon of plasma cortlsol followmg dexamethasone adnumstratlon (Asms et al, 1981. Poland et al. 1987) The changmg Interactions between pre-DST plasma cortlsol and plasma dexamethasone dunng treatment appear to largely determme the test-retest differences In DST status

In the majonty of patients chrucal Improvement, as measured by change m Hanulton scores on follow-up. uas accomparued by a fall m preDST

plasma cortlsol

To the extent that elevated

4-p m plasma cortlsol concentrdtlons are d rehdble Index of Increased HPA axis function (Astus et al 1981, Chnstensen et al 1985). their fall durIng treatment with a concurrent change from non-suppresslon to suppresslon m some patients 15 conslstent with reports that normahsatlon of the

Chnstensen L

t 19851 rwn

J

Dlsord

Chn BJ

and

J

hfarkb

R

Kronfol

Z

Pavctiatrv

Holsboer

hl (1960)

tlcal Manual ctuatnc Arana

Assoclatlon

of hlental

Assoclatlon

G W

G hf

Sachar

Ostron 138

Arch

3rd edn

E J

and Stall>-

Amencan

Psb-

M

(1985)

Psq&atn

Halbrelch

U

F S (1981)

42

The

and progNathan

R

Cortlsol secretIon and

response m depressIon

Am

J

Pswzhratn

D

dersmethasone F

A

Haack

D and Vecsel

P (1986) Senal De~a-

Gerken

K

half-bfe Gen

G

Hunt

methasone

M

Parke

K -M , Kneg

The effect of #e&t

dexamethasone

18

levels

J-C

and

Von Zerssen

loss and mappropnate

on

the

DST

P\vchatr

D

plasma Re,

15

351-360 V

Moms

H

and Gdhland

serum dexamethasone BJ

Schroeder,

Femberg

M

methasone rponse

Metab Felnberg

Haskett

R

James

DeVlgne

(1986)

and

of

tn the dexamethasone

Mukhopadhvav

ulth

The effect

Johnson

S

Greden

J (1980)

cortlsol

endogenous

J F

Plasma dexa-

suppressjon

depresston

J

reClan

bup-

m dcprss-

E (1986)

Shortened non-

813-815

A

kanable

and Boll

E 11986)

m deprebw~n

htophase hmetlo Kerr

tcst-re-

Ps\chatrv

K

md

Reb 17

I

Catcrson

test (DST)

G

Hunt

G

\one levels Johnson

G

Kerr

K

supprewon

(1984)

and plasnw Pbbchatr

Proceedings

IV World

Phladelpba Hunt

G

U S 4

Kerr

dekamethasone test

K

plasma

dexa-

Res

13

(1986)

The

dexametha-

Congress on Bmlo@cal

Elsekler

Amsterdam

I

and Caterson

nlndo\s

In

1

and Catcrson test and

11987)

The

and the devamethasone

depresslon

N

Greden MLI

J and Young

J F

, Kronfol

Tanka Z

J

Lobr

Albald N

A

Stemer

E (1981) A speclflL laboraton Arch

Gen

Psvcbatn

SW

213-216

S

Ich&.wa

metabolic

and Halbrelch cortlsol

U

1

Blol

and Homma

propertles

dexamethasone

m

among

Ps\cbatn

Il\er

22

Endocnnol

Metahol

M J (1985)

Poland

R E

(1987)

and dexamethasone

Effect of treatment Btol

Psbcluatn

on 22

accelerated

flulure

J

Chn

60 848-854

SPSS-Y

Rubm

Advanced

R T

Lesser

Neuroendocnne

depressmn

SI~IISIICS Guide

II

Serum

Pshchatn K

sane bnetlo admuustratmn

I

hf

Lane

LA

aspects of pnman

deuamethabone

hvpoth~amcFpltult~,n’-adrcnal

Wledemann

dl>ea>es

In rend

m and

hlc-

Cbcago

P J (1987)

Gen

Dlfferenceb

predntsolone

mind rend

of dexamethasone

Norusls

hl (1985)

cortlsol

metdboh,m

1340-1348

18 15-22 pla>ma

Kaua~

nantr of the dexamethasone

51 433-437 M

test for the &agnosls of melanchoba Carson

(198-I)

19 2X1-291

Gerken

supprewon

dexamethasone

Gras-HIII

21 735-743

and Tanka,

concentrations

EndoLnnol BJ

K

, RIC~K J

In pattents

J

concentrations

suppresslon test BIOI Psychatry

M

P

1015-1039

(1985)

Carroll,

\ecsel

and dlfferenual

levels III depressed pa:lent>

suppressmn

Carroll

and

Psvcluatrv 43

G

Desamethasone

Res

Carr

4

for

97-103

The mfluence 45-64 Bergcr

Neuro-

20 266-271

and Boll

K

test ,tudles and earl\

plasma

Psvchtatr

Arch

m depressed dcvamcthasone

Wledemann

Pan III

banables

The pro-

J Nsurol

Chem

BIOI Ps\cbatn

Arch

methasone SuppressIon Tests In psvch~atnc Illness of mtenemng

Carroll

of melJncholla

concentrations

Wledemann

Pskcbatn

1218-1221

Baumgartner,

L

Supprerslon

305-313

1193- 1204

&an-u

Grunbau\

response of cornsol and CortIcosterone F

Johmon

DC

Test for dlagnow

Gen

L and Halpem

dexamethasone

Dtagnostlc

R J and Omsteen

SuppressIon

noIts m psqcluatry Asms

Dlsorderr

Washmgton

Baldessanru

Dexamethasone

(1980)

D

Dexamethasonr

Chn

The plasma dexamethasone Psvchatnc

J

4 F (1974~ Radw1mmunodb,a\

m plasma

Haack

suppressors

Amencan

9

Eur

4 ratmg for dcprebslon

sI\es and control>

Holsboer

(1975)

treatment

Plasma dexamethasone

Holsbocr

4

and test-retebt reproduclblht\

and Hogans

pre,slon

V and Parhe

23 56-62

dexamethasone F

H ‘I

III deprcs-

40 493-500

.rurg Psbchatn

cal recovery m patients Nlth depresslon should. however, take mto account the effect of \anahlhty

cortlsol

for dexamethasone

hng (1983)

Tebts m antIdepressant

hl

Chn>tenwn

9 239-244

Gardner

cew of normallratlon Gen

P

and Thomsen

plasma

procedure

Pharmacol J F

0 L

8 271-278

Chahrabortb

Greden

Kragh-Sorenwn

Pedersen afternoon

radlolmmunoassa\

Hlchem

References

L F

C B

J 4ffec1

Enghsh

Studies exanunmg the chmcal utlhty of the dexamethasone suppresslon test to motutor chru-

m plasma dexamethasone concentrations To do ths requires simultaneous measurement of plasma dexamethasone and plasma cortlsol

Gram

Spontansous

Harmlton

DST comcldes with chrucal Improvement

P

Knrtensen

and Hart endogenous

concentratmns

cortical suppres\ton

rlctnlt\

dnd

as deternu-

test response

4rLh

44. 790-796

and Holxhoer dunng of

F

the DST the

te\t

(1987) after drug

Plasma dewmethdoral and Intra\enou\ BIOI

Ps\cbJtn

72